Written exam

Question 1

Cardiovascualr system - What is the frank starling law?

Answer 1

Frank Starling law represents the relationship between stroke volume and end diastolic volume.
It highlights the idea hearts ability to change its force of contraction and therefore the stroke volumes in response to changes in venous return.

Question 2

Explain the role of the frank starling law in cardiac physioloigy.

Answer 2

• The importance lies mainly with adapting to changes with left and right ventricular output.
• The myocardium and the cardiac muscle has an ability to increase contracility in response to stress or tension.
• The Frank-Starling law states that the force or tension developed in a muscle fiber depends on the extent to which the fiber is stretched

Question 3

How does increased preload affect stroke volume?

Answer 3

• This relationship is shown in frank starling law.
• An increase in pre load leads to an increase in stroke volume. This is because when more blood that is being pushed into the ventricals, the stretch of the myocytes increase. This makes more tension being developed on the ventricular wall leading to a greater force when conteraction is generated.

Question 4

Atherosclerosis - What does damage to the endothelial cells do?

Answer 4

• Endothelial cells are damaged from hypertension, smoking, hyperglycemia.
• damage to the endothelial cells increases permaebility of the arterial wall. This allows LDLS to enter the tunica intima.

Question 5

What happens to the macrophages when the endothelial cells are damaed in atheroscelosis?

Answer 5

White blood cells are moving through the blood vessel in the adventitia layer but when the endothelial cells are damaged they express adhesion molecules which signal for white blood cells to move towards the sight of damage.

Question 6

What do white blood cells release in atheroscelosis?

Answer 6

They release free radicals which cause oxidation rection of LDLs meaning they become macrophages.

Question 7

What will the white blood cells do once they have became macrophages?

Answer 7

The white blood cells engulf the LDLS forming foam cells. Once the lipid laden foam cells accumulate in big amounts they form a lesion called a fatty streak.

Question 8

How does a fatty streak become a fibrous plaque?

Answer 8

The smooth muscle cells proliferate in the afftected muscle and produce collagen. Collagen is a critical component im forming lesions. The endothelial cells and smooth muscle cells cover the fatty streak creating the fibrous plaque.
The collagen, fibrogen and calcium salts will adhere creating a fibrous plaque.

Question 9

What can be a reason that the atherscleotic plaque can rupture?

Answer 9

If the endothelial cells that are covering the plaque are damaged, the plaque will be exposed and can become dasmaged and eventually rupture.

Question 10

Define bronchial asthma -

Answer 10

Bronchial asthma is caused by the thick mucus production, mucosal odema and smooth muscle spasm causing obstriction to the small airways. This can cause breathing to become laboured and expiration can become be more difficult.

Question 11

What initates an adaptive immune response in asthma?

Answer 11

Airway epithelial exposure to allergy antigens.

Question 12

What does antigen exposure to the bronchial mucosa cause?

Answer 12

The activation of the dendritic cells which are the macrophages. These present to the antigen CD4T which then differentiate into TH2 cells.

Question 13

In early asthmatic response what does the TH2 cells do?

Answer 13

Releases cytokines and will stimulate B cell activation and the activation of antigen specific IGE.

Question 14

What does IL5 do in Asthma?

Answer 14

IL5 stimulates the activation, migration and proliferation of eosinophils. This will cause direct tissue injury and the release of toxic neuropeptides. This will contribute to airway scarring, endothelial injury and bronchial hyperresponsiveness.

Question 15

What is asthma often the result of?

Answer 15

A strong immune reaction to allergens.

Question 16

What does inhaled irritants stimulate?

Answer 16

TH2 cell proliferation which will cause the production and release of TH2 cytokines, IL4 and IL13.

Question 17

What does IL4 (interlukin) do?

Answer 17

IL4 is a key mediator if allergic inflammation. It also alongside IL13 promotes the production of immunoglobin E (IGE) antibodies.

Question 18

What does IL13 do?

Answer 18

IL13 impairs mucocillary clearence and enhances fibroblast secretion contributing to airway remodelling. It also helps IL4 to produce immunoglobin E (IGE) antibodies.

