Cardiovascular Pathology

Question 1

What is the pericardium?

Answer 1

Outer layer
Fixes the heart to the mediastinum
Provides barrier against infection
Provides lubrication for the movements of the heart
The visceral layer of serous pericardium is also called the epicardium

Question 2

What is the myocardium?

Answer 2

Provides a scaffolding for the heart chambers
Essential for contraction and relaxation of the cardiac walls so that blood can pass between chambers
Allows electrostimulation conduction through it own tissues and into the endocardium

Question 3

What is the endocardium?

Answer 3

Important role in heart genesis, valve and great vessel formation
Contains Purkinje fibres
Transmit electrical impulses
Provides a low friction lining reducing frictional damage to circulating cells and prevents valves sticking together

Question 4

What are some cardiac disorders?

Answer 4

Ischaemic Heart Disease
Heart Failure
Cardiomyopathies
Rheumatic Heart Disease
Other Forms of Carditis

Question 5

What are some vascular disorders?

Answer 5

Arteriosclerosis
Hypertension
Vasculitis

Question 6

What is the systolic section of blood pressure?

Answer 6

Correlates to when the left ventricle contracts
Measuring the amount of pressure that is put under the arterial walls
We measure the pressure at the brachial artery

Question 7

What is the diastole section of blood pressure?

Answer 7

When the ventricle is filling
The large arteries are elastic & can stretch, and then they snap back  but they continue to propagate blood through
so diastolic shows how well your large arteries recoil (how elastic they are)

Question 8

What are the Limitations when taking BP in a healthcare setting?

Answer 8

White coat syndrome
Mask syndrome – BP goes down in front of the health care practitioner.
Best practice, on going BP at home when relaxed

Question 9

What is normal Blood pressure?

Answer 9

Normal 120/ 80
Can have healthy people in and around those values

But population wise:
if elevated over 120/80 over a period of time  hypertensive
If decreased under 120/80 over a period of time  hypotensive

Question 10

What are the two types of hypertension?

Answer 10

Primary (essential)
Secondary (due to something else)

Question 11

What is primary hypertension?

Answer 11

most common type - 90– 95% of cases
As we age, our BP increases
Unsure what causes this.
Known as the silent killer as it is asymptomatic. A high cause of death.
50% of adults in the US have hypertension – 50% of those, don’t know they have it.
The 50% that do know they have it, are being treated incorrectly it.
1 in 2 people with mismanaged hypertension will die of ischaemic heart disease
THIS IS WHY IT IS REALLY IMPORTANT TO CHECK IT!

Question 12

What is the blood pressure equation?

Answer 12

BP = Cardiac Output X Peripheral Vascular Resistance

CO = how much blood leaves the heart per minute
Heart Rate: How many times does the heart beat per min (approx. 70)
Stroke Volume: how many litres (approx. 5l) pumped out
Increase HR or SV = Increase CO

Vascular Resistance = the diameter of the blood vessels.
If you narrow the diameter of a blood vessel – you increase resistance – you increase BP.

Everything works back to this formula! Remember this.

Question 13

What is the Pathophysiology of (Primary)hypertension ?

Answer 13

The Sympathetic Nervous System
Kidneys & body Fluid - The Renin Angiotensin Aldesterone System
Vasculature
Sodium (ion) handling
All play a role in increasing blood pressure.

           BP = Cardiac Output  X  Peripheral Vascular Resistance

Question 14

What is the role of the sympathetic nervous system?

Answer 14

Has a role in the stress response – fight / flight
Release of adrenaline / noradrenaline – controlled by the hypothalamus
The SNS gets activated to keep you alive in that moment
Redirect blood
Increase blood
Breath more air in
Move blood to the muscles away from the skin
Dilate pupils to see

Hormones released in sympathetic response have an effect on blood vessels.
The SNS efferents target different organs
Heart – SA and AV nodes – speeds the heart rate up
Myocardium – increases the contractile force
Blood vessels – cause most arterioles to constrict
Adrenal glands – adrenaline release, which circulates around the blood stream and ramps up all of the above
Kidneys – causes them to release hormones

Question 15

What are the kidneys role in blood pressure?

