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Flashcards in Week 3 Deck (90):

What is vascular tone?

The amount of constriction in a blood vessel


Where does most of the calcium come from for smooth muscle contraction?

The extracellular fluid


What happens after Ca2+ and calmodulin bind in smooth muscle contraction?

The complex activates myosin light chain kinase (MLCK) which phosphorylates and activates myosin light-chains.


What are the three possible receptor molecules located in the membrane of the VSM cell that cause a rise in intracellular Ca2+?

L type voltage gated Ca2+
GPCR (affects SR store of Ca2+
Ligand-gated Ca2+


List three differences between smooth muscle and cardiac or skeletal muscle.

1. VSM consumption of ATP is much less, and contraction can be maintained for longer without using much ATP
2. VSM APs depend more on ECF calcium; relatively less stored in the SR
3. VSM has no troponin
4. VSM contracts and relaxes more slowly


Which vessels typically display the myogenic response?

Small arterioles


What are the two major impacts of the myogenic response?

1. Preserves/maintains organ blood flow in the situation of varying arterial pressure
2. Protects downstream capillary beds from exposure to excessive pressure


What would the myogenic response be to an increase in BP in that vessel?

Constriction - VSM increases in response to an increase in transmural pressure and relaxes in response to decreased transmural pressure


In which vessel type is the pulsatile wave of vasomotion seen?



The myogenic response is initial passive stretch followed by active contraction. What initiates the contraction of the VSMC?

Stretch-activated Ca2+ channels


In myogenic response, what perpetuates the contraction of the VSMC?

Tension-sensitive Ca2+ channels


Define metabolic active hyperaemia

Metabolic active hyperaemia describes an increase in tissue blood flow in response to an increased metabolic rate.


What are 4 metabolites that contribute to active hyperaemia?

Metabolites that contribute include CO2, lactate, adenosine, potassium


True or false: active metabolic hyperaemia and reactive hyperaemia have the same physiological control mechanism



What are three other compounds that might influence local hyperemia?

Thromboxane, serotonin (vasoconstriction, from platelets in clotting blood)

Histamine (vasodilation)


What effect on reperfusion flow rate and duration would occluding a vessel for 2 mins as oppose to 30 seconds have?

1. Higher peak blood flow when occlusion first released
2. Longer duration of reactive hyperemia in response to longer deprivation of flow


What is the effect of prostacyclin on VSM?

Inhibits platelet aggregation


What is the effect of endothelins on VSM?



What is the effect of adenosine on VSM?



Name two anti-clotting agents produced by endothelial cells?

1. Antithrombin III
2. Plasminogen activator


What is flow dependent relaxation?

The endothelial cells detect increased shear stress associated with increased flow; causes them to release NO, which induces vasodilation


What event causes NO synthetase to switch on in endothelial cells?

A rise in intracellular Ca2+


What is autoregulation? What are three components of vessel tone 'autoregulation'?

Autoregulation describes changes in vascular resistance that tend to maintain a constant blood flow despite a range of perfusion pressures.

1. Myogenic response
2. Accumulation of vasoactive metabolites * less important for pressure changes alone *
3. Endothelial flow-dependent relaxation


Which adrenoceptor type predominates in coronary circulation?

Beta2 (SNS stim causes


What effect does SNS stimulation of blood vessels have on venous return?

SNS stimulation to veins causes venoconstriction, which assists blood moving from the peripheral to the central vascular pool and back to the heart. Thus, SNS stimulation of the veins increases venous return (which will increase EDV and thence CO)


Define haemostasis

Retention of blood in veins and arteries


Briefly summarise normal haemostasis.

Injury damages the vascular endothelium, exposing sub-endothelial collagen.

vWF from the blood adheres to this, and binds activated platelets to the lesion.

Fibrin, produced by coagulation cascade, adheres to platelet plug and later contracts to stabilise it

Plasmin digests the fibrin clot, and the endothelium regenerates


What happens to blood flow in the area of endothelial injury? What mediates this, and why?

SNS mediates local vasoconstriction which helps to reduce blood loss from the lesion and allow clotting due to reduced blood velocity.


What is the role of thrombin in coagulation?

Cleaves inactive fibrinogen to form fibrin, which can then polymerise and become insoluble. Fibrin added to the clot contributes to clot stability.


Name three things contained in platelets.

Actin , myosin, serotonin


How do platelets get fibrin to bind them?

Externalise GpIIb/IIIa receptors


Define active hyperemia

Active hyperemia is increased blood volume due to arteriolar dilation and expansion of the perfused capillary bed (O2 blood)


Give three examples of active hyperemia

1. Increased blood flow to GIT following ingestion of food
2. Increased blood flow to skeletal muscles during exercise
3. Increased blood flow to the skin during hot weather to augment heat loss


How would you distinguish between active and passive hyperemia of organ or tissue in the LIVE animal?

