Thomas smith AAA Flashcards by Adam Fogarty

Alpha 1 agonist (sympathomimetic)
Examples
MOA
effect on blood vessels

Example:
Desglymidodrine
Pseudoephedrine
Phenylephrine

MOA:
* post synaptic action
* activates phospholipase C -> increases inositol pathway -> increases diacylglycerol -> increases intracellular calcium

Effect:
*Vasoconstriction/ increases BP.

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Alpha 2 agonist (sympathomimetic)
Examples
MOA
Effect of BP

Examples
*Clonidine

MOA
*pre-synaptic action- acts in CVS centre of CNS
*inhibits adenylyl cyclase
*reduces cAMP formation
*reduces activation of calcium channels
*increases potassium efflux
*causes hyperpolarisation and so norepinephrine cant be released

Effect:
*causes vasodilation by preventing catecholamines vasoconstrictive effect - drops BP

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Beta 1 agonist (sympatomimetic)
Examples
MOA
Effect

Example:
*Dobutamine

MOA:
*Post synaptic action
*Gs GPCR
*activates adenylyl cyclase
*increases cAMP
*activation of L-type calcium channels via phosphorylation
*increased calcium = increased contractile force
*increases opening of HCN channels in SA node = increased HR

Effect
*Increased rate + contractility of heart.
*no major effect on blood vessels.

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Beta 2 agonists (sympathomimetic)

Example
MOA
effect

Example
*Salbutamol

MOA
*post-synaptic
*Gs GPCR
*increases cAMP
*activates PKA
*reduces intracellular calcium influx
*inhibits phosphorylation of myosin light chain kinase.
*prevents constriction

Effects:
Bronchodilation.

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Alpha blockers (antagonists)
Sympatolytics
MOA
Example
Effect

Example
Doxazosin

MOA Inhibits phospholipase C
Inhibits inositol triphosphate
Inhibits diacylglycerol
Reduces intracellular calcium

Causes vasodilation
Anti-hypertensive drug

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Beta blockers/ antagonists

Propanolol- equal affinity for B1+2
Atenolol - selective to B1
Labetalol - antagonises alpha also

-blocks epinephrine/norepinephrine from binding to cardiac myocytes, SA + AV nodal cells.
- lowers intracellular calcium concentration

Effect: reduces HR and contractility

used for:
-arrythmias
- MI
- hypertension
-congestive heart failure

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Define shock and give 4 types.

Shock is the body’s response to systemic hypoperfusion of tissues caused by failure of the cardiovascular system, resulting in impaired tissue perfusion and cellular hypoxia

Hypovolemic
Cardiogenic
Obstructive
Distributive

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Causes of hypovolemic shock

(i) Excessive sweating, vomitting, diarrhea

(ii) Hemmorhage (internal/external)

(iii) uncontrolled diabetes mellitus resulting in polyuria

(iv) third space causes e.g. ascites

REDUCED PRELOAD

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Causes of cardiogenic shock

(i) MI
(ii) valve dysfunction
(iii) excessive afterload
(iv) cardiomyopathiese.g. Lt ventricle hypertrophy.

REDUCED CO

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Causes of obstructive shock

(i) cardiac tamponade
(ii) constrictive pericarditis
(iii) aortic stenosis
(iv) pulmonary embolism
(v) Tension pneumothorax

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Distributive/ vascular shock causes

(i) anaphylaxis: histamine induced vasodilation
(ii) Septic shock
(iii) Neurogenic- trauma to head causes damage to CVS centre of medulla

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Coarctation of the aorta most commonly occurs at what part of aorta?

List 5 complications of coarctation

Distal ligamentum arteriosum- distal to the left subclavian artery branch point.

Left ventricular hypertrophy
Cardiomegaly
Congestive heart failure
Aortic dissection
Systemic hypotension

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Describe the histology of large arteries

Large arteries include Aorta, subclavian, common carotids, iliac arteries.