Answer 15

Kidneys get a 5th of blood volume every minute.
Due to this, very suited to constantly check how much blood pressure is in the system and how much blood volume is being moved around
If it senses a change in BP, the kidneys respond - The Renin Angiotensin Aldosterone System

Main function of kidneys is to filter blood, and to do this, it needs a lot pressure to force plasma out of the blood to do its main filtration job.
If they can’t filter, the metabolites sit and accumulate in the body which can become toxic > death.

The kidneys respond to a drop in blood volume (reduced blood volume, reduced GFR)
Kidneys respond by releasing by renin.

Question 16

What is the The Renin Angiotensin Aldosterone System ?

Answer 16

The kidneys respond to a drop in blood volume (reduced blood volume, reduced GFR)
Kidneys respond by releasing by renin.
Three ways in which renin is released.

The pressure within the afferent blood arterioles has dropped, the granular cells within the blood vessels release renin.

2. A drop in blood volume causes a reduced GFR= there will be slow movement through the nephrons.
   So more time to reabsorb sodium back into the body through the tubules of the nephron
   Therefore by the time the sodium reaches the very end of tubules, the sodium will be low as a lot of it has had time to be reabsorbed back into the body.
   Therefore the macular denser cells which detect low sodium in the end of the tubules cause a release of renin.
   Sympathetic NS can innervate granular cells to release renin.

Now renin is released and circulates around the body and comes across angiotensinogen (ogen – inactive) which is released from the liver.
When Renin interacts with angiotensinogen, it activates it  angiotensin 1
Angiotensin 1 circulates in the blood until it reaches the lungs, where it meets the enzyme ACE.
Ace converts Angiotensin 1 into Angiotensin 2
Angiotensin 2 is one of the most potent vasoconstrictors of the body.
If you constrict blood vessels, you increase BP
Outcome of this system

Angiotensin 2

can further stimulate the nervous system – leading to further BP increase.
Travels to the Blood Brain Barrier, at the 3rd ventricle Angiotensin 2 can cross and stimulate the Sympathetic Nervous System.

Also releases aldosterone from adrenal glands.
Aldosterone causes reabsorption of sodium back into the body, and then water follows, so then you increase blood volume

At the Hypothalamus
Causes release of vasopressin – ADH
ADH reabsorbs back into the body (increasing blood volume, increasing BP).

Question 17

What are the 3 ways renin is released?

Answer 17

The pressure within the afferent blood arterioles has dropped, the granular cells within the blood vessels release renin.

A drop in blood volume causes a reduced GFR= there will be slow movement through the nephrons

Sympathetic NS can innervate granular cells to release renin

Question 18

What affects the vasculature and therefore the BP?

Answer 18

Anything that narrows the lumen will cause an increase in BP:

Ageing – elasticity reduces, replaced with collagen type tissue.
Atherosclerosis – can be both a cause of high BP and an effect.
Obesity
Smoking

There is also Local control

Question 19

What is sodium handling?

Answer 19

Sodium in the body is an ion (Na+ )
The body is predominantly made up of water, so due to the charge of ions, wherever sodium goes, water follows.

If an individual eats a lot of salt, a lot of water will be pulled with it into the body which causes:
Blood volume to increase, which causes BP to increase
Our bodies can mostly adapt and excrete out excess sodium.

Some people are salt sensitive, and their BP rises significantly with increase in salt - salt reduction diet intervention.
Salt sensitivity is present in 50% of primary hypertensive people
25% of people of normal tensive people – are salt sensitive.
Salt sensitive people – don’t have as adaptive vascularity can’t change blood vessels diameter quickly.
For most people this is transient, but if you’re salt sensitive, it will take a bit longer to respond to this.
No objective measure for this – hence why its primary hypertension, and generally advise people to reduce salt.

Question 20

What are the risk factors for primary hypertension?

Answer 20

Modifiable:
Stress
Obesity
Smoking
Physical Inactivity
Increased salt consumption

Non- Modifiable
Genetics
Low income countries or low socio economic income homes

Question 21

What is secondary hypertension?

Answer 21

Has a cause
If you remove the cause, BP reduces.