Question 19

What do TH17 cells produce in regards to asthma?

Answer 19

IL17 and IL22

Question 20

What does IL22 do?

Answer 20

Stimulates the airway endothelial cells which play an important role in stimulating further inate and adaptive responses. It also promotes cellular proliferation and wound healing.

Question 21

What does IL17 do?

Answer 21

Increases neutrophilic inflammation enhancing the inflammation response.

Question 22

What do the cytokines IL17 and IL22 do?

Answer 22

Induce airway inflammation and IL17A increases smooth muscle contractility.

Question 23

In asthma what does inflammation cause?

Answer 23

inflammation will lead to swelling of the airways which will cause them to narrow and will increase the production of mucus. This can occlude the airways.

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Question 24

What do TH1 cells do in asthma?

Answer 24

Promote cell mediated immune responses by producing interferon gamma, IL2 and tumour necrosis factor beta (multifunctional cytokine).

Question 25

Why are mast cells important in asthma?

Answer 25

Mast cells are important in how the body repsonds to certain bacteria and parasites. The FC proportion of the preformed IGE will bind to the receptors on the surface of the mast cells. Once bound to the antigen, the IGE will cause the mast cell to degranulate. This will cause the release of inflammatory mediatiors, together these will cause vasodilation and will increase capillaruy permability. This is an increase in fluid movement across the capillary wall. This narrows the airway and obstruct the airflow.

Question 26

In asthma, what happens in late asthmatic response?

Answer 26

The chemoatic recruitment of lymphocytes, eospinophils and neurophils that
are collected in the early phase cause a latent release of inflammatory mediators. This will cause bronchospasm, mucus secretion and odema.

Question 27

How is plugs in the airways caused in asthma?

Answer 27

The damage to the endothelial cells contribute to impaired mucocillary function. This causes the accumulation of debris and mucus, forming plugs in the airways

Question 28

What cause air trapping in asthma?

Answer 28

Airflow obstruction increases resirance to airflow and decreases flow rates, especially expiration rates. Impaired expiration can cause air trapping, hyperinflation distal to the obstruction and an increased WOB.

Question 29

What can continued air trapping cause?

Answer 29

An increase in intrapleural and alveolar gas pressure and a decrease in the perfusion at the alveoli.

Question 30

What can IL5 and IL13 do together?

Answer 30

Break down the endothelial layer, causing fluid to move into the airway. The eosinophils also bind with IGE to release toxic substances to damage some of the endothelial cells. Increased fluid movement and bronchospasm cause constriction.

Question 31

What does asthma cause to the body?

Answer 31

Due to inflammation, constriction of the airways and fluid movement asthma causes reduced amount of oxygen being diffused into the blood stream from the alveoli. This will reduce the amount of oxygen going to vital organs and surrounding tissues, making the body work harder.

Question 32

What is the most common form of angina?

Answer 32

Stable angina

Question 33

What is angina?

Answer 33

Angina is chest pain caused by the reduced blood flow and oxygen going to the heart muscles. It can feel like pressure, tightness or squeezing in the chest when the heart is not recieving enough oxygen. There can also be pain or a dull ache within the shoulders, neck or jaw.

Question 34

What are some other symptoms of angina?

Answer 34

Angina equivelent symptoms include SOB, fatigue, sweating and nausea.

Question 35

What happens during stable angina?

Answer 35

The gradual luminal narrowing or hardening of the arterial wall. This means that the affected vessels cannot dilate in response to the increase in myocardium demand.

Question 36

What is angina pectoris?

Answer 36

Substernal chest discomfort, ranging from a sensation of heaviness to pressure.

Question 37

What causes angina pectoris?

Answer 37

Buildup of lactic acid or abnormal stretching of the ischemic myocardium. This irriates the nerve fibres. The afferent sympathetic nerve fibres enter the spinal cord at locations c3-t4, accounting for the location and radiation of angina pain

Question 38

Define Athersclerosis:

Answer 38

A chronic inflammatory disease characterised by thickening and hardening of the arterial wall.

