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Semester 4 > systemic pathology 400 (CV class 3) > Flashcards

systemic pathology 400 (CV class 3) Flashcards

1
Q

arteriosclerosis

A

Group of diseases characterized by thickening and loss of elasticity of arterial walls

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2
Q

arterio

sclerose

A

sclerosing of arteries

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3
Q

arteriosclerosis also refers to…

A

“Hardening of the arteries”

and/or

“clogged arteries”

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4
Q

three forms of arteriosclerosis

A

Atherosclerosis

Monckebergs Arteriosclerosis

Arteriolosclerosis

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5
Q

arteriolosclerosis

A

Arteriolosclerosis is a form of cardiovascular disease involving hardening and loss of elasticity of arterioles or small arteries

is most often associated with hypertension and diabetes mellitus.

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6
Q

atherosclerosis

A

Atherosclerosis thickening or hardening of the arteries.

It is caused by a buildup of plaque in the inner lining of an artery.

Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin.

As it builds up in the arteries, the artery walls become thickened and stiff.

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7
Q

Monckeberg’s arteriosclerosis

(Mönckeberg’s sclerosis)

A

is a non-inflammatory form of arteriosclerosis,

differs from atherosclerosis traditionally.

Calcium deposits are found in the muscular middle layer of the walls of arteries with no obstruction of the lumen.

It is an example of dystrophic calcification.

This condition occurs as an age-related degenerative process.

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8
Q

dystrophic calcification

A

Dystrophic calcification (DC) is the calcification occurring in degenerated or necrotic tissue,

E.g.
as in hyalinized scars, degenerated foci in leiomyomas, and caseous nodules.

This occurs as a reaction to tissue damage,[1] including as a consequence of medical device implantation.

Dystrophic calcification can occur even if the amount of calcium in the blood is not elevated

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9
Q

dystrophy define

A

a disorder in which an organ or tissue of the body wastes away.

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10
Q

can the same person have all forms of arteriosclerosis?

A

yes.

All three forms of arteriosclerosis may be present in the same person in different blood vessels.

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11
Q

a note about the use of the terms atherosclerosis vs arteriosclerosis

A

technically, atherosclerosis is a type of arteriosclerosis

Frequently the terms arteriosclerosis and atherosclerosis are used interchangeably,

although technically atherosclerosis is the most common form of arteriosclerosis.

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12
Q

most common type of arteriosclerosis

A

atherosclerosis

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13
Q

atherosclerosis

A

Plaques or fatty deposits
form in the inner layer (intima)
of arteries
—> in lumen

“athero” = gruel;
“sclerosis” = hardening

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14
Q

simultaneous arterial hardening and softening (???)

A

atherosclerosis
—>
“Indicates simultaneous arterial
hardening and softening”

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15
Q

Monckebergs Arteriosclerosis

A

Involves the middle layer of arteries with destruction of muscle and elastic fibers and formation of calcium deposits

Age related

“Senile”

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16
Q

Arteriolosclerosis

A

Arteriolar sclerosis

Thickening of the walls of small arteries (arterioles)

Hypertension related

Doesn’t involve ATHEROMA

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17
Q

atheroma

A

“tumor/mass full of gruel-like matter”

“groats” –> hulled/crushed grain/oats

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18
Q

atheroma define

A

Atheroma refers to the fatty material that clogs your arteries.

It builds up over time and can lead to complications.

Atheroma (plaque) is the defining feature of a disease called atherosclerosis.

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19
Q

atherosclerosis… what accumulates in the lumen of arteries?

A

lipids,

macrophages,

T lymphocytes,

smooth muscle cells,

ECM (/ECF),

calcium,

necrotic debris

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20
Q

accumulation results in

A

Accumulation results in formation of plaque and narrowing of arterial lumen

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21
Q

atherosclerosis classificaitons (TYPES)

A

Coronary artery disease

Peripheral vascular disease

Cerebrovascular disease

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22
Q

Coronary artery disease

A

atherosclerosis of the coronary arteries

myocardial infarction

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23
Q

Peripheral vascular disease

A

atherosclerosis of the arteries supplying the extremities and organs

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24
Q

Cerebrovascular disease

A

atherosclerosis of the arteries that supply the brain

stroke

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25
Q

atherosclerosis – clinical manifestations

A

It can be asymptomatic

Ischemia

Infarct

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26
Q

atherosclerosis etiology and risk factors

A

Higher cholesterol levels

High blood pressure

obesity (visceral, abdominal fat)

diabetes

Smoking

Genetics

Age

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27
Q

atherosclerosis – Dx

A

Cholesterol checkups (blood work)

Angiogram

ECHO

Stress test

Ultrasound

MRI

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28
Q

atherosclerosis – Tx

A

Modify and reduce risk factors

Exercise

Medications

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29
Q

atherosclerosis (and relating Sx) — MEDICATION

A

ACE inhibitors and beta blockers help lower blood pressure and lower the heart’s workload.