Causes are grouped as:
Renal
Endocrine
Other
sleep apnoea
pregnancy
Drug induced

Question 22

What are the renal causes of secondary hypertension?

Answer 22

Kidney requires enough BP to maintain GFR

Chronic Kidney disease (reduction in GFR causing release of renin)

renal artery stenosis can’t bring blood to the whole kidney – again releases renin

Question 23

What are the endocrine causes of secondary hypertension?

Answer 23

A Primary aldosteronism (tumor)– Aldosterone enhances Na reabsorption at the distal tubule

Cushings – cortisol released from the adrenal glands. Cortisol is a stress hormone and stimulates SNS and therefore increases BP.

Hyperthyroidism/ hypo: T3/ T4 have a role in enhances in the sympathetic nervous system. Too much, more sensitive to BP- increases heart rate contractibility, increase HR and CO = high BP
Hypo – the opposite. Vasoconstriction of blood vessels.

Adrenal hyperplasia – tumour on medulla- causes release of adrenaline

Tumour in parathyroid gland – calcium homeostasis. If blood calcium is low, parathyroid is released. Helps reabsorption of Ca from bone, and reabsorption of calcium in intestines and kidneys (with vitamin D). Increased Ca2+ has an effect on the heart – increased contractibility o the heart and constricts the blood vessels.

Question 24

What are the other causes of secondary hypertension?

Answer 24

Sleep apnoea
Periods of decreased ventilation whilst sleeping e.g. obstructive or central.
The body will generally wake up, so you have poor quality of sleep.
Activate the SNS more often, no longer getting restorative sleep as much

Pregnancy
General blood volume increase
Hormonal effect from being pregnant has an effect on edema (more fluid on the body)

Drug induced
Cocaine – increase BP, has an effect on increasing adrenaline  SNS effect
Herbal remedies – St. John’s Wart.
NSAIDs – block prostaglandins (chronic use)
Anti depressant. – which increase serotonin or noradrenaline
Decongestants.

Question 25

Long standing hypertension is a risk factor for the brain. How?

Answer 25

haemorrhagic stroke (long term stress, effects the tissue composition, where it branches is the weakest point)
small vessel haemorrhages in the brain
retinal changes – vision changes

Question 26

Long standing hypertension is a risk factor for the heart. How?

Answer 26

Ischaemic heart disease (MI)
Cardiomegaly / hypertrophy of cardiac muscles

Question 27

Long standing hypertension is a risk factor for the kidneys. How?

Answer 27

Nephropathy – remodelling kidney changes due high BP, leads to kidney failure.

Question 28

Long standing hypertension is a risk factor for the arteries. How?

Answer 28

AAA – Abdominal Aortic Aneurysm
Dissecting Aneurysm- high pressure blood shears between the two layers of the blood vessels (tunica / media)
Peripheral Vascular Disease – significant atherosclerotic plaque – stops perfusion into the legs
Carotid changes – atherosclerosis at bifurcation.

Question 29

What is Edema?

Answer 29

Accumulation of excess fluid in tissues is termed edema
Under normal circumstances on a small amount of interstitial fluid leaks which is removed by lymphatic vessels.
Excess fluid leaks from capillaries in 3 main circumstances:

Increased hydrostatic pressure in vessels (heart failure)

More fluid leaves capillaries with reduced plasma oncotic pressure (hypoproteinemia)

More fluid leaves capillaries if vascular permeability is altered (allergic reaction liberating histamine, acute inflammation)

Question 30

What are the Two important types of edema due to cardiac failure?

Answer 30

Increased hydrostatic pressure in the pulmonary vascular bed
Due to left sided heart failure

2. Subcutaneous edema
   Increased hydrostatic pressure in the systemic venous
   system
   Due to right sided heart failure.

Question 31

What are the risk factors of Atherosclerosis?

Answer 31

Hyperlipidaemia
Hypertension
Diabetes mellitus
Cigarette smoking
Family history

Question 32

In Atherosclerosis, what are the 3 types of lesions?

Answer 32

Fatty streak (small, intracellular fat , innocuous)
Atheroma (raised, lipid centre, dangerous)
Fibrous plaque (intimal scar, innocuous)

Question 33

What are fatty streaks?

