Cardiovascular System Flashcards
1
Q
The heart accounts for how much total body weight?
A
0.6% (except in greyhounds and TBs
2
Q
The heart is usually located between which ribs?
Which side is closer to the thoracic wall?
A
3rd and 6th
Left side
3
Q
In the young animal, the cranial aspect of the heart is related to what?
A
The thymus
4
Q
The pericardium is a serous sac lined by ___________ ______________ ______________. It’s layers include:
1). ____, 2). _____, 3). _______.
What are its functions?
A
Simple squamous mesothelium
1) . Visceral pericardium
2) . Parietal pericardium
3) . Fibroelastic tissue layer of parietal pericardium
Function: maintain ❤️ position, minimise friction, prevent over-distension
5
Q
The fibroelastic layer of parietal pericardium continues dorsally over the great vessels. Caudally, it attaches to the sternum. What is this attachment called?
A
In ruminants, the attachment is a pair of sternopericardiac ligaments. In the horse, it’s a single midline sternopericardiac ligament.
In carnivores and the pig, it actually attaches to the diaphragm as the phrenico-pericardiac ligament
6
Q
Describe the cardiac notch and it’s clinical sig?
A
It’s the gap on the ventral border of the left and right lungs which allows the pericardium to make contact with the thoracic wall. It is greater on the left side thereby providing a useful acoustic window for echocardiography
7
Q
What is cardiac tamponade?
A
Compression of the heart
8
Q
The position of the interventricular septum is marked externally by the __________________ on the left and the ________________ on the right.
The auricular surface of the heart is which side?
A
Left interventricular (paraconal) groove Right interventricular (subsinuosal) groove
Left side (right side is called the atrial surface)
9
Q
How does the caudal border of the left ventricle compare in different species?
A
Carnivores: slightly convex
Horse: almost straight and vertical
Ruminants: slightly concave
10
Q
What are the four main openings of the right atrium?
A
Cranial VC
Caudal VC
Coronary sinus
Right atrioventricular orifice
11
Q
The azygous veins vary among species. Describe the differences:
A
Carnivores, horse and sometimes the pig: R. Azygous vein only
Pig: L. Azygous vein only
Ruminants: L and R azygous veins
12
Q
The right auricle is interlaced with muscles called ______________. What vestiges of the foetal circulation are present in the right atrium?
A
Pectinate muscles
Fossa ovalis Intervenous ridge (tubercle) Crista terminalis (from which most of the pectinate muscle arise)
13
Q
Blood from the right ventricle goes to the ______________.
The RV and RA are separated by the _____________ valve.
A
Pulmonary trunk Right atrioventricular (or tricuspid) valve
14
Q
What are chordate tendinae?
What are the septomarginal trabeculae? What else are they known as?
A
Tendinitis bands arising from papillary muscles that project from the ventricular wall and fan out to attach to the cusps of the A-V valve. Each muscle modulates 2 cusps
Rounded tissue bundle that crosses the ventricular lumen from the interventricular septum to the lateral wall. They distribute conducting fibres to the papillary muscles. Also known as moderator band.
15
Q
What are trabeculae carneae?
A
Subendocardial myocardial ridges on the ventricular wall (of the inflow channel) that protrude into the lumen
*papillary muscles contribute to the irregular surface of the inflow channel
16
Q
The RV has ___ papillary muscles. Where do they arise from?
A
3- 2 arise from IV septum. The third (great papillary muscle) arises from the outer parietal wall of the ventricle.
17
Q
Describe the outflow channel of the RV:
A
Origin- septomarginal trabeculae.
Consists of conus arteriosus which directs blood to pulmonary trunk. It has a smooth wall
18
Q
The thick muscular interventricular septum has two parts. Describe:
A
Larger muscular part caudally is thick myocardium formed by the combined walls of the two ventricles. Surface facing lumen of LV is concave
Collagenous thin membranous part exists dorsally. Marks final closure of embryonic interventricular foramen.
19
Q
The alternate name for the left A-V valve is….? It has how many cusps?
A
Mitral
2
20
Q
The pulmonary and aortic valve each have___ semilunar valvules.
A
3
21
Q
Aorta arises from the ____ and is divided into:
A
LV
Ascending aorta, aortic arch, descending aorta
22
Q
The fibrous rings composing the cardiac skeleton surround what?
A
Left AV valve Right AV valve Aortic semilunar valve Pulmonic semilunar valve The AV bundle
23
Q
What are characteristic features of cardiac muscle?
A
Intercalated disks Branching fibres Central nucleus Sarcoplasmic reticulum (associated with....) T-tubules
(Also, Purkinje fibres are present)
24
Q
Explain the basic mechanism for excitation-contraction coupling?
A
Action potential is propagated along T-tubules which are closely associated with the intracellular sarcoplasmic reticulum. The propagation of the AP stimulates release of Ca++ into the cell which causes tropomyosin to move aside thereby allowing cross-bridging between actin and myosin filaments. This enables a contraction.
25
How does cardiac muscle relaxation occur?
Active pumps return Ca++ to the sarcoplasmic reticulum and extracellular fluid. Intracellular Ca++ is exchanged for Na+ and the intracellular calcium concentration falls.
26
The amount of calcium release depends on what?
1. How much calcium is stored in the sarcoplasmic reticulum
| 2. Number of release channels activated
27
What is the difference between an isometric and isotonic contraction?
Isometric: muscle develops force at a FIXED length
Isotonic: muscular contraction in the absence of significant resistance with shortening of muscle fibres
28
Define the term contractility (relative to the heart):
The amount of tension that can be developed at any given stretch of cardiac muscle
29
What are inotropes?
Physiological or pharmacological agents that alter contractility.
30
In an ECG, what do the P, Q, R, S, and T phases represent?
P: atrial depolarisation
Q,R,S: ventricular depolarisation
T: ventricular repolarisation
31
What is a sinus bradycardia/ tachycardia?
Slowing/ fastening of HR governed by the SA node (due to increased/deceased vagal tone)
32
What are the layers comprising blood vessels?
```
Tunica intima (flat endothelial cells on bm)
Tunica media (concentric smooth muscle layers and elastic fibres)
Tunica adventitia (collagen and elastic fibres)
```
33
What are the anatomical groups of vessels?
1. Muscular
2. Elastic
3. Arterioles
4. Sinusoids
5. Capillaries
6. Postcapillary venules
7. Metarterioles
8. Muscular venules
9. Veins
34
What are the 5 functional groups of vessels?
1. Conducting
2. Distributing
3. Resistance
4. Exchange
5. Capacitance (reservoir)
35
Conducting arteries are ?thin/thick? walled. They have a high _____________ content. Examples include...?
Thick-walled
Elastin
Aorta, pulmonary, brachiocephalic, subclavian, common carotid
36
Distributing arteries are muscular and have more smooth muscle cells in their tunica media than capacitance arteries do. Their primary role is.......? They can actively change their diameter in response to.....? Examples include....?
Conduct flow to smaller arteries
Sympathetic innervation
Internal carotid, femoral, cranial mesenteric aa.
37
The main role of resistance vessels is to.....?
| Types of resistance vessels include...?
Control local blood flow to tissues (peripheral resistance)
Arterioles and metarterioles
38
Briefly describe the wall structure of arterioles.
TI- non fenestrated endo. supported by bm
TM- 1-2 layers of smc (metarterioles may have a single intermittent layer or none!)
TA- loose connective tissue
39
Define TPR
Total peripheral resistance= resistance to flow in entire systemic circ.
= (mean aortic pressure-vena caval pressure) / cardiac output
40
What is the mathematical definition of mean arterial pressure?
MAP= cardiac output x TPR
| = diastolic pressure + 1/3 pulse pressure
41
Exchange vessels include...?
Sinusoids, capillaries, post-capillary venules
42
What is a pericyte?
Endothelial cell "assistants" external to vessel wall
43
Describe the following:
1. Arteriovenous shunt
2. Thoroughfare channel
3. Glomeriform arteriovenous anastomosis
1. Connects arteriole with muscular venule
- sphincter like action
2. Connects metarteriole to post-capillary venule
3. Role in thermoreg (not covered as yet)
44
Capacitance vessels return blood to heart. They have a ?small/large? volume and ?low/high? pressure.
Large volume and low pressure
45
How does the tunica intima in veins differ to that in arteries?
No internal elastic lamina
46
What four factors control venous return?
1. Smooth muscle contraction (symp NS)
2. Skeletal muscle pump effect
3. One-way valves
4. Thoracic and cardiac pressure
47
What are the four "special circulations" covered?
