Aneurism and Atheroma (M2 20/11) Flashcards Preview

Case 3: Hypertension > Aneurism and Atheroma (M2 20/11) > Flashcards

Flashcards in Aneurism and Atheroma (M2 20/11) Deck (36)
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1

LO:

  • Describe the main types of aneurysms and describe the main pathogenic mechanisms, morphological features and clinical course
  • Apply the principles of clinical reasoning in formulating a differential diagnosis between the different presentations of cardiovascular disease
  • Describe the multifactorial nature of essential hypertension and causes of secondary hypertension
  • Describe the pathophysiology of hypertension particularly in end stage organ damage
  • Describe the causes, underlying pathophysiology and clinical consequences of arteriosclerosis
  • Describe the difference between atheroma and arteriosclerosis

These are the LO's dodo brain.

2

What is the definition of hypertension?

  • Chronic elevated blood pressure
  • 140/90 mm Hg
  • or 130/80 mm Hg in diabetics/ renal disease

3

How do we classify the level of BP elevation?

 

The diastolic pressure is generally regarded as the baseline for assessment of level of hypertension.

Mild: less than 105 diastolic

Moderate: between 105 and 115 diastolic

Severe: more than 115 diastolic

Malignant: more than 130 diastolic

4

How do we classify the types of primary/essential hypertension?

  • Primary or essential hypertension is when there is no identifiable cause of the high BP.
  • Primary/essential HP can be malignant or benign.
  • Primary/ essential hypertention is extremely high blood pressure that develops rapidly and causes some type of organ damage. A person with malignant hypertension has a blood pressure that's typically above 180/120. Malignant hypertension should be treated as a medical emergency.
  • Primary/essential benign hypertension: a form of high blood pressure that tends to develop slowly and may not cause any noticeable symptoms for a number of years.

5

Which factors regulate BP?

  • Mean Arterial Pressure is the average pressure in the arteries causing flow.
  • MAP: CO X TPR
  • CO: amount of blood the heart pumps through the circulatory system in a minute. 
  • TPR: resistance in the arteries, a function of the internal vessel diameter, vessel length, and blood viscosity.
  • CO is affected by blood volume (Na+/ Mineralocorticoids/ Atriopeptin) and cardiac factors (heart rate and strength of contractility).
  • Total peripheral resistance is affected by humoral (Constrictors: Angiotensin II, catecholamines,Thromboxane, leukotrienes. AND Dilators: Prostaglandins, Kinins, NO) and neural factors (Adrenergic constrictors and dilators).

6

What are the mechanisms for essential/primary hypertension?

  1. ABNORMAL RENIN ANGIOTENSIN ALDOSTERONE SYSTEM: Renin is produced by cells in the macula densa of the distal convoluted tubule in response to a decrease in sodium concentration.Renin converts angiotensinogen in the blood into angiotensin one. In the lungs ACE coonverts it into angiotensin 2. This causes vasoconstriction and aldosterone to be raised so there is more sodium retention, so BP increases.

  2. ABNORMAL SODIUM HOMEOSTASIS: 

  3. ABNORMAL SENSITIVITY TO CATECHOLAMINES OR INCREASED CATECHOLAMINES

7

Possible causes for secondary hypertension are?

•Some acute and all chronic renal diseases.

•Adrenal tumors: pheomchromacytoma

•Coarctation of the aorta: aortic narrowing, pressent from birth.

•Drug Therapy: Corticosteroids- these are man-made drugs that mimic the hormones produced from the adrenal glands and used as anti-inflammatories.

•Sleep apnoea: This is pauses  in braething that can last from a few seconds to minutes.They may occur 30 times or more an hour. Typically, normal breathing then starts again, sometimes with a loud snort or choking sound. Sudden drops in blood oxygen levels that occur during sleep apnea increase blood pressure and strain the cardiovascular system. 

This type of hypertension can be cured

8

What are the clinical effects of benign hypertension?

BENIGN HYPERTENSION results in chronic changes with risk of stroke and heart failure. Long term drug therapy is used to prevent these complications.

9

What are the clinical effects of malignant hypertension?

MALIGNANT HYPERTENSION is a relatively acute and serious condition which is rapidly progressive, and damages the kidneys and brain. This condition is a medical emergency

10

What is the effect of benign hypertension on the heart?

  • Benign hypertension is due to increased peripheral vascular resistance so there is increased cardiac workload for the hear. This leads to concentric hypertrophy of the left ventricle. This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress. This type of ventricle becomes stiff (i.e. compliance is reduced), which can impair filling and lead to diastolic dysfunction. Eventually the left ventricle may no longer be able to deal with the increased peripheral resistance, and the left heart fails (CHF).
  • The heart becomes prone to ventricular arrhythmia (abnormal heart rhythms) which can cause sudden death. This may be due to the scarring on the left ventricle preventing electrical signals being delivered normally.
  • Sudden cardiac arrest occurs when the electrical system to the heart malfunctions and suddenly becomes very irregular. The heart beats dangerously fast. The ventricles may flutter or quiver (ventricular fibrillation) and blood is not delivered to the body. In the first few minutes, the greatest concern is that blood flow to the brain will be reduced so drastically that a person will lose consciousness. Death follows unless emergency treatment is begun immediately.

 

11

What is the effect of benign hypertension on the brain?

There is a much increased risk of cerebral haemorrhage.

Patients with subarachnoid (a type of stroke caused by bleeding on the surface of the brain. It's a very serious condition and can be fatal) or intracerebral haemorrhage (a type of stroke caused by bleeding within the brain tissue itself) due to a ruptured aneurysm often give a history of hypertension.