Anti-platelet or anti-clotting medicines

Calcium channel blockers lower blood pressure by relaxing blood vessels

Medicines to control blood sugar

Nitrates, such as nitroglycerin, dilate your coronary arteries and relieve or prevent chest pain from angina.

Statins treat unhealthy blood cholesterol levels.

Other cholesterol-lowering medicines, such as ezetimibe, PCSK9 inhibitor, bempedoic acid, and omega-3 fatty acids, may be used if you are unable to take statins or when statins have not worked to treat unhealthy blood cholesterol and triglyceride levels.

Thrombolytic medicines, sometimes called clot busters, may be used to treat blood clots resulting from atherosclerosis. These medicines can dissolve blood clot that block arteries

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30
Q

can glucose contribute to atheroma formation?

A

yes (?)

“Prolonged exposure to hyperglycemia is now recognized a major factor in the pathogenesis of atherosclerosis in diabetes.”

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31
Q

peripheral vascular disease

A

Narrowing of the circulatory system outside of the brain or the heart

Any pathological condition of the blood vessels that supply the extremities and major abdominal organs, often the intestines and kidneys

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32
Q

PVD incidence/gender/age distribution

A

Incidence increases with increasing age (>50)

Men > women

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33
Q

most common PVD

A

Peripheral Artery Disease (PAD)

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34
Q

PVD classified according to

A

Classified according to pathology and blood vessel

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35
Q

note that PVD is a TYPE/classification of ATHEROSCLEROSIS

however, one can say that PVD is most commonly occurring as a result of…

A

Most commonly occur as a result of atherosclerosis

—> I.e. other causes exist (?)

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36
Q

does PVD most commonly occur in the upper or lower extremity

A

LE > UE

They occur more commonly in the legs than in the arms because the blood vessels in the legs are further from the heart.

—> correlation (??)

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37
Q

PVD –> SSx, clinical manifestations

A

can include…

intermittent claudication,

pain,
cyanosis,
fatigue,
gangrene,
cold extremities

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38
Q

claudication define

A

a condition in which cramping pain in the leg is induced by exercise, typically caused by obstruction of the arteries.

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39
Q

claudication etymology

A

claudus = lame

claudicare = to limp

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40
Q

vasculitis

A

inflammation of a blood vessel; can affect any organ or system including the peripheral nervous system (PNS)

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41
Q

arteritis (type of vasculitis)

A

inflammation of an artery

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42
Q

infective arteritis

A

inflammation of an artery due to infection

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43
Q

rheumatoid arteritis

A

inflammation of an artery associated with RHD/RF

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44
Q

what other structures does RF affect?

A

arteries (?)

myocardium?

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45
Q

giant cell arteritis (TEMPORAL ARTERITIS)

A

AKA cranial or temporal arteritis

A vasculitis primarily involving multiple sites of temporal and cranial
arteries

(i.e. arteries of
the head, neck, and
aortic arch)

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46
Q

why is it called giant cell arteritis

A

The term “giant cell arteritis” is often used because when one looks at biopsies of inflamed temporal arteries under a microscope, one often sees large or “giant” cells.

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47
Q

giant cell arteritis incidence

A

Most common vasculitis in the US

Incidence increases with increasing age after 50

Women > men (2:1)

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48
Q

giant cell arteritis risk factors

A

Menopause

Smoking

Heart murmurs (?)

Arthritis-related diseases
—> SLE, RA

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49
Q

what is the most common vasculitis in the US?

A

GIANT CELL ARTERITIS

I.e.
temporal arteritis

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50
Q

giant cell arteritis etiology…

A

Idiopathic

Multifactorial

Genetic

Infectious (VSV)

Hormonal

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51
Q

VSV

A

Vesicular stomatitis virus

negative sense RNA virus from the family of Rhabdoviridae,

whose replication is relatively fast and with infection culminating in cell death mediated by apoptosis.