1. Coronary
2. Pulmonary
3. Cutaneous
4. Cerebral
48
What are the specific species differences in regards to the coronary circulation?
In dogs and ruminants: 🐶🐮🐶🐮
- Right interventricular artery arises from the LEFT coronary artery
In horses and pigs: 🐴🐷🐴🐷
- Right interventricular artery arises from the RIGHT coronary artery
49
The venous drainage of the heart occurs through which vessels?
🔹Great cardiac vein
| 🔹Coronary sinus
50
In what ways does pulmonary circulation differ from systemic circulation?(4)
1. Pressures are low due to low pulmonary vascular resistance
- vessels are more compliant
- arteries and arterioles are shorter/thin walled
2. Basal tone is low
3. Sympathetic vasomotor nerves play no major role
4. Metabolic vasodilation has no role
51
What are the two main arteries supplying the head?
1. Common carotid arteries
| 2. Vertebral arteries
52
What is the functional significance of artery to artery anastomoses in the brain?
Provides for collateral circulation- preserves cerebral perfusion if carotid artery or vertebral arteries or their branches are obstructed
53
What is preload? What is it affected by?
The degree of tension on the myocardium when it begins to contract (considered to be the volume of blood in the ventricle at the end of diastole (EDV)).
EDV and venous return
54
What is afterload? What determines its magnitude?
The load against which the cardiac muscle exerts its contractile force (ie the pressure in the arteries).
Arteriolar pressure, aortic stenosis
55
What is the Frank-Starling Law of the Heart?
The energy released during contraction depends on the initial fibre length (allows for equalisation of output from left and right sides)
56
How does noradrenaline affect cardiac muscle contractility?
It is a positive inotrope released from sympathetic nerves. Binds to beta adrenoceptors
57
How does an increase in heart rate cause an increase in cardiac contractility?
Increased frequency of action potentials causes an increase in intracellular sodium and increased calcium in the sarcoplasmic reticulum (due to decreased diastolic interval).
58
What is the flow equation?
Flow = pressure gradient/ resistance
59
What two factors maintain mean arterial pressure?
Cardiac output
| Arteriolar resistance
60
What is your systolic and diastolic pressure?
Systolic: peak pressure during systole
Diastole: peak pressure when aortic valve is closed
61
Stroke volume=.....?
SV= EDV - ESV
62
How might the force of cardiac muscle contraction be increased? Explain the mechanism (7 steps).
Binding of noradrenaline to beta adrenergic receptor.
Activates adenyl cyclise ➡️ increased IC cAMP ➡️ phosphorylation of voltage op Ca channels ➡️ Ca influx ➡️ Ca release from SR ➡️ increased actino-myosin cross bridging ➡️ increased force of contraction
63
In relation to the cardiovascular system, what may cause cyanosis?
🔹Pulmonary oedema/effusion
🔹R. to L. patent ductus arteriosus
🔹Pulmonary stenosis
🔹Pulmonary hypertension
64
Pulse strength is a measure of ___________ minus ______________ pressures. Therefore, a bounding pulse may be indicative of____________or _________________ and a weak pulse may be indicative of _____________, ________________, or _________________
Systolic - diastolic pressures.
Bounding pulse: PDA, aortic insufficiency
Weak: shock, cardiac tamponade, aortic stenosis
65
What types of murmurs are these:
- Aortic stenosis
- Mitral regurgitation
- Aortic regurgitation
- Mitral stenosis
- Aortic stenosis= systolic ejection murmur
- Mitral regurgitation= pansystolic murmur
- Aortic regurgitation= early diastolic murmur
- Mitral stenosis= pre-systolic accentuation
66
Where on the dog can you auscultate the following:
1. Pulmonary valve
2. Aortic valve
3. Right AV valve (tricuspid)
4. Left AV valve (mitral)
1. Pulm. valve: Left 3rd intercostal space
2. Aortic: Left 4th intercostal space
3. Tricuspid: Right 4th intercostal space
4. Mitral: Left 5th intercostal space
67
The radio graphic appearance of the heart is influenced by...?
🔹positioning
🔹phase of respiration
🔹phase of the cardiac cycle
🔹conformation
68
On a lateral projection, features of cardiomegaly include...?
🔹Elevation of trachea
🔹Increased apicobasilar projection
🔹Decreased distance between heart and spine
🔹Increased craniocaudal diameter of heart
🔹Straightening of caudal heart border
🔹Expansion of left atrium into caudal lobar area
69
There are two broad groups of excitation-contraction coupling. These are...?
1. Electromechanical coupling (depolarisation of the vascular smooth muscle cell leads to opening of L-type voltage gated Ca channels)
2. Pharmacomechanical coupling (binding of signalling molecule to receptor causes increase in IC Ca via G-protein coupled release of IC stores or opening of receptor operated Ca channels)
70
Increase in [Ca++] ➡️ Ca-calmodulin complex ➡️ _____1.__________➡️ _____2.________➡️ myosin forms crossbridge with actin ➡️ contraction of SMC
1. [Ca-calmodulin]- myosin light chain kinase
| 2. Phosphorylation of myosin light chains
71
Amlodipine and Nifedipine are what type of drugs?
Ca++ channel blocker
Used for hypertension
72
What controls vascular tone?
1. Intrinsic mechanisms
- Myogenic response
- Vasoactive metabolites
- Endothelial secretions
2. Extrinsic mechanisms
- Neural control (vasomotor nerves)
- Hormonal control (vasoactive hormones)
73
What is the myogenic response?
Vascular smooth muscle contracts in response to stretch and relaxes with a reduction in tension (depol. initiated by stretch-activated channels)
74
Vasoactive metabolites contribute to _________ and _________ hyperaemia.
Metabolic
| Reactive
75
What is reactive hyperaemia?
Temporary increase in blood flow following a period of reduced blood flow.
76
What are some vasodilator and vasoconstrictors released by endothelial cells?
```
Dilatory= NO and prostacyclin
Constrictor= endothelin
```
77
Explain nitric oxide signalling on smooth muscle cells.
NO released by endothelial cells activates guanylyl cyclise.
GC converts GTP to cyclic GMP
cGMP activates kinases that promote relaxation
78
What is nitroprusside?
Nitric oxide donor
79
Sympathetic fibres terminate in the tunica ________ of vessels and release _____________which activate adrenoceptors and cause vasoconstriction
Media
| Noradrenaline
80
Parasympathetic fibres release _______ which activates M3 muscarinic receptors on endothelial cells. This stimulates synthesis of ______.
ACh
| NO
81
Beta2 receptors predominate in the _________; alpha receptors predominate in __________.
Coronary circulation and skeletal muscle
Most tissues
82
What are the three steps in haemostasis?
1. Vascular spasm
2. Platelets ether (platelet plug formation)
3. Clot formation
83
Platelets are activated by...?
```
Collagen
vWF
Tissue factor
Thromboxane A2
ADP
Thrombin
```
84
What prohibits platelet binding to undamaged endothelium?
NO and prostacyclin which are activated by ADP
85
What are three anticoagulant mechanisms?
1. Tissue factor pathway inhibitor (secreted by EC)
2. Thrombomodullin
Thrombin + thrombomodullin ➡️ thrombomodullin- thrombin complex ➡️ activates protein C ➡️ inactivates factor V and VII
3. Antithrombin III (joins with and inactivates thrombin)
86
What is the process of fibrinolysis?
1. Plasminogen binds fibrin
2. Bound plasminogen is activated by tissue plasminogen activator
3. Plasminogen is cleaved to plasmin
4. Plasmin dissolves clots
87
What are the components of the baroreflex (6)?
1. Stimulus
2. Sensory receptors
3. Afferent pathways
4. Integrating centre in the CNS
5. Efferent pathways
6. Effector organs
88
Where are arterial baroreceptors located?
🔹Aortic arch (pulsatile flow)
🔹Carotid sinus (non-pulsatile stretch)
🔹Atria, at junctions of great veins and atria, ventricles and pulmonary veins (respond to absolute pressure)
89
Afferent pathways for the baroreceptors reflex are in what nerves?
Glossopharyngeal (9) and vagus (10)
90
Central integration for the baroreflex is at the ______________. This has two regions. Explain.
Medullary cardiovascular centre
1. Pressor region: provides normal tonic sympathetic stimulation to vessels and ❤️
2. Depressor region: stimulated by baroreceptor firing. Inhibits sympathetic discharge form pressor region
91
What are meant by the terms "active hyperaemia" and "passive congestion"?