3 layers:

(i) Tunica Intima
-Endothelial cells (simple squamous epithelium) with tight junctions.
-Sub-endothelial layer
-internal elastic lamina (separates intima from media)

(ii) Tunica media
-Thickest layer in large arteries.
-Smooth muscle cells.
-These SMCs produce collagen, proteoglycans and elastin forming lamellae sheets.
- External elastic lamina

(iii) Tunica Adventitia
-connective tissue
-Fibroblasts
-Macrophages
-Collagen fibres
-Vasa Vasorum

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list 5 functions of endothelium

Exchanging of nutrients between blood and surrounding tissue.
Converts angiotensin I -> II in order to cause vasoconstriction to raise BP
Nitric oxide synthesis
Lipolysis - fat break down to prevent accumulation in intima
Conversion of inflammatory, clotting and vasoconstriction mediators to an inert form to dampen their effects i.e. bradykinin, serotonin, thrombin

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In capillaries, what is the only layer to form their walls? List 3 types of capillaries.

They are surrounded by pericytes, list 3 functions of pericytes. What is their origin?

Tunica intima is the only layer present; Its walls are made of the following
-Endothelium
-Basal lamina
-Pericytes

3 types of capillaries
(i) Continuous - continous endothelial layer and basement membrane BBB, lungs, lung, exocrine glands

(ii)Fenestrated - endothelial layer fenestrated but basement membrane is continuous Intestine, endocrine glands, Glomeruli

(iii)Sinusoids/Discontinuous - both endothelial layer and basement membrane fenestrated. Liver, bone marrow, spleen

3 Functions of pericytes
-Regulate blood flow through contraction
-Help mediate vessel permeability as acting as a barrier to influx/efflux of molecules.
-Can contribute to vessel repair by differentiating into endothelial or SMC’s

They are undifferentiated mesenchymal cells.

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What layer of vein wall is the largest? How can you differentiate them from arteries?

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Tunica adventita

-Their walls are not well defined
-Thinner walls
-There is no internal or external elastic layer
surrounding muscle layer
-They contain valves

Outline the 3 stages of shock

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Non-progressive
- normal body compensatory mechanisms allow for full recovery
Progressive
-Requires intervention to prevent death.
Irreversible
-Loss of ATP -> death

Outline 5 effects of shock on the cellular level

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Reduction in active transport of sodium + potassium
- results in accumulation of sodium + chloride in cell, potassium is lost to the ECF -> cells swell
Reduction in mitochondrial activity
-impaired liver function
-loss of detoxification mechanisms
release of hydrolases from lysosomes -> damages cell
increased production of lactic acid from anaerobic glycolysis
Depletion of ATP -> excess adenosine diffuses into blood forming uric acid

outline 4 complications of massive blood transfusion

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Hypocalcaemia
- Citrate within the blood product can bind the calcium thereby reducing the concentration of ionized calcium.
Coagulopathy
-Dilution of platelets and clotting factors, hypothermia and platelet dysfunction.
Hypothermia
-rapid infusion of cold products - can lead to coagulopathy
Hyperkalemia
-Lysis of RBC’s while in storage -> increased extracellular potassium.

How does hypothermia cause coagulopathy?

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Reduces the release of Thromboxane A2
leads to reduction in platelet stimulation and aggregation and so affects platelet plug formation.

*Can affect the normal function of essential clotting enzymes.

Why are infra-renal AA’s more common than supra-renal?

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Poorer vascularisation via vasa vasorum in infra-renal aorta making it more prone to ischemic damage. Relies more so on direct diffusion of nutrients from blood passing through its lumen.

The infra-renal aorta also has less lamellar sheets making it less elastic so less able to distribute stress.

Define an abdominal aortic aneurysm

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AAA is a localised dilation of the aorta which is > 50% larger than the normal diameter ( >3cm diameter).

5 risk factors for AAA

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Atherosclerosis
Smoking
Diabetes
Hypertension
Age > 65

How does smoking contribute to AAA

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Endothelial damage, chronic inflammation and expression of cytokines, chemokines + leukocyte (mostly macrophage) infiltration.
Degrades elastin + collagen through oxidative stress (mainly via superoxide dismutase)
Increases activity of metalloproteinases -> elastin + collagen break down.
Can cause increased LDL’s and reduced HDL’s -> atherosclerosis

List 5 indications for intervention for AAA

1. > 5.5cm 2. increase in size > 0.5cm in 6 months 3. Abdominal pain 4. Thromboembolic complications 5. PAD lower limbs

2 AAA repair options and mortality rates associated

1. Open repair - 7% MR 2. Endovascular aneurysm repair (EVAR)- 2% MR

how does diabetes increase risk of AAA

Chronic hyperglycemia -> endothelial dysfunction -> increased vascular permeability -> LDL uptake -> athersclerosis

At what level does the abdominal aorta bifurcate?