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52
Q

stomatitis define

A

inflammation of the mucous membrane of the mouth.

etymology:
mouth + itis

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53
Q

sense (molecular biology)

A

In molecular biology and genetics, the sense of a nucleic acid molecule, particularly of a strand of DNA or RNA, refers to the nature of the roles of the strand and its complement in specifying a sequence of amino acids.

IN VIRUSES:
In virology, the term “sense” has a slightly different meaning. The genome of an RNA virus can be said to be either positive-sense, also known as a “plus-strand”, or negative-sense, also known as a “minus-strand”.

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54
Q

giant cell arteritis clincal manifestations

A

Onset is usually sudden

Severe, continuous, unilateral, throbbing headache and temporal pain as the first symptoms

Pain may radiate to the occiput, face, or side of the neck

55
Q

giant cell arteritis – visual symptoms

A

Visual disturbances

—> Can lead to irreversible blindness
(if ophthalmic artery is involved)

56
Q

GCA other SSX/clinical manifs

A

Enlarged, tender temporal artery,

scalp sensitivity,

jaw/tongue claudication

Heart murmur

57
Q

GCA – polymyalgia

A

“Polymyalgia rheumatica and giant cell arteritis are closely linked inflammatory disorders that almost always occur in people older than age 50.”

“Polymyalgia rheumatica is a condition that causes aches, pain and stiffness in large muscle groups, including your hips and shoulders.”

58
Q

why is polymyalgia rheumatica common in patients with GCA

A

Polymyalgia rheumatica and giant cell arteritis are related conditions, with some people having symptoms of both. About 10 percent of people with polymyalgia rheumatica have giant cell arteritis, and about 50 percent of those with giant call arteritis have polymyalgia rheumatica.

Inflammation causes polymyalgia rheumatica and giant cell arteritis, but scientists do not know what triggers it. Some studies have linked certain gene variants with the disorders, but these genetic links have not been consistent across different populations. Because the disorders occur in older people, the aging process may contribute to the disease onset

59
Q

GCA – Dx

A

Based on symptoms
Palpation
Blood tests (ESR, CRP)
Biopsy*

60
Q

GCA – Tx, Px

A

Anti-inflammatories and corticosteroids

Left untreated, the condition may lead to blindness and rarely a stroke, heart attack, or aortic dissection.

Overall prognosis is normal life expectancy

61
Q

aortic dissection

A

An aortic dissection is a serious condition in which a tear occurs in the inner layer of the body’s main artery (aorta).

62
Q

thromboangiitis obliterans

(AKA Buerger’s disease)

A

A vasculitis affecting the peripheral blood vessels, primarily in the distal extremities

63
Q

thromboangiitis obliterans…

A

Thromboangiitis obliterans (Buerger disease) is caused by small blood vessels that become inflamed and swollen.

The blood vessels then narrow or get blocked by blood clots (thrombosis).

Blood vessels of the hands and feet are mostly affected.

64
Q

TO etiology – risk factors

A

Idiopathic

Smokers and users of tobacco products

65
Q

TO – men vs women

A

Men > women

66
Q

TO – pathogenesis

A

General inflammatory concepts apply

Inflammatory lesions of the peripheral blood vessels are accompanied by thrombus formation and vasospasm,

occluding and eventually
obliterating small and medium sized vessels of the feet and hands

67
Q

TO – clinical manifestations

A

Intermittent claudication = first sx

Pain, tenderness

Edema

Cold sensitivity

Rubor or pallor

Cyanosis

Trophic changes to the skin

Paresthesia

68
Q

recall intermittent claudicaiton

A

Intermittent claudication is muscle pain that happens when you’re active and stops when you rest.

69
Q

TO – complications

A

Ulcerations, Gangrene

70
Q

TO – Tx, Px

A

Treatment includes cessation of smoking, increasing circulation, medication,

and amputation… (extreme cases)

Px:
It can result in progressive disability from pain and loss of function.

71
Q

Polyarteritis nodosa

A

Polyarteritis nodosa is a serious inflammatory blood vessel disease. The small and medium-sized arteries become swollen and damaged. Polyarteritis nodosa, seen here on a lower extremity, produces painful, erythematous nodules.

“PAN affects medium-sized blood vessels, causing inflammation of the skin, nervous system, joints, kidneys, gastrointestinal (GI) tract, and heart, among other organs. Depending on the form of the disease, PAN may affect only the skin, a single body organ, or multiple organ systems.”