The colour for active hyperemia is much redder, passive more purple
The temperature of active hyperemia is warm, vs passive is regular - cold.


What are the three major scenarios for the development of generalised congestion?

Congestive heart failure (most common)


Define ascites

Accumulation of non-inflammatory oedema fluid within the peritoneal cavity


Define hydrothorax

Accumulation of non-inflammatory oedema fluid within the pleural cavity


Define hydropericardium

Accumulation of non-inflammatory oedema fluid in the pericardial sac


Define hydrocoele

Accumulation of non-inflammatory oedema fluid within the cavity of the tunica vaginalis of the scrotum


Define anasarca

Severe, generalised oedema


What are two mechanisms for development of oedema in tissues upstream of venous congestion?

1. Increased plasma hydrostatic pressure at venular end of capillary > net filtration
2. Distension of capillaries, venules and veins makes them more permeable to fluid by expanding gaps between adjacent endothelial cells


Why doesnt increased arterial pressure cause oedema formation (usually)?

Because this leads to reflex vasoconstriction of the arterioles (myogenic reflex) and their precapillary sphincters to protect the delicate capillary beds


If no increase in plasma hydrostatic pressure, how low does albumin concentration have to become before get fluid transudation from vessels?

Less than 10-15g/L


What are the five major mechanisms for oedema?

Increased plasma Hydrostatic pressure
Decreased plasma Oncotic pressure
Impeded Lymphatic drainage
Increased Vascular permeability
Sodium retention


What are five examples of disease processes leading to oedema, with one example from each of the major mechanisms?

H - portal hypertension due to cirrhosis (localised) or R sided CHF (generalised)
O - Johnes disease causing excessive protein loss (generalised)
L - lymphadenitis impeding drainage (localised)
V - inflammation due to bee sting (localised) or vasculitis due to Oedema Disease (generalised)
S -


What are two examples of disease processes that would lead to localised oedema?

Local inflammation generating inflammatory mediators which cause widening of gaps between endothelial cells causing increased vascular permeability (e.g burns)

Obstruction of venous outflow of an intestinal segment due to volvulus in a horse


What are three examples of disease processes that would lead to generalised oedema?

Vasculitis leading to generalised oedema through increased vascular permeability e.g Oedema disease in pigs (e. coli)

Glomerulonephritis in dogs causing chronic protein loss in urine

Gastrointestinal parasitism in lamb causing protein malabsorption and loss leading to panhyproproteinaemia


What two things determine diastolic pressure?

Blood volume
Tone of arterioles


What two factors affect SV for a given preload and afterload?

EDV (venous return)


What are the two types of baroreceptors? Where are they found?

High-pressure stretch receptors detect changes in pressure, found aortic arch and carotid sinus

Cardiopulmonary low-pressure stretch receptors detect absolute pressure by monitoring stretch produced by blood volume, are located in pulmonary vessels, atria and ventricles


Which region of the medullary cardiovascular centre does baroreceptor firing stimulate? What is the effect of this?

The depressor region - serves to inhibit aberrant SNS discharge from the pressor region when all is well.


What are three mechanisms for SNS stimulation to the veins and heart improving stroke volume?

1. SNS stimulation of veins to venoconstrict increases venous return, which increases stretch on myocardium during diastole. Due to FS Law of the heart, increased cardiomyocyte length corresponds with increased tension generated by contraction (+ contractility)
2. NA stimulation of cardiomyocytes increases Ca2+ levels in the sarcoplasm, leading to an increase in contractility (more fore generated for a given length)
3. NA stim to SA node increases HR. Increased HR increases cardiomyocyte contractility as less time spent in diastole, so less time for Ca2+ to be extruded from the cell. Thus Ca2+ accumulates in cell with each depolarisation, increasing contractility.


What are the two effects of increasing arteriolar tone in the baroreflex?

1. Increase TPR, which raises/maintains BP
2. Reduce capillary hydrostatic pressure, which favors reabsorption at the post capillary venule, boosting blood volume


Define haemorrhage by rhexis

A substantial tear in a blood vessel or heart chamber leading to rapid escape of a substantial volume of blood


Define haemorrhage by diapedesis

Escape of RBC one by one through minute or microscopically impercetable defects in vessel walls


Haemothorax describes haemorrhage into which body cavity?



What is the clinical term for haemorrhage into a synovial joint?



What is the clinical term for coughing blood?



Define melaena

Diffuse, dark red-black discolouration of faeces due to upper alimentary tract haemorrhage or swallowing blood from respiratory tract (blood is digested)


Define hypaemia

Haemorrhage into the anterior chamber of the eye


What three factors determine the clinical severity of haemorrhage?