Active: increased blood volume due to arteriolar dilation and expansion of the perfused capillary bed
Passive: increased blood volume within the vasculature of a tissue is due to the impairment of venous outflow
92
In what circumstances does active hyperaemia develop? Why is it a local phenomenon?
Exercise, hot weather, embarrassment, inflammation
Why? Ere is insufficient blood volume to permit generalised active hyperaemia whilst maintaining adequate systemic blood pressure
93
In what circumstances does congestion occur? What are the potential consequences?
Circumstances: luminal obstruction of vein, intestinal strangulation, pooling in recumbent or inactive animals (hypostatic congestion), congestive heart failure
Consequences: venous hypertension, development of collateral venous channels
94
How would you grossly distinguish between active hyperaemia and passive congestion of an organ/tissue in a live animal?
Congested tissues appear red-purple to black (active hyperaemia tissues are red)
Cold vs warm
95
What gross lesions might you find in an animal that has died in left-sided congestive heart failure? Why do these lesions develop?
🔹Dark red to red-purple lungs
🔹Heavy lungs that don't fully collapse when the chest is opened
🔹Subpleural and interstitial tissues are distended with oedema fluid
🔹Foam is present in the lumina of bronchioles
🔹Stiff lungs (chronic) and tan-brown discolouration
96
What gross lesions might you find in an animal that has died in right-sided congestive heart failure? Why do these lesions develop?
🔹Swollen, dark red-purple liver
🔹Venous blood oozes from cut surface of liver
🔹Coagulated fibrin over capsule of liver
🔹Hilar lymphatics are distended
🔹Pooling of venous blood upstream in the venae cavae
🔹Enlarged, firm liver (chronic)
🔹Sugar frosting, nutmeg liver
97
Oedema is the accumulation of excess body fluid. The following terms relate to oedema in what part of the body?
1. Ascites
2. Hydrothorax
3. Hydropericardium
4. Hydrocoele
5. Anasarca
1. Peritoneal cavity
2. Pleural cavity
3. Pericardial sac
4. Tunica vaginalis of the scrotum
5. Severe generalised oedema
98
What are the five mechanisms that can lead to oedema development? Which is most likely to be responsible for localised oedema? Which is most likely to be responsible for generalised oedema?
1. Increased plasma hydrostatic pressure (G)
2. Decreased plasma oncotic pressure (G)
3. Lymphatic obstruction (L)
4. Increased vascular permeability (L)
5. Sodium retention
99
What circumstances are likely to lead to increased plasma hydrostatic pressure within a capillary bed?
Venous hypertension
100
Why is extracellular oedema not expected in animals with systemic hypertension?
Because increased arteriolar blood pressure causes reflex vasoconstriction of the pre-capillary arteriolar sphincter in order to protect the delicate capillary bed downstream
101
What 2 assays are initially used to categorise oedema fluid samples in a lab?
1. Protein concentration
| 2. Cell count
102
In which organs can severe oedema prove fatal?
Cerebral and pulmonary oedema
103
What are the potential consequences of oedema?
🔹Impaired wound healing
🔹Susceptible to secondary bacterial infection
🔹Fibroplasia and permanent fibrosis
104
What is meant by "haemorrhage by rhexis" and "haemorrhage by diapedesis"?
1. Rhexis- substantial tear in blood vessels or heart chamber leading to rapid escape of a substantial volume of blood
2. Diapedesis- escape of RBCs one by one through minute defects in vessel walls
105
What are the following terms:
1. Haemothorax
2. Haemopericardium
3. Haemoperitoneum
4. Haemarthrosis
5. Haemoptysis
6. Dysentery
7. Hyphaema
1. Haemothorax- pleural cavity
2. Haemopericardium- pericardium
3. Haemoperitoneum- peritoneal cavity
4. Haemarthrosis- synovial joint
5. Haemoptysis- coughing of blood
6. Dysentery- diarrhoea with blood
7. Hyphaema- anterior chamber of eye
106
How do bruises and haematomas resolve? Which pigments contribute to the discolouration of bruises and haematomas?
Resolved by lysis and phagocytosis
Pigments: poorly oxygenated Hb (red-blue)
Bilirubin/ biliverdin - green/ yellow
Haemosiderin (brown)
107
What factors determine the clinical significance of haemorrhage?
Location
| Rate and volume of blood loss
108
What is the most common cause of haemorrhage in domestic animals?
What are other potential causes?
Physical trauma!!!!
Other:
🔹Severe tissue infl.
🔹Sponataneous organ rupture, tumour, neoplasm
🔹Parasites
🔹Passive congestion
🔹Inherited or acquired defects in primary or sec. haemostasis
109
What are haemorrhagic diatheses?
Clinical disorders of haemostasis characterised by a bleeding tendency. Subdivided into disorders of primary and secondary haemostasis or combined.
110
What clinical signs would make you suspicious that an animal has a defect in primary haemostasis?
🔹Multiple short-lived bleeds that cease once fibrin is generated.
🔹Bleeding typically commences immediately after venipuncture
🔹Multiple petechiae, purpura or ecchymoses or paintbrush haemorrhages
🔹Epistaxis
🔹Haematuria, haematemesis, melaena/ haematochezia
111
List the four major mechanisms responsible for defects in primary haemostasis.
1. Thrombocytopaenia
2. Thrombocytopathies
3. von Willebrand's Disease
4. Blood vessel disorders
112
What are the major mechanisms responsible for thrombocytopaenia in domestic animals? Which is most likely to be clinically sig?
1. Decreased platelet production*
2. Increased platelet destruction
3. Consumption of platelets
4. Sequestration of platelets
5. Haemorrhage
113
What is the most common mechanism responsible for clinically significant thrombocytopaenia in cats? What are common underlying conditions?
Decreased platelet production
Retro viral infection, myeloproliferative or lymphoproliferative disease.
114
What is the most common mechanism responsible for clinically significant thrombocytopaenia in dogs? What can trigger it?
Platelet destruction
Disease process (eg. systemic lupus erythematosus (SLE))
Neoplasia (esp. lymphoma)
Viral, bacterial or rickettsial infection
Drugs (NSAIDs, digoxin, aspirin, penicillin)
115
What do thrombocytopathy, thrombopathy and thrombopathia mean? What are some causes of these conditions in animals?
All are synonyms for platelet function disorders.
```
🔹SLE
🔹Myeloproliferative diseases
🔹Retroviral infections in cats
🔹Hyperglobulinaemia
🔹Chronic liver disease
🔹Renal failure
🔹Snake envenomation
```
116
What role does vWF play in primary haemostasis?
Mediates adhesion of platelets to exposed subendothelial collagen via surface GpIb receptors. It's a glycoproteins.
117
What breeds are most commonly affected with vWD in Australia? How is it inherited?
Dobermans, welsh corgis, GSDs, golden retrievers and poodles (type 1)
German short haired and wire haired pointers (type 2)
Scottish terriers, Shetland sheepdogs (type 3)
All three forms are AUTOSOMAL RECESSIVE
118
What are some blood vessel disorders that can manifest as petechiae and ecchymoses in the skin or mucous membranes?
(7)
```
🔹Endotheliotropic viral infections
🔹Infectious vasculitis
🔹Immune mediated vasculitis
🔹Scurvy
🔹Inherited collagen dysplasia syndromes
🔹Skin fragility syndromes (caused by diabetes or hyperadrenocorticism)
```
🔹Also, toxaemia and bacteraemia and uraemia
119
What clinical signs would make you suspicious that an animal has a defect in secondary haemostasis?
```
🔹Bleeding after venipuncture is delayed
🔹Bleeding may be prolonged and severe
🔹Deep haematomas are common
🔹Severe haemorrhage in body cavities
🔹Haemorrhage from mm (occasionally)
```
120
What are the clinical signs of von Willebrand's disease?
🔹Excessive haemorrhage triggered by hair clipping, venipuncture or other trauma
🔹Perinatal mortality
🔹Excessive bleeding during tooth eruption or oestrus
🔹Epistaxis, GI bleeding, haematuria
121
List the four major mechanisms responsible for defective secondary haemostasis?
Which is most common?
1. Inherited coagulation factor deficiencies
2. Vitamin K antagonism or deficiency**
3. Severe acute or chronic liver disease
4. Excessive fibrinolysis or fibrinogenolysis
122
In which domestic animals are inherited coagulation factor deficiencies most often recognised?
Dogs
123
Why can some animals have a hereditary deficiency of a particular coag factor and either never bleed excessively or suffer from only minor haemorrhage?
