4/4 Flashcards

1
Q

4 types of arteries

A
  1. elastic: aorta & beginnings of branches
  2. muscular: thick smooth muscle t. media
  3. small: autonomic blood flow regulation
  4. arterioles: fewer that 5 layers of muscle
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2
Q

Lipoproteins are…

formed in…

A
  1. any complex of lipids with proteins

2. usually formed in liver or intestine

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3
Q

Atherosclerosis
definition
pathology process
nomenclature

A

Atheroschlerosis is the #1 killer in US.
1. It is a response to injury featuring the accumulation of cholesterol-rich fat in the intima of the large and medium-sized arteries (these are macrophages that have appetite for LDL cholesterol forming plaques or atheromas).

  1. Plaques occlude arteries (slowly over time or suddenly by rupture of plaques) causing ischemic heart disease, myocardial infarction, stroke and gangrene of the extremities.
  2. This term derives from Greek word meaning “hardening” or “induration”.
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4
Q

Pathologists recognise four kinds of arteriosclerotic lesion:

A
  1. atherosclerosis
  2. arteriolosclerosis
  3. hypertensive arteriosclerosis
  4. medial calcific sclerosis (produces calcification in the media of large arteries in elderly people)
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5
Q

6 risk factors for atherosclerosis are:

A

a) high LDL level - heredity, diet, exercise
b) cigarette smoking - smoke oxidizes LDL
c) high blood pressure - intima damage
d) lack of exercise - change in lipoprotein receptor count
e) heredity - familial hypercholesterolemia
f) low HDL levels - HDL keep LDL from binding to plaques

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5
Q

The risk factors for atherosclerosis can be divided into three groups:

A
  1. factors that we cannot do anything about: heredity, male sex, and advancing age
  2. “deadly quartet”: hypertension, hyperlipidemia (cholesterol and LDL), cigarette smoking, and diabetes mellitus
  3. “soft” factors of uncertain importance: obesity, inactivity and personality characteristics
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6
Q

Examination of the ocular fundus is an important test for :

A

monitoring of any patient who is liable to develop any form of arteriosclerosis.

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8
Q

Vascular smooth muscle is important factor in atherosclerosis because (2)

A
  1. it has receptors for LDL

2. it can get into intima through holes in the internal elastic membrane.

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8
Q

Atherosclerosis development has different stages, it starts with:

A

an early lesion of the endothelial surface of large arteries.

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9
Q

Pathogenesis of atherosclerosis is today explained as

response-to-injury hypothesis (3)

A
  1. the development of focal areas of chronic endothelial injury: fatty streaks, intimal masse
    proliferation of smooth muscle cells in the intima with the formation of connective tissue
  2. insudation of lipoproteins (oxidized LDL and VLDL) producing cell injury
  3. accumulation of macrophages & platelets and formation of fibrous cap & atheroma
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10
Q

fibrolipid plaque phase:

A

At this point intimal changes are not reversible.

In general the intimal surface shows a layer of fibrosis - “fibrous cap” which encloses a zone of fatty, necrotic, and partly calcified debris full of elongated smooth muscle cells, fibroblasts and macrophages.

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11
Q

Two kinds of this early lesion are described:

A
  1. fatty streaks: are lesions which begin in children in all populations and show collections of foamy lipid-laden macrophages and smooth muscle cells just beneath the intimal surface of the arteries.
  2. diffuse intimal fibrosis: is also a change that develops over the first few decades of life, and may be related to the development of atheroma.
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13
Q

When plaques are formed they may become confluent and (3)

A
  1. calcified: producing the “eggshell aorta”
  2. ulcerate: this is more important complication that may lead to
    embolization of plaque debris - atheroembolism, and also provides a naked non-endothelialized surface which is a site for thrombosis and possible thromboembolism
  3. bleed: haemorrhage into plaques can also occur
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13
Q

Hypertension : pressures

A

systolic blood pressure over 160 mmHg and /or diastolic pressure over 90 mmHg

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14
Q

With expansion of plaques, what would happen to the the internal layer of the intima?

What do Media damages lead to?

If it is not surgically repaired what is the most important complication of aneurysm?

A

With expansion of plaques, the internal layer of the intima may become broken up and the lesion may induce pressure changes on the tunica media.

Media damage leads to the formation of atherosclerotic aneurysm that can be fusiform or saccular, depending of the shape. Most common location of this aneurysm is in the aorta below the a. renalis, and often going down into the iliac arteries.

If it is not surgically repaired the most important complication of aneurysm is rupture followed by severe haemorrhage into the peritoneal cavity.

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16
Q

Hypertension is result from an imbalance in the interactions between: (4)

A
  1. cardiac output: systemic pressure, venous return
  2. renal function: renin-angiotensin-aldosteron
  3. peripheral resistance: arteriosclerosis
  4. sodium homeostasis: diet, pheochromocytoma
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16
Q

Aneurysms

A

Abnormal dilatations of arteries or veins are called aneurysms. They develop as a result of marked weakening of the wall of a vessel (t. media). Any vessel may be affected, but they are much more frequent in aorta.