72
Q

polyarteritis nodosa – from notes

A

Systemic inflammation and necrotic lesions in the arterial system, causing damage to organs, muscles, joints, and skin

73
Q

where does polyarteritis nodosa typically NOT OCCUR

A

Typically not the lungs

74
Q

PAN — etiology

A

Etiology - idiopathic

Possible link to bacterial or viral infections

75
Q

polyarteritis nodosa …

A

sdf

(??)

76
Q

PAN – clinical manif

A

Polyarteritis nodosa affects medium-sized blood vessels, resulting in a variety of clinical S&S depending on the arteries involved.

Namesake nodes of aneurysms in effected arteries

Subcutaneous nodules

Rash

Muscle and joint pain

77
Q

PAN – Dx, Tx, Px

A

Diagnosis – blood test, imaging (Rosary Sign), biopsy

Treatment – meds (corticosteroids, immunosuppressants)

Prognosis – poor without treatment; every good with treatment

78
Q

aneurysm

A

An abnormal stretching (dilation or dilitation) in the wall of an artery, vein, or the heart with a diameter that is at least 50% greater than normal.

79
Q

aneurysm a few classificaitons based on shape/state

A

saccular aneurysm

fusiform aneurysm

ruptured aneurysm

80
Q

aneurysm classification – based on…

A

Location

Pathology (atherosclerosis, infection)

Type of vessel (artery)

81
Q

aortic aneurysm

A

Most common site of aneurysm
Abdominal > thoracic

Thoracic - involves the ascending,transverse, or first part of the descending portion of the aorta

Abdominal - generally involves the aorta between the renal arteries and iliac branches

82
Q

mycotic aneurysm

A

Caused by bacterial or fungal infection

Salmonella and syphilis most common

83
Q

atherosclerotic aneurysm

A

Due to the build-up of fatty deposits on the inner wall of the arteries

84
Q

aneurysm – etiology/ risk factors

A

Atherosclerosis

Congenital connective tissue weakness (Marfan’s, Ehler-Danlos)

Genetics

Trauma/inflammation/infections

85
Q

Marfan’s and aortic aneurysm

A

In people who have Marfan syndrome, this is most likely to happen at the aortic root — where the artery leaves your heart.

86
Q

Ehler-Danlos – aneurysms

A

Vascular type EDS can cause aneurysms, arterial dissection, and pseudoaneurysms (“false” aneurysms)

and while aneurysm formation is relatively rare in EDS, an aneurysm rupture is unpredictable.

Aortic dissections may cause pain and compromise blood flow to the extremities or internal organs.

87
Q

aneurysm – pathogenesis

A

Plaque formation erodes vessel wall predisposing the vessel to stretching of the inner and outer layers of the artery and formation of a sac

With time, the aneurysm becomes more fibrotic

Force of blood pressure can cause a tear or rupture of the wall

88
Q

Aneurysm – Dx

A

Palpation

CT (can be with dye)

89
Q

aneurysm – clinicla manif

A

Variable
Asymptomatic
Pain
Dyspnea
Cough
Hoarseness
Edema
Distended neck veins

Ischemia
MI
Renal failure
Stroke
Paraplegia
Death

90
Q

aneurysm – Tx, Px

A

Tx:
Watch and wait
Surgery
Medications

Px:
Poor

91
Q

***IN CLASS FLASHCARDS

A

..

92
Q

arteriosclerosis

A

umbrella term – > includes 3 diseases

atherosclerosis (most common)

2) Monckberg’s Arteriosclerosis

3) Arteriolosclerosis

93
Q

2) Monckeberg’s arteriosclerosis

A

calcium deposits

—> middle layers of arteries
—> destruction of mm and elastic fibres
—> formation of calcium deposits

common (?) in old people
–> in 70s/80s

some suggest that it is just a typical event in getting this old
—> some might be more susceptible, etc.

94
Q

arteriolosclerosis

A

does not involve atheroma
–> no fatty deposits, etc.

–> only in small arteries (arterioles & small arteries (?))

95
Q

WHICH CARDIOMYPATHY HAS POTENTIAL AUTOSOMAL DOMINANT ETIOLOGY

A

HYPERTROPHIC MYOPATHY

96
Q

NOTE PLAQUE IS NOT EXPOSED TO BLOOD (IN ATHEROSCLEROSIS)

A

A LAYER OF ENDOTHELIUM COVERS THE PLAQUE

“Plaque rupture happens when the fibrous cap that covers the plaque breaks open. With plaque erosion, the fibrous cap stays intact, but endothelial cells around the plaque get worn away. Both events lead to the formation of a blood clot. The clot blocks blood flow and can lead to a heart attack or stroke.”