Location, volume and rate of blood loss


What is the relationship between speed of blood loss and volume of blood loss required to induce shock?

The faster the blood loss, the smaller the volume needed to induce shock


What types of bleeds are likely to be visible if you have a disorder of primary haemostasis?

Petechiae, purpura, ecchymoses
- bleeding stops when fibrin coagulum is formed
- small, finite volume


What are some clinical signs that might indicate a patient has a disorder of primary haemostasis?

Epistaxis, haematuria, haematemesis, haematochezia, ecchymoses, purpura, petechiae


What are the four major disorders of primary haemostasis?

von Willebrands disease
Blood vessel disorders


What is the most common acquired haemostatic disorder of dogs and cats?



What is the most common mechanism of thrombocytopenia in dogs?

Immune mediated platelet destruction


What is the most common mechanism of thrombocytopenia in cats?

Decreased platelet production due to FeLV or FIV infection


How low must platelets drop before risk of petechial haemorrhages?

Below 40-50 x 10^9 / L


Other than DIC, what are some conditions that could cause excessively fast consumption of platelets, leading to thrombocytopenia?

Heartworm infection
* will not drop platelet count low enough for spontaenous haemorrhage

* will not drop platelet count low enough for spontaenous haemorrhage




What is the most common inherited bleeding disorder in dogs?

von Willebrand's disease


What are the two major mechanisms of von Willebrand's disease?

a) absolute deficiency in vWF
b) reduced functional activity of vWF


Is vWF essential for platelet plug formation in blood vessels with high velocity blood flow or low velocity bloodflow?

High velocity blood flow - otherwise platelets would be washed away by the flow!


Name three sources of vWF for a dog.

Endothelial cells
Subendothelial tissues

NOT platelets! cats only


How does vWF sustain itself in circulation?

Complex with factor VIII (8) which stabilises it and protects from proteolytic degradation


Give three potential causes of damage to small blood vessels which could cause a disorder of primary haemostasis.

1. Canine adenovirus-1 infection (endotheliotrophic)
2. Bacteraemia or toxaemia (e.g LPS)
3. Uraemia due to renal failure


Deficiency of which clotting factor constitutes haemophilia C? Why is this coagulopathy only problematic in severe trauma?

Factor XI (11)
Need factor XI to mediate sustained fibrin activation, where the extrinsic pathway shuts off and the intrinsic is required for sustained clotting. Short term clotting demand can be managed by extrinsic system


Under what circumstances might a dog develop vitamin K deficiency?

Oral antibiotic use kills significant numbers of intestinal flora
Chronic fat maldigestion or malabsorption (e.g complete extrahepatic bile duct obstruction, EPI)


What are the four major mechanisms for secondary haemostatic dysfunction ?

Deficiency in one or more clotting factor e.g haemophilia A (factor 8)

Vitamin K deficiency or antagonism e.g ratbait

Hepatic parenchymal disease

Excessive fibrinolysis or fibrinogenolysis


What are two ways that chronic hepatic disease can impact primary haemostatic function as well as secondary?

1. Death of hepatocytes > damage endothelial cells of sinusoids > consumption of platelets in haemostasis > thrombocytopenia

2. Chronic hepatic disease can cause thrombocytopathy.


Define fibrinolysis

Enzymatic lysis of fibrin by plasmin


How much of the hepatic mass must be compromised before the animal is thought to be predisposed to haemorrhage or thrombosis?

70% or more


In which condition is excessive fibrinolysis a contributor to defective secondary haemostasis in domestic animals?



In which conditions is excessive fibrinogenolysis thought to be a contributor to defective secondary haemostasis in domestic animals?

Snake envenomation e.g rattlesnakes of USA
Administration of plasminogen activators for therapeutic reasons (e.g tPA, streptokinase)
Excessive endothelial release of tPA e.g shock, heat stroke, severe tissue trauma


What are the parameters for fluid classification as a transudate?

protein from 0 - 25g/L

nucleated cells from 0 - 1.5 x 10^9 /L


What are the parameters for fluid classification as a modified transudate?

protein from 25-75g/L

nucleated cells from 1.0 - 7 x 10^9 /L


What are the parameters for fluid classification as an exudate?

protein from 30g/L

nucleated cells from 7 x 10^9 /L


What are the three factors that determine the colour of a subcutaneous haemorrhage?

Arterial or venous blood
Amount lost
Time since bleed


What are the three factors that determine the consequences of haemorrhage?

Amount of blood lost
Rate of blood loss (the faster this is, the less volume needs to be lost to become significant)


Name three things that can activate plasminogen > plasmin

Circulating kallikrien
Activated factor 11 or 12
tPA (from endothelial cells)