H
124
Which of the inherited coagulopathies predispose to severe haemorrhage?
Inherited deficiencies of factors
1, 2, 10 (rare)
Or
8, 9
Or combined factor deficiencies
125
Why do haemophilia A and B mainly affect male animals?
Because it's inherited as an X-linked recessive disorder
126
Which coag factors are deficient in the inherited coagulopathy recognised in Devon Rex cats?
Factors 2, 7, 9 and 10 (vit K dependent factors)
127
What role does Vitamin K play in hepatic synthesis of coag factors? Which factors are vit K dependent?
It's required as a cofactor by the enzyme gamma-glutamyl carboxylase. This enzyme is involved in the synthesis of vit K dependent coag factors
II, VII, IX, X
128
What's the most common cause of vit K antagonism in domestic animals?
Ingestion of anticoagulant rodenticides
129
How can large animal species become poisoned by coumarin-type anticoagulants?
Ingestion of mouldy sweet clover or sweet vernal grass
130
Why do more potent anti coag rodenticides pose a greater hazard to small animals than does warfarin?
Warfarin generally causes poisoning after repeated ingestion.
More potent anti coags may induce severe life-threatening haemorrhage cats and dogs after a single episode of ingestion. Also, their longer half life permits secondary intoxication pets that consume poisoned rodents.
131
In what circumstances might a dog develop vit K deficiency? How common is it?
🔹Dietary vit K deficiency (rare)
🔹Prolonged anorexia or malnutrition
🔹Oral antibiotic use
🔹Chronic lipid maldigestion/ malabsorption syndromes (rare)
132
What role does the liver play in haemostasis?
It synthesise coagulation factors (in hepatocytes)
133
How much hepatic functional mass needs to be compromised before an animal is likely to be predisposed to haemorrhage due to inadequate synthesis of coag factors?
70%
134
In which condition is excessive fibrinolysis a contributor to secondary haemostasis?
Disseminated intravascular coagulation (DIC)
135
In which conditions is excessive fibrinogenolysis thought to be a contributor to a defective secondary haemostasis?
🔹Snake envenomation
🔹Administration of plasminogen activators
🔹Excessive endothelial release of t-PA
136
What vessels form the circle of Willis?
Internal carotid artery and the basilar artery
137
Heparin enhances the activity of...?
Antithrombin 3
138
Warfarin acts how?
Inhibits reduction of vit K
139
What is meant by the term thrombosis? How is it different from a physiological blood clot (haemostatic)?
= inappropriate formation of a blood clot within the CVS
It differs in that it is always attached to an area of damaged vessel wall and protrudes into the vessel lumen, thereby compromising blood flow.
140
What are the three major mechanisms that predispose to thrombosis?
1. Hypercoagulability
2. Abnormal haemodynamics (blood stasis or blood turbulence)
3. Endothelial injury
(Virchow's triad)
141
How does endothelial damage promote thrombosis?
Injured or activated endothelial cells adopt a procoagulant phenotype that promotes local coagulation of blood--> thrombosis
142
Where in the CVS is there a natural tendency for blood turbulence to develop?
In areas of hydraulic stress (eg. sharp bends, changes in vessel lumen diameter, valves and branching points)
143
How does abnormal haemodynamics predispose to thrombosis?
🔹Blood turbulence:
➡️direct endothelial injury and formation of blood counter currents and local pockets of blood flow
➡️ accelerates intravascular procoagulant and enzymatic rxns that lead to coag.
🔹Blood stasis
➡️ decreased venous blood flow --> increased blood viscosity--> blood hypercoagulability/ hypoxic injury to endothelial cells (procoagulant phenotype)
144
What are some circumstances that can lead to blood hypercoagulability?
Increased procoagulant factors or decreased inhibitory factors.
Eg. Oral contraceptives, disseminated malignancies, pancreatic necrosis, severe tissue trauma.
145
What are the basic events in thrombus formation?
1. Activation of normal haemostatic mechanism
2. Platelet adherence and activation
3. Platelet aggregation via binding of soluble fibrinogen
4. Activation of coagulation cascade forming a coagulation that is adherent to the point of injury
146
What is a mural thrombus? What is an occlusive thrombus?
Mural thrombus: coagulation that protrudes only partially into the vessel lumen
Occlusive thrombus: coagulation that completely obstructs the vessel lumen
147
What is thrombus propagation?
Gradual enlargement of a blood clot due to continued flow of blood over a mural thrombus which allows repeated layering of platelets and fibrin and entrapment of RBCs and WBCs
148
What are lines of Zahn and what do they signify?
Gross and microscopic lamination caused by episodic blood coagulation
149
What is the expected gross appearance of a thrombus in an artery or within the heart?
In a vein?
Artery or intra-cardiac: firm and pale yellow with a dull, dry rough surface (because they are chiefly composed of fibrin and platelets)
Vein: smooth shiny surface, moist and are dark red due to entrapped RBCs
150
What is vegetative valvular endocarditis?
Large thrombotic masses attached to the heart valves which are usually septic and containing bacterial colonies and leukocytes.
151
What gross features would allow you to distinguish between an antemortem venous thrombus and a post mortem red currant blood clot?
Ante mortem venous thrombi have a weak attachment to the vessel wall, have fine tangled strands of pale grey-yellow fibrin on their cut surface, and are accompanied by congestion and oedema of tissue upstream
152
What is a thromboembolus?
=fragments dislodged from an upstream thrombus that travel downstream in the blood to become trapped in distant vessels of smaller calibre.
153
Why are venous thrombi more likely (cff. arterial thrombi) to give rise to thromboemboli?
Because they have longer unattached thrombus tail that are susceptible to fragmentation
154
What is a septic thrombus? Bland thrombus?
Septic thrombus= thrombi infected with bacteria or fungi
| Bland= sterile thrombus
155
What is fibrinolysis? Which enzyme is responsible for it?
Enzymatic breakdown of fibrin
Plasmin
156
Which organ synthesises the precursor to plasmin?
Hepatocytes in the liver synthesise plasminogen
157
When is fibrinolysis most effective in degradation of a thrombus?
Most effective in recently formed thrombi
158
How do thrombi undergo organisation?
Via phagocytosis (by leukocytes) and via ingrowth of endothelial cells and vascular smooth muscle cells and fibroblasts
159
What is meant by recanalisation of a thrombus?
Process by which capillaries grow into an occlusive thrombus from either end
160
What is meant by the term embolus?
Intravascular solid, liquid or gaseous mass transported by the blood to a site distant from its point of origin (embolism is a blockage of a downstream vessel by an embolus arising upstream).
161
What is the most common type of embolus?
Thromboembolus
162
What is a saddle thromboembolism?
Thromboemboli lodged at sites of vessel bifurcation (common in cats)
163
How would you grossly distinguish between a thrombus and thromboembolus?
Need to search for a thrombus upstream
164
Where do most venous thromboemboli become trapped?
If arising from the GIT, spleen or pancreas then the vascular bed of the liver. If arising from anywhere else, then the vascular bed of the lungs.
165
What are the potential consequences of pulmonary thromboembolism?
🔹May occlude main pulmonary artery
🔹May impact across bifurcation of right and left pulmonary arteries or pass into smaller arterial branches.
🔹Pulmonary hypertension
🔹Cor pulmonale
166
What are some different types of emboli?
```
🔹Fungal
🔹Malignant tumour cells
🔹Bacterial colonies
🔹Lipid emboli
🔹Gas bubbles
🔹Parasites
🔹Fibroblasts/fibrocartilage
🔹Amniotic fluid
```
167
Define ischaemia and infarction.
Ischaemia= hypoxic, anoxic tissue injury due to decreased blood flow
Infarction= ischaemic necrosis of local area
168
Name some conditions (other than thrombosis, thromboembolism or embolism) that can cause ischaemia?
```
🔹Arteriosclerosis
🔹External compression of vessels
🔹Mesenteric torsion
🔹Diaphragmatic hernias
🔹Pneumonia
🔹Paracetamol poisoning
```
169
Why is infarction more commonly deferrable to arterial obstruction?
Because many tissues lack an arterial blood supply whereas collateral venous channels may be numerous
170
What are the major factors that determine the prognosis for an animal that has a local reduction in blood flow? (4)
1. Location
2. Alternative blood supply
3. Size of vessel
4. Rate of development and degree of occlusion
171
Why are infarcts less likely to develop in the lungs or liver than other organs?
They have a dual blood supply
172
What happens to necrotic debris in an infarct over time in surviving patients?