12

What is the effect of benign hypertension on the arteries?

Increased incidence of atheromatosis (fatty deposit/plaque) leading to ischemia

13

What are the consequences of malignant hypertension, and what is the quantative measure for MH?

A diastolic BP greater than 130 mm Hg

MH results in:

  • Cardiac failure with left ventricular hypertrophy and dilation
  • Blurred vision due to papilloedema (swelling of the blind spot) and retinal haemorrhages
  • Haematuria (red blood cells in the urine) and renal failure due to fibrinoid necrosis ( a form of cellular death that results in the formation of fibrous tissue) of glomeruli
  • Severe headache and cerebral hemorrhage

14

What are the effects of malignant hypertension on the heart?

There is risk of acute left heart failure.

The radiograph shows typical fluffy shadowing

 

15

What are the effects of malignant hypertension on the eye?

Ophthalmoscopy shows papilloedema (optic disc/ blind spot swelling that is caused by increased intracranial pressure) and retinal hamorrhages leading to blurred vision.

16

What are the effects of malignant hypertension on the kidney?

The small vessels undergo myxoid (mucus?) occlusion and / or fibrinoid necrosis.

The patient develops haematuria (RBC in urine) and then renal failure.

17

What are the effects of malignant hypertension on the brain?

Widespread small ischaemic lesions can result in hypertensive encephalopathy (brain dysfunction/ neurologic symptoms that are associated with the malignant hypertensive state in a hypertensive emergency) leading to severe headache, seizures and  reduced conscious level.

There is risk of cerebral haemorrhage.

18

What is a true aneurysm?

A true aneurysm is a localised permanent dilatation of part of the vascular tree. Basically, an aneurysm is a swelling in a vessel.

19

What is a false aneurysm?

A false aneurysm is a blood-filled space around a blood vessel

20

Name the types of aneurysms

•Atherosclerotic:  these are aneurysms caused by atherosclerosis and typically occur in the abdominal aorta, thus generating abdominal aortic aneurysms. 

•Dissecting: an aneurysm in which the wall of an artery rips (dissects) longitudinally. They tend to affect the thoracic aorta.

•Berry: these are berry shaped aneurysms arising at bifurcations of the intracranial arteries.

•Capillary micro-aneurysms: tiny aneurysms in the capillaries.

•Syphilitic Aortis: inflammation of the aorta associated with the tertiary stage of syphilis infection. Begins as inflammation of the outermost layer of the blood vessel, including the blood vessels that supply the aorta itself with blood, the vasa vasorum. As SA worsens, the vasa vasorum undergo hyperplastic thickening of their walls thereby restricting blood flow and causing ischemia of the outer two-thirds of the aortic wall. Starved for oxygen and nutrients, elastic fibers become patchy and smooth muscle cells die. If the disease progresses, syphilitic aortitis leads to an aortic aneurysm

•Mycotic: 

•Cardiac

21

Describe abdominal aortic aneurysms

  • It is an ATHEROSCLEROTIC ANEURYSM
  • AETIOLOGICAL FACTORS: Atheromatosis
  • It is a common condition with multifactorial causes: DNA variants and Polygenic

22

What is the clinical course of abdominal aortic aneurysms?

1.Pulsatile abdominal mass

2.Rupture into the retroperitoneum and from there to the peritoneal cavity

3.Atheroembolism from associated atheroma

4.Erosion of adjacent vertebrae or compression of the ureter

23

How does abdominal aortic repair happen?

see slide 30

24

How does endovascular open repair happen?

see slide 32

25

What is a dissecting aneurysm?

An intimal tear develops which allows blood to track into the media.

Blood proceeds along the media forming a dissection.

The patient presents with severe pain usually in the back, and often shock.

As it proceeds, branches of the aorta are blocked, causing acute ischaemic damage.

26

What is the Clinical Course of a Dissecting Aneurysm?

1.Rupture

2.Cardiac tamponade / haemopericardium (dissection into the pericardial sac).

3.Aortic insufficiency

4.Myocardial infarction

5.Extension of dissection into the great arteries of the neck, coronary arteries and mesenteric arteries

6.The aneurysm may re-enter the aorta giving a “double barrelled” aorta.

7.There is a very high mortality.

27

Describe thoracic aortic aneurysm.

DISSECTING ANEURYSM)

AETIOLOGICAL FACTORS à Degeneration of media in most cases.

Atheroma may serve as entry point.  Hypertension is associated, but not a direct cause.

Associated to a single DNA mutation

Monogenic

Autosomal dominant transmision

Rare condition

28

What are the FAMILIAL PATTERNS IN DEGENERATIVE AORTIC DISEASES like TAA

  • Inherited syndromes  - Genes encoding Transforming Growth Factor  (TGF- β) receptors mutations

  • •Marfan Sd.

    •Ehlers Danlos Sd.

    •Loeys-Dietz Sd. (2005)

    •Aneurisms-Osteoartrits Sd (2011)

    •LDS4 (2012)

    •Arterial tortuosity Sd.

29

Describe berry aneurysms

May be due to a congenital defect in elastica or media

Occur in the arteries at the base of the brain, especially the Circle of Willis

Associated with polycystic kidney disease

May rupture to give subarachnoid haemorrhage

30

Describe CAPILLARY MICROANEURYSMs

<0.5mm

Also known as Charcot Bouchard aneurysms

Associated with both hypertension and diabetes

Precursor of primary hypertensive intracerebral haemorrhage