97
Q

plaque is made of

A

lipids

but also:
macrophages,
Tlymphocytes,
smooth mm cells (???)
ECM (ECF?)
CALCIUM
necrotic debris (?)

98
Q

NOTE HYPERTENSION & ATHEROSCLEROSIS COMBO

A

HTN damages endothelial cells

99
Q

small LDLs genetics

A

some have smaller LDLs (genetically)

LDLs sneak between the endothelial cells and embed themselves in the artery wall (atherosclerosis)

ALSO HTN contributes to endothelial cell structural changes/damage that allows the LDLs & other substances to sneak between the endothelial cells

___

TO make matters worses, macrophages get past the endothelial cells to try to get rid of the deposits
—> But the macrophages once engulfing the deposits, they transform to FOAM cells, and are unable to leave from under endothelial cells

—> THUS MACROPHAGES ADD TO THE PLAQUE/DEPOSITS

100
Q

FOAM CELLS

A

“Foam cells are a type of macrophage that localize to fatty deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance.”

101
Q

what can ultimately happen

A

if deposits are excessive, the endothelial layer covering it can become damaged

A PLAQUE CAP forms on the protruding apex (?) of the deposits (on endothelium?)

plaque cap can rupture and lead to EMBOLISM that can cause, for instance, a MI (if they block coronary arteries)

–> IF CAP RUPTURES AND BECOME EMBOLISM, the deposits/plaque still remains – and new cap potentially forms

102
Q

note what happens to ____ at the spot where plaque/deposits build up

A

the outer wall (including ADVENTITIA?) weakens/softens (in contrast to sclerosing/HARDENING of inner wall)

—> can lead to aneurysm in the spot where the sclerotic plaques/atheromas

103
Q

peripheral vascular disease

A

anything that is not involving the heart or the brain

104
Q

peripheral vascular disease

A

not necessarily atherosclerosis

—> but most commonly atherosclerosis (?)

105
Q

most common symptom of atherosclerosis

A

VERY COMMONLY NO SYMPTOMS

—> asymptomatic until embolus forms and heart attack/stroke/necrosis takes place

106
Q

common end organs / target organs of atherosclerotic embolism

A

“Cholesterol crystal embolism is a multisystemic disorder characterized by the occlusion of small arteries by cholesterol crystal emboli deriving from eroded atherosclerotic plaques of the aorta (1–7). The proximity of the kidneys to the abdominal aorta makes the kidney the most frequent target organ.”

“6. End-Organ Damage”
“However, the following organs are most commonly involved: the brain, the kidneys, the gastrointestinal tract, and the skin and skeletal muscles of the lower extremities.”

–> “Virtually any organ or tissue can be affected by cholesterol embolization syndrome.”

107
Q

CHOLESTEROL EMBOLIZATION SYNDROME

A

“Cholesterol embolization syndrome occurs when atheromatous plaques in large arteries release cholesterol emboli and atheromatous debris into the circulation.

“These can then become lodged downstream in smaller arterioles and cause varying degrees of ischemia in target organs.

“This can result in worsening renal function, distal ischemia, hypertension, or acute multiorgan dysfunction.

“The partially occluded arterioles display an intense giant cell foreign body inflammatory response with fibrosis and eventually complete occlusion.”

108
Q

unrecognized cases of cholesterol embolization syndrome (?)

A

“Subsequent waves of arterial embolization are associated with increasing symptoms and signs of the syndrome and may explain why about 20% of cases go unrecognized. This is generally seen after an invasive arterial procedure but can occur spontaneously.”

109
Q

Tx – atherosclerosis

A

BP meds (E.g. beta adrenergic blocker)

statins (cholesterol meds)

110
Q

statins

A

“Statins are a group of medicines that can help lower the level of low-density lipoprotein (LDL) cholesterol in the blood. LDL cholesterol is often referred to as “bad cholesterol”, and statins reduce the production of it inside the liver.”

111
Q

beta adrenergic blockers

A

“They also may be called beta-adrenergic blocking agents. The medicines block the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause the heart to beat more slowly and with less force. This lowers blood pressure.”