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17
Q

Vasculitis (3)

A

Vasculitis is defined as inflammation and necrosis of blood vessels (aortitis).

a) Raynaud phenomenon (vasculitis)
b) polyarteritis nodosa
c) thromboangiitis obliterans - Buerger disease
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19
Q

Aneurism caused by wide variety of disorders: (3)

A
  1. congenital (atherosclerosis)
  2. infections (syphilis),
    1. trauma.
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19
Q

Dissecting aneurysm is:

A

a lesion which occurs when blood is forced through an intimal defect into the wall of an artery, under arterial pressure. This may lead to extension of a column of blood that may travel for a considerable distance along the arterial tunica media, and separate the wall into two planes - “dissection.”
Dissecting aneurysm is associated with hypertension, but it may also be the result of the arterial wall degeneration seen in cystic medial necrosis or Marfan’s syndrome.

20
Q

There are two ways to classify dissecting aneurysms according to their aorta location:

A

type A - if it involves the ascending part

type B - if it involves the descending part

21
Q

Dissecting aneurysm
def
associated with…

A
  1. a lesion which occurs when blood is forced through an intimal defect into the wall of an artery, under arterial pressure. This may lead to extension of a column of blood that may travel for a considerable distance along the arterial tunica media, and separate the wall into two planes - “dissection.”
  2. Dissecting aneurysm is associated with hypertension, but it may also be the result of the arterial wall degeneration seen in cystic medial necrosis or Marfan’s syndrome.
22
Q

Therapeutically proximal dissection need to be treated how?

A

surgically with a synthetic graft while distal descending type may be treated with drugs.

23
Q

what does cor pulmonole do?

A

causes PE block BF and die

24
Q

Varicose veins

A

abnormally dilated, tortuous veins caused by increased vessel intraluminal pressure.

25
Q

What is affected–varicose veins?

A

Any vein in the body may be affected, but superficial veins of the leg are by far the most frequently involved (beside legs hemorrhoidal plexus of veins at the anorectal junction, and esophagus are also common locations).

26
Q

Berry aneurysms
where do they develop
what are they?
why do we care?

A
  1. characteristically develop at branch points of arteries in the basal cerebral circulation.
  2. They are saccular outpouchings of the arterial wall which may fill with thrombus and which may bleed to produce subarachnoid bleeding.
  3. Their pathogenesis is controversial.
  4. It is important cause of intracranial bleeding in young patients.
27
Q

5 Risk factors for varicose veins are

A
  1. sex
  2. age
  3. heredity
  4. posture
  5. obesity
28
Q

Hemangioma

A

benign tumor of blood vessel usually located in the skin, but can be found in internal organs. This tumors are composed of masses of capillary-like channels filled with blood

29
Q

Deep venous thrombosis
what 2 words are used to describe thrombus formation?

What is associated with the condition?

A
  1. Thrombophlebitis and phlebothrombosis = thrombus formation in deep veins (usually legs) in presence and absence of infection or inflammation.
  2. The condition is associated with prolonged bed rest and can be threat to life because of embolization to the lung.
30
Q

Hemangiosrcoma

A

rare, highly malignant tumor that usually begin as small, painless red nodule located in skin, liver.

31
Q

Congenital heart disease Statistics

A

Congenital anomalies in general are the leading cause of death in children under one year old.
Of these fatal lesions congenital heart disease (CHD) is the most prevalent.
in less than 1 year old 18 deaths / 100.000 births
in 1 to 4 years old 2.2 deaths / 100.000 births
in 5 to 14 years old 0.8 deaths / 100.000 birth

32
Q

Congenital heart disease:

A

CHD is a broad term which can describe a number of different abnormalities affecting the heart.
By definition, present at birth although its effects may not be obvious immediately.
CHD may be a single lesions or in combinations with majority occurring as an isolated defect not associated with other disease.
However, CHD is a part of genetic and chromosomal syndromes (Down’s or Turner (XO) syndrome, trisomy 13, Marfan syndrome etc.
Drugs, chemicals, alcohol and infections (rubella) may also produce CHD.

33
Q

Why are CHD deaths during the first year of life highest?

A

Deaths during the first year of life are highest because severe cardiac abnormalities which are not corrected are generally not compatible with more than a few months of life.

34
Q

Shunt: Right-to-left

A

divert blood containing reduced hemoglobin away from the pulmonary circuit into the systemic circulation, reducing O2 saturation of the arterial blood that results in cyanosis.

35
Q

What are shunts?