Replaced by fibrous tissue
173
In what circumstances does venous hypertension develop?
Results from impairment of outflow of venous blood from the tissues.
Can also result from a congenital or acquired arteriovenous anastamosis.
174
What is pulmonary hypertension? What are some causes in domestic animals?
= a sustained increase in systolic blood pressure in the pulmonary artery
175
What is cor pulmanale?
= right heart disease caused by pulmonary hypertension
176
What is systemic hypertension?
= a sustained increase in systemic arterial blood pressure
177
What factors contribute to arterial blood pressure?
```
Cardiac output (HR x SV)
TPR
```
178
What is primary or essential hypertension?
Systemic hypertension of multifactorial origin
179
What are some diseases that may be responsible for the development of systemic hypertension in dogs and cats?
```
🔹Renal disease
🔹Hyperadrenocorticism
🔹Hyperthyroidism
🔹High salt diets
🔹Diabetes mellitus
🔹Liver disease
🔹Hyperaldosteronism
🔹Chronic anaemia (cats)
```
180
Why is systemic hypertension self-perpetuating and why is it not adequately treated?
H
181
Which body organs are most susceptible to damage from systemic hypertension?
Eyes, kidneys, brain and heart
182
What are the potential consequences of sustained systemic hypertension on a dog or cat?
Onset of blindness, PU/PD, systolic cardiac murmur, epistaxis, strokes
183
What is systemic hypotension?
Sustained decrease in systemic arterial blood pressure
184
What is meant by the term shock? What is characteristic for all forms of shock?
=generalised phenomenon of peripheral circulatory failure
Systemic hypoperfusion and systemic hypotension
185
What is cardiogenic shock and what are some causes?
Peripheral circulatory failure resulting from a rapid decrease in systolic cardiac output despite the presence of adequate blood volume.
Causes: primary disorders of myocardium, acute heart valvular dysfunction, severe dilated cardiomyopathy (most common)
186
What is hypovolaemic shock and what are some causes?
Peripheral circulatory failure resulting from a significant reduction (>20-25%) in the circulating blood volume.
Causes: severe, acute or chronic haemorrhage, severe fluid loss (vomiting, diarrhoea, polyuria), sequestration of fluid
187
What is distributive shock? Why does it cause a decrease in effective circulating blood volume?
Peripheral circulatory failure due to inappropriate vasodilation of arterioles with pooling of blood in capillary beds and venous channels.
Leads to reduced TPR and reduced effective circulating blood volume
188
What circumstances can trigger neurogenic shock? Why does it cause a decrease in effective circulating blood volume?
Electrocution, acute brain or spinal cord injury, anaesthetics or vasodilator drugs
Inappropriate vasodilation of arterioles--> pooling of blood in capillary beds and venous channels--> reduced TPR (vascular)--> decreased effective circulating blood volume
189
What circumstances can trigger anaphylactic shock? Why does it cause a decrease in effective circulating blood volume?
```
Anaphylactic (IgE and prior exposure) or anaphylactoid reaction. Other triggers include:
🔹Foreign antigens
🔹Administered drugs
🔹Hormones
🔹Heterologous proteins
🔹Dietary components
```
Inappropriate vasodilation of arterioles--> pooling of blood in capillary beds and venous channels--> reduced TPR (vascular)--> decreased effective circulating blood volume
190
What circumstances can trigger septic shock? Why does it cause a decrease in effective circulating blood volume?
Most often attributable to Gram-negative bacterial infection with release of endotoxins. Can also be caused by overwhelming bacterial infections, Gram +ve bacterial infections, fungal infections or superantigens.
Inappropriate vasodilation of arterioles--> pooling of blood in capillary beds and venous channels--> reduced TPR (vascular)--> decreased effective circulating blood volume
191
During septic shock, what happens to the microcirculation that contributes to the poor prognosis?
Widespread microthrombosis (DIC) and stimulation of systemic inflammatory response leads to multiple organ dysfunction syndrome (mechanism below).
Increased lipopolysaccharides from endotoxins ➡️ high concentrations of NO, cytokines, prostacyclin and platelet activating factor ➡️ systemic arteriolar vasodilation ➡️ hypotension and decreased effective circulating blood volume
NO ➡️e erased cardiac contractility ➡️ decreased CO
PAF ➡️ platelet activation ➡️ intrinsic coagulationcascade ➡️ widespread endothelial injury and inhibition of fibrinolysis ➡️ DIC
192
What are compensatory neurohormonal mechanisms activated in the initial stages of cardiogenic or hypovolaemic shock? (8)
1. Detection of hypotension by baroreceptors
2. Detection of hypercapnia by chemoreceptors
3. Release of glucocorticoids from adrenal cortex
4. Release of catecholamines from adrenal medulla
5. Generalised stimulation of autonomic SNS
6. Activation of RAAS
7. ADH release from posterior pituitary
8. Aldosterone release from zone glomerulosa of adrenal cortex
193
What happens during stage 2 of shock?
1. Glomerular filtration rate declines
2. Tissue hypoxia in non-essential organs
3. Blunting of vasoconstriction response--> pooling of blood in microcirculation
4. DIC
5. Signs of organ dysfunction and mental confusion
194
What has happened by stage 3 of shock?
Widespread hypoxia cell necrosis, failure of multiple organs +/- DIC
Renal shutdown, failure of neurological reflexes and vital organs
195
What clinical signs might suggest that an animal is in shock?
🔹increased HR
🔹subnormal temperature due to decreased metabolic rate
🔹hypotension, tachycardia, threads pulse, tachypnoea, cool dry or clammy skin, pallor (hypovolaemic and cardiogenic shock)
🔹injected mm, rapid CRT, normal to increased body temp in distributive shock.
196
Which form of shock has the best prognosis if appropriate therapeutic intervention is given in stage 1 or 2?
Hypovolaemic shock
197
What is DIC?
Disseminated intravascular coagulation.
A complex disorder of haemostasis that starts with widespread activation of blood coagulation within the microcirculation and may progress to sustained fibrinolysis and haemorrhage.
198
What're the major mechanisms by which DIC can be triggered?
1. Release of tissue factor (iii) or tissue factor-like procoagulant factors
2. Widespread endothelial injury
199
What are some disease conditions that can trigger DIC?
```
Bacteraemia
Heartworm
Infectious canine hepatitis
Feline infectious peritonitis
Hog cholera
```
200
What is happening in phase 1 (subclinical phase) of DIC?
🔹Blood is hypercoagulable
| 🔹Extrinsic coagulation cascade activated but thrombin is counterbalanced by anticoagulant molecules
201
What is happening in phase 2 (decompensated) of DIC?
🔹activation of endothelial cells to a procoagulant phenotype
🔹platelet activation
🔹suppression of fibrinolysis
➡️widespread thrombosis within the microcirculation
202
What is microangiopathic haemolytic anaemia or fragmentation anaemia?
Formation of fibrin strands within the microcirculation leading to fragmentation trauma to circulating RBCs
203
What are schistocytes?
Red blood cells damaged by shearing forces
204
What happens in phase 3 of DIC?
Consumption of platelets and coagulation factors in formation of microthrombi ➡️ thrombocytopaenia and inadequate coagulation factor activity ➡️ hypercoagulable/haemorrhagic phase of DIC
205
If an animal is bleeding due to DIC, what are the characteristic features of the bleeding?
Characteristics of defects in both primary and secondary haemostasis
206
Why are systemic inflammatory responses and cytokines cascade activated in DIC?
🔹factor XII activates the complement system ➡️ chemotaxis of leukocytes
🔹factor Va, thrombin and fibrin activate endothelial calls ➡️ synthesis of pro-inflammatory cytokines
207
Why does DIC often lead to shock?
Factor XIIa activates the kallikrein-kinin system ➡️ generation of kinins ➡️ vasodilation and increased vascular permeability ➡️ systemic hypotension and shock
208
What post mortem lesions might you find in an animal that has died in DIC?
🔹Thrombi may be identifiable microscopically in association with oedema, congestion, haemorrhage and/or ischaemic necrosis
🔹Mucosal, serosal and/or cutaneous petechiae, purpura and ecchymoses, deep haematomas and haemorrhage within body cavities or joints
209
What are the most common congenital anomalies in:
1. Dogs
2. Cats
3. Pigs
4. Cattle
5. Horses
6. Alpacas/llamas
1. Dogs: PDA, pulmonic/subaortic stenosis, AV valve dysplasia, PRAA
2. Cats: AV valve dysplasia, ASD, VSD, excessive moderator bands in LV
3. Pigs: subaortic stenosis, endocardial cushion defects
4. Cattle: ASD, VSD, valvular haemocysts, transposition of major vessels
5. Horses: VSD
6. Alpacas/llamas: VSD, valvular haemocysts
210
Where is the most common position for ectopic cordis?