What vertebral levels: Aorta passes through diaphragm with azygous vein + thoracic duct Coeliac trunk Testicular + Ovarian arteries branch from aorta Inferior mesenteric branch of aorta Abdominal aorta bifurcation

Aorta/thoracic duct/Azygous vein: T12 Coeliac trunk: T12 Testicular and ovarian artery: L2 Inferior mesenteric artery: L3 AA bifurcation: L4

Explain the Bainbridge Reflex

The bainbridge reflex is a compensatory increase in HR in response to increased Rt Atrial pressure i.e. Increased central venous pressure. This response is seen with fluid overload The increased pressure within the vena cava -> rt atria increases HR by directly stretching the SA node fibres + by activating atrial baroreceptors which send firing signals to the medulla thereby increasing Sympathetic firing to the heart thereby increasing HR. The effects are mediated by carotid sinus / aortic arch baroreceptors once blood pressure within the arteries rises -> opposite response occurs and parasympathetic nervous system reduces the HR.

List 3 common blood products used in AAA surgical repair and outline the purpose behind them

1. Packed red blood cells -will help improve oxygen carrying capacity of blood and offset anaemia by increasing hemoglobin levels -> This will help maintain tissue perfusion during/after sx. 2. Fresh frozen plasma - Will help replenish lost clotting factors. Will minimize risk of bleed out during surgery. 3. Platelets - Can be given if there is low platelet count (thrombocytopenia) which can occur following blood loss/ massive transfusion reactions. This will improve the bloods clotting ability.

How does hypothermia affect coagulation?

Inhibits release of Thromboxane A2 = reduced platelet activation, aggregation and platelet plug formation. Inhibits normal function of clotting factors within the coagulation cascade.

list 4 histological features that may be seen at biopsy of an aorta that underwent AAA

1. Loss/ degradation of elastin fibres. 2. Thinning of tunica media with loss of or disorganisation of smooth muscles cells. 3. Inflammatory infiltrate, particularly monocytes/macrophages. 4. Calcification of artery wall. 5. Foam cells 6. Cholesterol clefts

list the 3 types of Arteriosclerosis

(1) Atherosclerosis (most common) - in large/medium elastic arteries. (2) Arteriolosclerosis ->hyaline ->hyperplastic Thickening of arteriole walls usually due to hypertension or diabetes mellitus (3) Monckeberg medial calcific sclerosis -> calcium deposits in muscular arteries.

What is the most common cause of AAA

Atherosclerosis of the aorta due to hypertension, smoking, hyperlipidemia, hyperglycemia.

Describe the mechanism behind a plaque rupture

Unstable plaques have less fibrous cap and more inflammatory cells compared to stable plaques. The stability is dependant on collagen production by the SMC's which makes the plaque harder and more stable. However, macrophages also produce metalloproteinases which break down collagen. Therefore, if the balance is lost between collagen production and collagen breakdown, coupled with factors such as high blood pressure, then the plaque can rupture leading to thrombus formation.

What is central venous pressure and what is a normal CVP?

CVP refers the the blood pressure within the thoracic/superior vena cava. It can be used as a means of determining pressure within the right atrium since SVC is a direct continuation. It is used to monitor venous return to the heart. Normal 2-8mmHg

What are the equations for the following: CO BP MAP What is a normal cardiac output

CO = SV x HR BP = CO x TPR MAP = CO x PR Normal CO is 5.25L/min

outline the formation of platelet plug via primary hemostasis

Damage to endothelium results in transient vasoconstriction due to endothelin release and neural reflexes. von-willebrand factor, found in alpha granules of platelets and weibel palade bodies of endothelial cells, binds to exposed collagen at site of injury. Platelets then use vWF as anchorage, binding to it via GPLB receptors. Activated platelets release TXA2, serotonin, vWF, ADP and Ca2+ to enchance activity of other platelets. More platelets bind to ADP using P2Y12 receptors which stimulates expression of GIIb/IIIa on platelets surface. Fibriogen can then bind to these glycoproteins and become activated to fibrin via Thrombin. Fibrin can then cross link the platelets, forming a meshwork which traps platelets and red blood cells thereby forming a fibrous plug/growing thrombus.

Thomas smith AAA Flashcards

(39 cards)