Question 39

What happens in atherosclerosis?

Answer 39

• Lesions and plaques that are composed of lipids, calcium and other substances such as cellular waste products develop on the vessel wall and harden overtime.
• Development of these lesions casues platelet aggregation (collection), vasoconstriction, vessel obstruction and thrombosis.

Question 40

What happens to the heart when the arteries are hardened and narrowed?

Answer 40

The heart must work harder to pumb oxygen and blood through the arteries causing hypertension.

Question 41

What happens to the injured endothelial cells in atheroscelrosis?

Answer 41

The injured cells become more pearmable, become inflamed and signal T cells and monocytes to attach to the artery wall.
These cells then move into the artery wall where they transform into foam cells. These cells accumulaste in large amounts and form a lesion called a fatty streak.

Question 42

Where can the plaques grow?

Answer 42

The plaques can either grow into the artery lumen or into the artery wall.

Question 43

What happens if the plaque grows into the artery lumen?

Answer 43

Tissue perfusion can become compromised.

Question 44

What happens when the plaque ruptures?

Answer 44

The cells and material on the inside becomes exposed which can trigger thrombisis.

Question 45

If the plaque has formed in the coronary artery what can be the sign?

Answer 45

Chest pain during exertion

Question 46

What do sudden occlusions in the cerebral arteries cause?

Answer 46

Strokes and sudden occlusions in the leg arteries.

Question 47

Define what an MI is:

Answer 47

An MI is the death of the myocardium through a sudden blockage of the coronary artery blood flow.

Question 48

What differs an MI to Angina?

Answer 48

Angina is the result of narrowed arteries rather than blocked.

Question 49

What can cause an MI?

Answer 49

Vasospasm, atheroscerosis and a thrombus.
In most cases tears in the plaque buildup associated with atheroscerosis and cause a thrombus to form. As a result of the occlusion, the myocardium cannot meet the bodys needs for oxygen and nutrients

Question 50

Describe an NSTEMI

Answer 50

• When the thrombus breaks up before complete distal necrosis has occured, the infarction will only include the myocardium directly beneath the endocardium.
• This is called a subendocardial MI and results in T wave inverstion and ST depression

Question 51

What is the presentation of a NSTEMI?

Answer 51

• changes with blood pressure, high and low
• Substernal chest pain

Question 52

Define a STEMI

Answer 52

• if the thrombus lodges permantley in the vessel, the infarction will extend all through the myocardium, going from the endocardium to the epicardium
• This is called a transmural MI and results in severe cardiac disfunction.
• This shows as ST elevation

Question 53

During an MI, what is oxygen deprivation accompanied with?

Answer 53

Poor buffering capabilities and disturbances with electrolytes. Specfically the loss of calcium, potassium and magnesium. Loss of nutrients and oxygen can affect the hearts contractility, therefore reducing the hearts pumping ability.

Question 54

What happens to the oxygen stores in an MI?

Answer 54

Oxygen reserves are used within 8 seconds of no coronary blood flow. Glycogen stores then decrease as anerobic metabolism begins. This causes lactic acid to accumulate and hydrogen ions.

Question 55

What do ischmeic myocadial cells release?

Answer 55

Epinephrine and noepinephrine. This prediposes the individual to imbalances of the parasympatheic (change in heart rate) and sympathetic (increase in HR and contractility).

Question 56

What do cathelomoines (adrenaline) do?

Answer 56

Mediates the release of glycogen, glucose and sotred fat from body cells. This means that plasma concentrations rise 1 hour after the onset of an MI. Excessive levels can be harmful to the cell membranes.

Question 57

What does Norepinephrine do during an MI?

Answer 57

Elevate blood glucose levels through the stimulation of the liver and skeletal muscle cells. It also supresses pancreatic B cell acidity which reduces insulin secretion, highering blood glucose levels further.

Question 58

What does Angiotensin 2 do in an MI?

Answer 58

Released through the RAAS system.
Released locally where it is a growth factor for smooth muscle cells, myocytes and cardiac fibroblasts.