Pre-stern also subcutaneous position
211
What is the clinical consequence of an absent parietal pericardium?
Usually asymptomatic
212
What is a congenital peritoneopericardial diaphragmatic hernia?
Herniation of abdominal viscera into pericardial sac (due to defect in ventral diaphragm and parietal pericardium). Often clinically silent
213
In which species is a PDA most common?
Dogs! Especially females
214
In which species is a patent foramen ovals a common finding?
Ruminants (not really an issue because RA is low pressure)
215
What are the potential post-natal consequences of an atrial septal defect?
Blood shunts from LA to RA ➡️increased central venous pressure ➡️ volume overload on RA ➡️ dilation ➡️ chronic eccentric hypertrophy ➡️ return of extra blood from lungs into LA ➡️ volume overload on LA
216
What are the potential post-natal consequences of a ventricular septal defect?
Small VSDs may be clinically insignificant.
Otherwise:
L-->R shunt ➡️ RV overload ➡️ dilate ➡️ concentric/eccentric hypertrophy ➡️ increased workload of LA ➡️ pulmonary hypertension ➡️ shunt reversal
217
Why do some VSDs eventually close?
Reparative marginal fibrosis due to blood turbulence
218
In which species are endocardial cushion defects common?
| What are possible defects associated with endocardial cushion defects?
🐱🐱🐱🐷🐷🐷
| Lack of atrial/ventricular divisions, AV valve dysplasia, high VSD, low ASD
219
What is a persistent truncus arteriosus?
Incomplete separation of truncus arteriosus into pulmonary a trunk and aorta. Common in calves
220
What is an overriding aorta (dextropositioned aorta)?
Aorta is positioned too far to the right and straddles te entricular septum --> blood from RV enters aorta
221
What are the four components of a tetralogy of Fallot?
1. A VSD
2. Pulmonic stenosis
3. Overriding aorta
4. Concentric hypertrophy of the RV
222
What are the consequences of pulmonic stenosis? In which species is it common?
Dogs (inherited in beagles)
Narrow RV outflow tract ➡️ systolic pressure overload on RV ➡️ chronic concentric hypertrophy
Also get post-stenotic dilation of the pulmonary artery
223
What are the consequences of subaortic stenosis? In which species is it common?
Pigs and dogs
Sub-valvular stenosis ➡️ systolic pressure overload on LV. ➡️ concentric hypertrophy
Leads to post-stenotic dilation of the aorta
224
What are the consequences of AV valve dysplasia? In which species is it common?
Cats
| Volume overload --> congestive heart failure
225
What is the most common vascular ring anomaly in animals? Which species is most commonly affected?
Persistent right aortic arch
Dogs and calves
226
What are the potential consequences of PRAA?
Right aorta descends to the right of midline, arches over the origin of the right bronchus and then descends to the left or right of the vertebral column --> ligamentum arteriosum traps oesophagus and compresses it
Oesophageal obstruction--> megaoesophagus--> aspiration pneumonia
227
What can excessive moderator bands in the LV cause in cats? At what age?
Decreased cardiac compliance ➡️ decreased diastolic filling of LV ➡️ LS congestive heart failure
Middle aged or older cats
228
What is endocardial fibroelastosis?
Localised subendocardial lymphoedema ➡️ progressive subendocardial collagen and elastin deposition ➡️ prominent gross white thickenening of endocardium ➡️ decreased cardiac compliance
229
In which species are congenital valvular cysts common?
Calves, alpacas, llamas
230
What is myocardial rhabdomyoma?
Anomalous malformations of myocardial fibres
231
Hydralazine is what type of drug? In what circumstances is it used?
It is a potent direct acting arteriolar dilator. It is used in severe chronic heart failure
232
What are some examples of localised forms of DIC?
🔹bilateral renal cortical necrosis
🔹haemorrhagic adrenocortical necrosis
🔹gangrene of the extremities
🔹haemolytic-uraemic syndrome
233
What lines the pericardial sac and what is the function of this lining?
```
Squamous monolayer of mesothelial cells.
Functions include:
🔹phagocytosis
🔹production of plasminogen activator
🔹production of polysaccharide (lubricant)
```
234
What is meant by the term "constrictive heart disease"? Which conditions are likely to cause it?
Diseases of the pericardial sac that cause reduced ventricular compliance (especially impaired diastolic filling of the right ventricle).
May result from rapid pericardial effusion or chronic pericardial fibrosis.
235
What is meant by cardiac tamponade? What may cause it?
An excess volume of fluid in the pericardial sac.
May be caused by:
🔹hydropericardium
🔹haemopericardium
🔹pericarditis
236
What do the following terms mean: hydropericardium, pericarditis?
Hydropericardium- non-infl. oedema of the sac
| Pericarditis- infl. of the epicardium and parietal pericardium
237
How may hydropericardium develop and what is its typical gross appearance?
```
Causes:
🔹RSCHF
🔹hypoalbuminaemia
🔹local venous or lymphatic obstruction
🔹increased vascular permeability
```
Appearance:
Sac has excess fluid that is clear to faintly cloudy and colourless to pale yellow. If rich in fibrinogen, may form a gel (occurs with increased vascular permeability). If chronic, may see villus hyperplasia of the mesothelium and cream white opacity of serosa.
238
Why is haemopericardium commonly fatal? What are some causes of it?
Because it leads to cardiac tamponade
Causes:
🔹bleeding haemangiosarcoma (or other bleeding tumours)
🔹idiopathic spontaneous rupture of the intrapericardial aorta or the pulmonary artery during exercise or mating 🐴
🔹hardware disease
🔹spontaneous rupture of a heart chamber, aorta or coronary artery 🐷
239
What are the two major types of pericarditis? Which is more common**?
Fibrinous** and suppurative.
240
What is the most common cause of fibrinous pericarditis and what is the typical gross appearance?
Usually results from haematogenous localisation of an infectious agent (esp. bacterium but occasionally a virus or protozoa).
Small volume of exudate present; no sac distension; inflamed serosal membranes are hyperaemic and may have haemorrhages; fibrin sticks parietal and visceral pericardial layers together.
241
What is cor villosum, shaggy heart or bread and butter pericarditis?
Fibrinous pericarditis where the exudate is drawn into villus projections at necropsy (when visceral and parietal pericardial membranes are pulled apart)
242
In which species is suppurative pericarditis most commonly seen? Why?
Cattle due to traumatic reticuloperitonitis
243
Is there a difference between suppurative and fibrinous pericarditis in terms of their effect on cardiac function?
Yes, scar tissue formed in fibrinous pericarditis is is not usually dense and hence there is usually no compromise on cardiac function.
Suppurative pericarditis causes intense and deep infl. leading to dense scar tissue formation and constrictive pericarditis ➡️ RSCHF
244
What would serous atrophy of the epicardial fat indicate?
It reflects recent rapid mobilisation of epicardial fat depots in anorexia, starvation and cachectic illnesses.
245
What are common causes of haemorrhage over the epicardium and parietal pericardium?
🔹Bacteraemia, septicaemia, toxaemia, viaremia
🔹Disorders of primary haemostasis
🔹Mulberry heart disease 🐷
Common in 🐴🐴🐴, uncommon in small animals
246
What is gout?
Deposits of uric acid crystals over the pericardial membranes, liver capsule, renal tubules and ureters.
Crystalline deposits called tophi.
🐦🐦🐦🦎🦎🦎
247
What are some post mortem artifactual lesions you might find in pericardial sac?
Serosanguinous fluid that does not clot (also accumulates in pleural and peritoneal cavities).
Red discolouration of pericardial membranes
Cream white barbiturate crystals
248
What gross change might suggest subendocardial fibrosis?
Endocardium is still smooth and shiny, but appears milky white and opaque.
249
What is the usual cause of diffuse subendocardial fibrosis?
Chronic dilation of heart chambers
250
What is meant by the term jet lesion?
Streaks of fibrosis in the atrium due to static pressure injury to the subendocardium as a result of turbulent regurgitating blood (caused by AV valve insufficiency).
251
In what circumstances can mineral be deposited in the endocardium? Provide examples of causes.