A

During embryogenesis, when oxygenated blood is being supplied via the umbilical veins, communication between right and left heart atriums (right-to-left shunt) is imperative
After birth, these shunts should be closed in order to establish the normal adult blood flow. If not heart shunt disorders develop.
Two possible shunts are:
a. right-to-left
b. left-to-right

36
Q

Left-to-right shunt

A

divert blood from the systemic into the pulmonary circulation depriving tissues of O2. which may result in cyanosis
Additional blood volume demands on the right side and the pulmonary circulation results in hypertrophy of the pulmonary arterioles walls and increased pulmonary resistance that cause right ventricle hypertrophy leading to shunt “reversal”.

37
Q

Depending of the shunt CHD can be divided into:
cynaosis (3)
w/o cynaosis (4)

A

those with cyanosis

  1. tetralogy of Fallot
  2. transposition of great vessels
  3. patent ductus arteriosus

those without cyanosis:

  1. atrial septal defect (ASD)
  2. ventricular septal defect (VSD)
  3. coarctation of aorta
  4. pulmonic stenosis
38
Q

Tetralogy of Fallot

A
  1. prime example of right-to-left shunt.
  2. It is a combination of four (tetrad) anatomic defects including pulmonary stenosis.
  3. The severity of the disease is related to the amount of pulmonary artery stenosis.
40
Q

Ductus arteriosus persistant

A
  1. (PDA) is congenital heart defect where ductus arteriosus (embryonic blood vessel that connects the pulmonary artery to the aorta that drains major part of the pulmonary artery output directly into the aorta) is not closed at birth.
  2. In PDA after the birth blood flow from the aorta to the pulmonary artery, and than to the lungs which is the opposite direction than before the birth due to the high pressure in the left ventricle and aorta.
41
Q

Anatomical defects of

Tetralogy of Fallot

A
  1. pulmonary stenosis (severity of the disease is related to the amount of pulmonary artery stenosis)
  2. ventricular septal defect (missing part of wall)
  3. dextroposition of aorta - allows blood from right and left ventricle to be pumped into the aorta
  4. right ventricular hypertrophy
42
Q

Transposition of the great vessels (TGA) (3)

description

A
  1. two main arteries, aorta and pulmonary artery are transposed (aorta arises from the right ventricle, and the pulmonary artery from the left ventricle.)
  2. usually associated with an atrial or ventricular septal defect (VSD) or patient ductus arteriosus which will keep child alive

because:
Combination of transposition of great arteries and septal defect will allow mixing of blood from both sides of the heart, so there is enough oxygen supplied to the different organs to permit adequate but not normal function

43
Q

Ventricular and atrial septal defect (VSD and ASD)
def
due to
large VSD and ASD can cause

A
  1. opening in the wall between the ventricles or atria.
    This opening may be small, medium or large and may be single or multiple.
  2. Due to the left-to-right shunt more blood than normal flows into the lungs causing breathing difficulty in children.

Large VSD and ASD defects may cause heart failure (right ventricle cannot pump increased blood volume) that is associated with rapid shallow breathing, sweating, inability to feed, constant crying and failure to grow normally.

43
Q

Coarctation of the aorta
what is it
clinical signs for upper and lower extremities

A
  1. local constriction of this vessel (more frequent in males) immediately below the origin of the a. subclavia. (subclavian artery)
  2. Clinically upper extremities exhibit increased blood pressure (and left ventricular hypertrophy), but lower extremities show decreased blood pressure, diminished peripheral pulses, pallor and coldness predisposing to intermittent claudications [cramp and pain in calf because diminished blood supply for energy and oxygen] in calf muscles.
44
Q

Heart failure (4)

A
  1. insufficient to pump blood at the rate required by the tissues
  2. associated with defective myocardial function.
  3. The failing heart usually shows dilatation of one or more chambers.
  4. Longer standing heart failure is often accompanied by ventricular hypertrophy
46
Q

Left heart failure
associated with
symptoms
CHF

A
  1. is usually associated with pulmonary congestion and (2) respiratory symptoms like dyspnea and orthopnea [cannot breath lying down] progressing to pulmonary edema.
  2. Congestive heart failure usually implies significant infarction of the left ventricle (30-40% of the ventricular mass).
47
Q

Right heart failure
usually causes
associated with…
what happens with sever liver venous congestion

A
  1. usually causes chronic passive congestion of the liver, spleen and gut
  2. is associated with peripheral edema and ascites.
  3. Severe cases of liver venous congestion may produce necrosis of the centrilobular zones and result in destruction of the normal liver tissue. Edema of the gut may lead to “cardiac cachexia”
48
Q

cor pulmonale
def
acute
chronic

A
  1. secondary disease- right ventricular enlargement and associated heart failure
  2. Acute type is seen in acute pulmonary embolism.
  3. Chronic type is seen in chronic obstructive pulmonary disease that is associated with loss of pulmonary vascular cross section area and constriction of remaining vessels due to response to acidosis and hypoxia.
49
Q

Plasma proteins are classified on the basis of density (lipid content) as: (3)

A
  1. High - HDL - 50%lipids / 50%proteins
  2. Low - LDL- large amount of cholesterol
  3. very low - VLDL - 25% cholesterol