Answer 33

Almost all children older than 10 in developed countries have fatty streaks, with coronary fatty streaks beginning in adolescence.
It consists of aggregates of foam cells, which are lipoprotein-loaded macrophages.
Fatty streaks may also include T cells, aggregated platelets, and smooth muscle cells.
It is the precursor lesion of atheromas.

Question 34

What is Atheroma?

Answer 34

Atheroma is an accumulation of degenerative material in the intima of an artery wall.
The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.
It develops in areas of turbulent flow due to increased hydrostatic pressure at that point, whereas it is not seen in low pressure systems such as the Pulmonary artery or vein

Question 35

What are Aneurysms?

Answer 35

Change in the structure of the tunica media may result in loss of elasticity of the vessel wall.
Major factor in the pathogenesis of aneurysm formation.
Mainly occurs in large arteries affected by severe atherosclerosis,
Abdominal aorta

An aneurysm which continues to grow in size, will cause progressive weakening of the artery wall.
The larger the aneurysm becomes, the greater the risk of rupture.
This requires surgical intervention
Prevention of a rupture is the most important goal in medical therapy

Question 36

Shapes of aneurysms can be described as..?

Answer 36

Fusiform
bulges or balloons out on all sides of the blood vessel.
usually due to atheroma
often below renal arteries; may affect iliac arteries

Saccular
E.g. Berry Aneurysm in the circle of Willis.
bulges / balloons out on one side

Pseudoaneurysm
aka False aneurysm
Not an enlargement of any of the layers of the blood vessel.
May be as a result of prior surgery.
Blood fills between the layers of the blood vessel wall creating a pseudo aneurysm.

Question 37

What is a dissecting aneurysm?

Answer 37

An aneurysm that occurs with a tear in the artery wall that separated the 3 layers of the wall

(rather than ballooning out the entire wall)

Question 38

What are the causes of aneurysms?

Answer 38

Multifactorial reasons which lead to the breakdown of structural proteins in the artery walls which provide support and stability to the vessel wall.

Atherosclerosis plays an important role in aneurysm formation
risk factors associated with atherosclerosis
e.g. male, genetics, hyperlipidemia, hypertension, smoking, diabetes, obesity.

Question 39

What are some specific causes of aneurysms related to their location?

Answer 39

Abdominal Aortic Aneurysm (AAA)
Atherosclerosis
Genetic
Giant Cell Arteritis

Cerebral Aneurysms
Hypertension
Atherosclerosis
Head Trauma

Iliac Artery Aneurysm
Atherosclerosis
Pregnancy
Post lumbar / Hip surgery

Femoral / Popliteal Aneurysm
Atherosclerosis
Trauma

Question 40

What is Thrombophlebitis?

Answer 40

acute inflammation of veins which triggers a thrombus
Caused by:
bacteria
parasite
physical / chemical stimuli

Superficial thrombophlebitis – visible, localised swelling, erythema

Question 41

What is Deep vein thrombosis?

Answer 41

Deep vein thrombosis – global swelling but no localised erythema visible due to thrombosis within muscle compartment

Question 42

What are varicose veins?

Answer 42

Not primarily inflammatory
Abnormally dilated veins

Sites for varicose Veins:
Legs
Osoephagus
Testes, Vuvla,
perianal (haemorrhoids)

Question 43

What is pericarditis?

Answer 43

Inflammation of the pericardium

Causes:
Infective – Bacterial or Viral
immune-mediated
Chest trauma e.g. RTA
Ischaemic – e.g. following a trans-mural MI causing an inflammatory pericarditis +/- effusion

Resolution may result in:

Constrictive pericarditis - Fibrosis, Fusion + Occasionally calcification
or
Cardiac tamponade – too much fluid in the pericardial space

Both conditions can lead to cardiac failure

Question 44

What is Cardiomyopathy?

Answer 44

Disease of the myocardium
Inherited or acquired

3 main types:
HOCM (Hypertrophic obstructive cardiomyopathy) – 1 in 500
DCM (Dilated cardiomyopathy) - 50% inheritance (inherited + acquired types)
ARVC (Arrthymogenic right ventricular cardiomyopathy) - rare

Question 45

What are the causes of Acquired Cardiomyopathy?