Can be deposited in necrotic -dystrophic- or in healthy -metastatic- tissues (due to an increased blood concentration of calcium and phosphate).
```
Causes:
🔹chronic dilation of heart chambers
🔹Johne's disease
🔹uraemia endocarditis
🔹vitamin E deficiency in lambs and calves
```
252
What is endocardioisis? In which animal is it most common?
=myxomatous degeneration of the heart valves
Common in dogs, especially the cavalier King Charles spaniel and daschunds due to its polygenic inheritance in those breeds
More common in males than females
253
Describe the aetiopathogenesis of endocardiosis in dogs. Which heart valves are commonly affected?
It's an inherited degenerative disease of connective tissues, esp. collagen.
Most frequently affected breeds are of the chondrodystrophoid type.
Mostly mitral valve, less commonly the tricuspid valve
254
What gross lesions would suggest endocardiosis?
🔹Lesions at the margins of the valve leaflets.
🔹Cores of valve leaflets become thickened by loose fibroelastic tissue and deposits of protoglycans.
🔹Affected valves become short and thick.
🔹Nodules form at margins
🔹Overlying endocardium remains smooth and glistening.
🔹Thickening of chordae tendinae
255
What are the potential consequences of endocardiosis?
```
Valvular insufficiency ➡️ blood regurgitation leading to
🔹decreased cardiac output
🔹volume overload on atrium
🔹dilation
🔹subendocardial fibrosis
🔹jet lesions
🔹thrombosis
🔹congestive heart failure
```
256
What is endocarditis and what is the most common cause? (In which animals?)
=inflammation of the endocardium
Bacteraemia.
Large animal species
257
Where are valvular endocarditis lesions most commonly located?
At lines of apposition of valve leaflets exposed to the forward flow of blood
258
What is the typical gross appearance of valvular endocarditis lesions? Where are they most common?
Valve leaflet swelling; irreg. ulceration. Older lesions are friable, rough surfaces, yellow-grey-red vegetations largely composed of thrombus (thrombi usually contain deeply buried bacterial colonies and leukocytes).
259
What are potential consequences of valvular endocarditis?
Often fatal
Thrombi leads to ingrowth of granulation tissue ➡️ fibrosis +/- dystrophic mineralisation
Valves may become stenotic or insufficient
Risk of bland or septic thromboembolism
260
What is mural endocarditis and what are the distinct forms (3)?
May develop as an extension of valvular endocarditis. May also result from extension of infection from the underlying myocardium.
1. Parasitic endocarditis in horses (strongylus vulgaris)
2. Blackleg in ruminants (clostridium chauvoei)
3. Uraemia ulcerative endocarditis in dogs (most common)
261
What can cause haemorrhages over the endocardium?
Bacteraemia, toxaemia, viraemia, septicaemia
| Disorders of primary haemostasis
262
What are the possible adverse effects of myocardial degeneration, necrosis, infl., or neoplasia on cardiac function?
May cause depression of myocardial contractility and/or induction of cardiac arrhythmias. This can in turn lead to cardiogenic shock or congestive heart failure.
Tumours may also lead to intrapericardial haemorrhage
263
What is the most common cause of cardiac arrhythmias?
Most significant ones are secondary to myocardial damage rather then lesions of the conduction system
264
What are potential causes of hydropic of fatty degen. of cardiac myofibres?
Severe anaemias (or other causes of hypoxia), toxaemias and systemic febrile infections.
265
What is meant by the term brown atrophy of the heart? In which species is it most common and in what circumstances?
Myocardial atrophy accompanied by gross dark brown discolouration of the myocardium due to severe intra-cellular accumulation of lipofuscin pigment caused by cumulative peroxidative injury to phospholipids of cell organelle membranes.
Most common in ruminants with chronic starvation/ malnutrition or chronic wasting disorders
266
For the two types of mineralisation, provide examples of causes.
Dystrophic: white muscle disease in lambs and calves due to vitamin E or selenium deficiency
Metastatic: vitamin D toxicity and vit D analogue poisoning
267
Where are foci of myocardial necrosis most likely to occur and why?
Left ventricle (esp. in the subendocardial myocardium of the interventricular septum and in the papillary muscles) because these are sites of greatest chamber wall tension development during systole.
268
How long must a patient survive after necrosis of cardiac myofibres before the lesions are likely to become grossly obvious? What gross lesions might you see?
Subtle pallor: 4-12 hrs later
Pale, dystrophic mineralisation, fibrin, haemorrhage over the overlying epicardium: 18-24hrs
Reactive hyperaemia: 2-4 days
Fibrosis (cream white pallor): 7 days
269
What are some examples of agents that can be responsible for myocardial necrosis?
Infectious agents
Ischaemia/hypoxia (hypovolaemic shock)
Excess catecholamines (tumour of adrenal medulla)
Nutritional deficiencies (taurine, vit E)
Inherited/metabolic disease (eg. Equine rhabdomyolysis)
270
For how long can cardiac myocytes tolerate hypoxia conditions?
Why is infarction so common in humans?
20-30 mins before there is irreversible cardiac myofibre injury
As a consequence of artherosclerosis of coronary arteries compounded by systemic hypertension
271
What are some causes of myocardial hypoxic/ischaemic injury in animals?
```
🔹severe anaemia
🔹hypovolaemic shock
🔹thrombosis/ thromboembolism of coronary arteries
🔹arteriosclerosis of coronary arteries
🔹hypertrophied heart chambers
```
272
What are the circumstances in which beta adrenergic stimulation of the myocardium can result in myocardial necrosis?
Catecholamine toxicity
273
List 5 plants capable of causing myocardial necrosis.
1. Avocado 🥑 🐦🐴🐑
2. Phalaris 🐑
3. Lantana 🐑
4. Fluroacetate-containing plants (ruminants)
a. Acacia
b. Oxylobium
274
How is the inner half of the wall of a blood vessel supplied with oxygen and nutrients?
Diffusion from the vessel lumen
275
How to vascular smooth muscle cells respond to a sustained increase in blood volume and pressure?
They undergo hypertrophy and to a lesser extent, hyperplasia
276
What are myointimal cells?
Smooth muscle cells of the tunica media that have migrated through pores in the internal elastic lamina into the subendothelial layer
277
What causes hypertrophy of arteriolar SMCs?
Systemic hypertension, pulmonic hypertension, pregnancy
278
In what circumstances does sustained arteriolar vasoconstriction occur?
Systemic hypertension
| Mycotoxins (eg. Ergotism)
279
What is arteriosclerosis and artherosclerosis? Which is more common**?
Arteriosclerosis**= a chronic degenerative disease of arteries characterised by hardening, loss of elasticity, and luminal narrowing
Artherosclerosis= arteriosclerosis in which there is significant lipid deposition and fatty degeneration of the vessel wall
280
What are characteristic lesions of artherosclerosis?
Artheromas (fibrofatty plaques)= a focal, raised intimal plaque with a core of lipid covered by a fibrous cap
Fatty streak= a soft, smooth non-elevated, lipid-rich intimate degenerative plaque
281
In what circumstances is artherosclerosis likely to develop in animals?
Pigs on high fat/cholesterol diets
| Dogs with diseases promoting persistent hypercholesterolaemia (hypothyroidism, diabetes mellitus)
282
What is hyaline degeneration of arterioles? What is fibrinous change of arterioles and in what circumstances does it develop?
Hyaline degen.= spectrum of arteriolosclerotic lesions involving deposition of collagen, elastin, glycosaminoglycans or amyloid in the tunica intima and/or tunica media of damaged arterioles.
Fibrinous change= an EC degen. change in damaged small arteries and arterioles (renal failure, systemic hypertension, vasculitis, vit E def., oedema disease in pigs)
283
What are potential causes of arterial rupture?
```
🔹Physical trauma
🔹Fungal infections of guttural pouch 🐴
🔹Parturition (uterine artery) 🐴
🔹Exertion/exercise (aorta) 🐴
🔹Copper deficiency 🐷
```
284
What is an aneurysm/ dissecting aneurysm?
=localised abnormal dilation or outpouching of a blood vessel (dissecting= blood enters the vessel wallthrough endothelial tear and dissects between layers of the tunica media to create a cavity within the vessel wall)
285
What are some causes and consequences of vasculitis?
```
Causes:
🔹Infectious agents
🔹Circulating toxins
🔹Deposition of immune complexes
🔹Extension of inflammation from adjacent tissues
```
Consequences:
🔹Thrombosis
🔹Infarcts/ischaemic injury
286
What is verminous arteritis? Provide an example.