112
Q

exercise long term benefit

A

CV exercise increases BP for the duration of exercise

But overall, and in the long run, regular CV exercise reduces BP

113
Q

CABG vs stent

A

TITLE OF ARTICLE (2005 – MAY BE OUTDATED)
“Five-Year Outcomes After Coronary Stenting Versus Bypass Surgery for the Treatment of Multivessel Disease: The Final Analysis of the Arterial Revascularization Therapies Study (ARTS) Randomized Trial”

“The overall MACCE-free survival at five years was 58.3% in the stent group and 78.2% in the CABG group (p < 0.0001). At five years, there was a significant difference in the presence of anginal symptoms between the two treatment groups (21.2% of the stent patients vs. 15.5% of the CABG patients, p < 0.05).”

114
Q

most common PVD (peripheral vascular disease)

A

PAD (peripheral arterial disease)

115
Q

which part of body is most commonly affected during vascular disease

A

LE (lower exremity)

—> harder to get blood up from LE (against gravity – and larger distance from heart)

therefore, usually LE is affected – but there are occasionally vascular diseases that have predilection for UE (upper extremity)

116
Q

claudication (during vascular disease)

A

“a condition in which cramping pain in the leg is induced by exercise, typically caused by obstruction of the arteries.”

117
Q

claudication is simply just

A

“angina” of a part of the body that isn’t the heart

In other words, the mechanism is the same

118
Q

intermittent claudicaiton deinfe

A

“Intermittent claudication is muscle pain that happens when you’re active and stops when you rest. It’s usually a symptom of blood flow problems like peripheral artery disease.”

119
Q

vasculitis

A

inflammation – inflammation of BV

arteritis – inflammation of artery

infective arteritis – inflammation of artery due to infection

rheumatoid arteritis – inflammation of an artery (associated w/ RF/RHD)

120
Q

MOST COMMON vasculitis in US

A

GIANT CELL ARTERITIS

AKA cranial/TEMPORAL arteritis

121
Q

which gender does giant cell arteritis most commonly affect?

A

WOMEN

122
Q

giant cell (temporal arteritis) correlation with…

A

arthritis / autoimmune conditons:
E.g.
SLE, RA

123
Q

note reason for giant cell arteritis affecting women more commonly

A

women are more commonly affected by autoimmune conditions

124
Q

which arteritis is linked with visual disturbances and potential vision loss?

A

temporal arteritis (giant cell arteritis)

can lead to irreversible blindness if the ophthalmic aa is involved

125
Q

POLYMYALGIA vs giant cell arteritis

A

“Inflammation causes polymyalgia rheumatica and giant cell arteritis, but scientists do not know what triggers it. Some studies have linked certain gene variants with the disorders, but these genetic links have not been consistent across different populations.”

“However, genetic predisposition, immune system problems and environmental factors seem to play an important role in development of these disorders.”

—>
I.e.
the polymyalgia could just be related to the autoimmune nature of the original giant cell arteritis

126
Q

reconsider – why is it called giant cell arteritis?

giant cells
granulomas
type 4 hypersensitivity

A

“Granulomas, which are accumulations of immune cells, are the hallmark of type IV hypersensitivity. Activated T-helper 1 cells produce pro-inflammatory cytokines, such as TNF-α and IFN-γ, leading to recruitment of monocytes to the tissue and massive activation of the macrophages.”

“A giant cell is a mass formed by the union of several distinct cells (usually histiocytes), often forming a granuloma.”

127
Q

giant cell arteritis – risk factors

A

Incidence increases with increasing age after 50

Women > men (2:1)

Menopause

Smoking

128
Q

THROMBOANGIITIS OBLITERANS – biggest risk factor

A

SMOKING

very common among males who smoke

“Buerger’s disease (thromboangiitis obliterans) is a rare disease most often found in those who smoke. The blood vessels in their legs, arms, feet and hands get inflamed, making it hard for blood to travel through.”

129
Q

polyarteritis nodosa – where does the n”odosa” come from?

A

nodosa refers to the node-like appearance of aneurysms in affect arteries

the condition also involves subcutaneous nodules – however, the “nodosa” does not refer to these nodules

130
Q

note the appearance of aneurysms in medical imaging (“string of pearls” / “rosary sign”)

A

looks like a string of pearls

131
Q

gangrene

A

LARGE area of necrotic tissue

132
Q

polyarteritis nodosa – brief description

A

many arteries are inflamed, leading to aneurysms that look like nodes on an angiogram

133
Q

which part of the aorta is MOST COMMONLY affected by aneurysms?

A

ABDOMINAL is more commonly affected compared to thoracic aorta

134
Q
A

Semester 4 (22 decks)

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