Answer 45

Takosubo/Broken Heart Syndrome
Follows acute physical or emotional stress in 85% of cases
Can cause fatal arrthymias/heart rupture
Myocarditis
autoimmune or viral
Ischaemic
Endocrine
Diabetic/hyperthyroidism
Poisons
chemotherapy, alcohol, drugs

Question 46

What is Rheumatic Fever?

Answer 46

An autoimmune response to an untreated Strep A infections
Scarlet Fever, Strep Throat
Causes an inflammatory disease which can involve:
Heart, skin, joints and brain
The disease typically develops 2 – 4 weeks after a streptococcal throat infection.
the heart is involved in about half of cases
Damage to the heart valves is known as rheumatic heart disease

Question 47

What is Chronic Rheumatic Heart Disease?

Answer 47

Subsequent changes in the heart: Thickening of valve cusp, especially along lines of closure
Fusion of commissures
Result is aortic stenosis, insufficiency or often both
Aortic stenosis> LV hypertrophy
Aortic insufficiency> LV hypertrophy and dilatation

Subsequent changes in the heart:

Predominantly left-sided valves (almost always mitral)
Mitral > Aortic > Tricuspid > Pulmonary
Mitral alone 48%, Mitral + aortic 42%

Question 48

What is Myocardial Infarction?

Answer 48

Occlusion of a coronary artery leading myocardial hypoxia > cell death.
usually due to thrombotic occlusion of a coronary vessel
It is generally accepted that the cross sectional area of the coronary artery lumen must be reduced by > 75% to significantly affect perfusion.
underlying coronary artery disease
Coronary arteries are prone to atheroma due to their unique flow pattern of being empty during systole and filling in diastole. This spurt—flow pattern causes turbulence and arterial wall trauma.
causes a rapid drop in systolic function

Time from Onset Gross Morphologic Finding
18 - 24 Hours Pallor of myocardium

24 - 72 Hours Pallor with some hyperaemia

   3 - 7 	Days 		Hyperaemic border with 								central yellowing                  
10 - 21	Days 		Maximally yellow and soft 								with vascular margins
 	    7 		Weeks 	White fibrosis

Question 49

What is the treatment for Myocardial Infarction?

Answer 49

Anti- coagulants

Stents fitted

Question 50

What are examples are Ischaemic Heart Disease?

Answer 50

Angina Pectoris
Characterised by paroxysmal attacks of exercise related chest pain
Anterior chest pain usually
Caused by myocardial ischaemia

Stable Angina (typical)
Increases on exertion
Resolves completely with rest or vasodilators

Unstable Angina
Occurs at rest or minimal exertion and usually lasts more than 20 minutes.
Severe and of recent onset (i.e. within 1 month).
Occurs with a crescendo pattern (brought on by less activity, more severe, more prolonged or increased frequency than previously.

Question 51

What is congestive heart failure?

Answer 51

Cardiac function is insufficient to pump blood at the rate required by the tissues in the body
Heart failure can also affect the kidney’s ability to dispose of Sodium & water > leading to edema.
As glomerular filtration rate decreases

Divided it into:

Left sided heart Failure
Right sided heart Failure

Question 52

What are the 2 types of left sides heart failure?

Answer 52

Systolic Failure
aka Heart Failure with reduced ejection fraction
the left ventricle loses its ability to contract normally, & so can’t push enough blood out into circulation.

Diastolic Failure
aka Heart Failure with preserved ejection fraction
The left ventricle loses its ability to relax normally (because the muscle has stiffened) & therefore the heart is unable to properly fill with blood between each beat.

If fluid collects in the lungs, it can cause shortness of breath – particularly when a person is lying down
 this is known as pulmonary edema.

Question 53

What is right sides heart failure?

Answer 53

NB. Blood returns from the body to the heart via the right atrium > into the right ventricle.
The right ventricle  then pumps back to the lungs.

Can occur as a result of left sided heart failure
When the left ventricle fails, increased fluid pressure is transferred back to the lungs – damaging the hearts right side.
When the Right side loses power, the blood backs up into the body’s veins
this causes swelling in the ankles and abdomen.