Inflammation of vessels caused by worms 🐛
Strongylus vulgaris
Dirofilaria immitus
Angiostrongylus vasorum
287
What is steroid-responsive meninges arteritis? Which species are affected?
Polyarteritis that is thought to be immune-mediated. It's characterised by sever necrotising arteritis of meninges like arteries +/- coronary and mediastinal arteries.
Esp. seen in young beagles but other dog breed as well
288
What is polyarteritis nodosa?
A form of immune mediated arteritis characterised by severe necrotising infl. of small-medium arteries, often in a nodular pattern and with a predilection for branching points.
289
What is thrombophlebitis? What are common causes of jugular thrombophlebitis?
Inflammation of the veins leading to thrombosis.
Inept/repeated venipuncture, injection of irritant solutions, use of indwelling catheters, intro. of bacteria
290
What are some bacterial agents that commonly cause lymphangitis?
```
🔹Bacillus anthracis
🔹Mycobacterium species
🔹Actinobacillus lignieresii (wooden tongue)
🔹Actinobacillus equuli
🔹Corynebacterium pseudotuberculosis
```
291
What is phlebectasia?
Dilation of a vein
292
What is the usual cause of lympoedema? What is the difference between primary and secondary?
Impaired lymphatic drainage.
Primary: results from anomalous development of the lymphatic system with inadequate drainage
Secondary: due to obstruction of previously normal efferent lymphatics
293
What is intestinal lymphangiectasia?
Dilation of mesenteric lymphatics- a common cause of protein-losing enteropathy
294
What is chylothorax? What are possible causes?
=free chylomicron-rich lymph within the thoracic cavity due to leakage from a ruptured thoracic duct
Causes: thoracic trauma, severe coughing, intrathoracic malignant neoplasms, dirofilarias, pleuritis, RSCHF, lung lobe torsion, congenital anomalies
295
What are the two most common neoplasms arising from vascular endothelium? How are they different? Where are they commonly found?
1. Haemangioma= benign, most common in dermis and subcutis
2. Haemangiosarcoma= malignant
🐶 most common in spleen, RA/RAu, skin subcutis and liver
🐱 spleen, intestines, subcutis
🐴 conjunctival/ cutaneous tumours or multicentric neoplasia
296
Chronic activation of the sympathetic nervous system leads to...?
1. Reduced baroreceptors sensitivity
2. Down regulation of beta receptors in the heart
3. Chronic activation of RAAS
- persistent vasoconstriction
- increased blood volume
- increased angiotensin
297
What are some compensatory mechanisms in heart failure?
Release of ANP and prostaglandins
298
Eccentric hypertrophy occurs in response to __________? Concentric hypertrophy occurs in response to.......
Volume overload
Pressure overload
299
The first stage of heart development is the formation of what?
The pleuropericardial cavity and cardiac primordium from the lateral mesoderm
300
The embryonic heart is supported dorsally by a membrane called what?
Dorsal mesocardium
301
The primitive bulbous cordis and the truncus arteriosus become divided into what by the spiral septum?
Pulmonary trunk and the aorta
302
The ?cranial/caudal? extensions of the endocardial tubes beyond the cardiac region constitute the start of the main efferent channels or aortae
Cranial
303
What are the main arteries from the aorta to the yolk called?
What foetal circulation regresses and is transformed into the hepatic-portal circulation?
Omphalo-mesenteric arteries
Vitelline
304
Blood from all parts of the embryo is collected by what?
The cardinal veins
305
Most of the blood in the pulmonary trunk is shunted via the ......?
Ductus arteriosus (6th aortic arch)
306
The definitive aorta (4th aortic arch) arises from...?
Left ventral aorta
Left fourth aortic arch
Left dorsal aorta
307
The large vascular channel between the left umbilical vein and the hepatic part of the caudal vena cava is what?
Ductus venosus
308
What are the three pairs of channels that drain into the sinus venosus in the early embryo?
Vitelline
Umbilical
Cardinal
309
What changes occur in the cardiovascular system at birth?
```
Change in vascular resistance
Closure of umbilical arteries
Closure of ductus venosus
Closure of the foramen oval
Closure of the ductus arteriosus
```
310
Nitrates are direct acting ______________ that are metabolised to release __________. This stimulates the formation of cGMP to initiate __________.
Examples include:
Vasodilators
Nitric oxide
Smooth muscle relaxation
Glyceryl trinitrate, nitroglycerin
311
Hydralazine is a potent direct acting __________. It is used in cases of _____________. It's mechanism of action is not well understood but it probably acts similarly to nitrates.
Side effects include:
Arteriolar dilator
Severe chronic heart failure
Hypotension and reflex tachycardia
312
Calcium channel blockers bind tightly to receptors in the inactive state and delay recovery to resting state. They allow for ____________. Examples of L-type calcium channel blockers include...?
Vasodilation
Verapamil (1:1)
Diltiazem (7:1)
Amlodipine (14:1)
313
What type of drugs are prazosin and propanolol?
What are their effects?
Prazosin is an alpha one adrenoreceptor blocker. It causes arteriolar and venous dilation.
Propanolol is a beta adrenergic blocker. It reduces heart rate and stroke volume and inhibits renin release (thereby reducing angiotensin formation).
314
Benazapril and enalapril are what sort of drugs? How do they work?
ACE inhibitors.
They inhibit formation of angiotensin II --> reduced vasoconstriction. They also decrease alsdosterone release--> reduced blood volume and reduced preload/afterload
315
Losartan and candesartan are what type of drugs?
Angiotensin II receptor blocking agents
| They don't cause increase bradykinin levels like ACE inhibitors do
316
Heparin is an ______________ that acts by enhancing the activity of ___________ (which does what?).
Anticoagulant
Antithrombin III (inactivates factor X and thrombin)
317
How does warfarin work?
It inhibits the reduction of vit K thereby inhibiting gamma carboxylation of glutamate in factors II, VII, IX, X
318
Clopidogrel is what type of drug?
ADP receptor antagonist. Prevents ADP binding to platelets thereby preventing platelet activation.
319
What is aspirin and how does it work?
Aspirin in an irreversible cycle-oxygenase inhibitor (thromboxane synthesis inhibitor). It binds irreversibly to COX and prevents formation of thromboxane which is a potent activator of platelets, promoting their endothelial adhesion and the formation of a platelet plug.
320
Streptokinase is what type of drug?
A fibrinolytic drug. It activates plasminogen in order to break down fibrin clots. It's antigenic so can only be used once IV
321
Cardiac glycosides were originally derived from the ________ plant.
How do they work?
What are some examples?
🦊 foxglove
Bind to and inhibit the Na/K ATPase pump on cardiac myocytes (compete with K) --> increased IC Na --> reduced exchange of Ca out of cell. Increased IC Ca increases contractility ***may lead to Decreased K
Digoxin, digitoxin
322
What are the effects of cardiac glycosides at the level of the medullary CV centre? Why are signs of toxicity quite common?
Increase vagal activity--> slow rate of SA node--> slow conduction through atria and AV node conduction --> increase AV node refractory periods. They decrease symp drive and catecholamine levels and partially restore baroreceptors reflexes
They have a low therapeutic index. Digoxin has long half life and is cleared by kidneys
323
Beta adrenoreceptor agonists such as ____________, __________ and ___________ are used in cases of ___________. Adverse effects include ____________
Adrenaline (beta 1 & 2), dopamine (beta 1 & 2) and dobutamine (beta 1 specific).
Severe, acute heart failure
Arrhythmias
324
Phosphorites tears even catalyses the breakdown of ________. Therefore PDE inhibitors such as _________ lead to increased IC cAMP--->_________--> increased cardiac contractility.
cAMP
Amrinone
Increased Ca influx
**note: no longer registered for use in dogs
325
Pimobemdan is what type of drug? It's an inotropic drug with vasodilator properties. As such, its main effects include.....?
Calcium sensitiser.
Increased ventricular contractility
Reduced preload and afterload
326
Negative inotropes include what type of drugs?
Beta adrenergic antagonists (eg. Propanolol) and calcium channel blockers (eg. Amlodipine)
327
Classes of anti-arrhythmic drugs include...?
1. Sodium channel blockers
2. Beta blockers
3. Outward potassium channel blockers
4. Calcium channel blockers (verapamil)
5. Other (digoxin- a cardiac glycoside)
328
Examples of sodium channel blockers include...? They are used primarily in the treatment of ...?
Lignocaine, quinidine, procainamide
Ventricular arrhythmias (act of fast Na channels)
