Cardiovascular disease ppt Flashcards

1
Q

Atherosclerosis is characterized by intimal lesions called ________, which protrude into and obstruct vascular lumens and weaken the underlying media

(it’s actually 3 names)

A
  • atheromas
  • or atheromatous
  • or fibrofatty plaques
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2
Q

atherosclerosis primarily effects what type of arteries?

A

elastic/muscular arteries

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3
Q

what are elastic and muscular arteries that atherosclerosis usually effects?

elastic?

muscular?

most common?

A
  1. elastic- Aorta, carotid, iliac
  2. Muscular- Coronary, popliteal
  3. most common- in smaller arteioles
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4
Q

symptomatic atherosclerotic disease most often involves the arteries supplying what organs

A
  1. Heart
  2. Brain
  3. kidneys
  4. LE
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5
Q

the major consequences of atherosclerosis are

A
  1. MI
  2. Cerebral infarction
  3. Aortic Aneurysm
  4. PVD
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6
Q

where does atherosclerosis start?

A

endothelial cells

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7
Q

what do the endothelial cells do?

4

A
  1. form semipermeable membrane
  2. thromboresistant smooth surface (anticoagulation)
  3. modulate vascular tone, inflammation
  4. modify lipoproteins and other cell growth
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8
Q

***************

what begins the cycle of atherosclerosis

A

vascular injury in the endothelial cells

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9
Q

after vascular injury with atherosclerosis in the endothelial cells what occurs

(it’s alot but well break it down shortly)

A
  1. endothelial dysfunction
  • rapid- induced by mediators
  • slow- activation and alterations in gene expression
  1. Vascular smooth muscle
  • provides risistance
  • synthesis of new tissue
  • ***** intimal thickening in response to injury
  1. Vascular injury begins the cycle
  • turbulent blood flow= HTN
  • ***** shear stress on the endothelium
  • the inability of the endothelium to adequately regulate lipoprotein proliferation and other cell growth
  • development of intimal thickening and fatty streak (xanthoma)
  1. over time Atheromas
  • raised focal plaque- cholesterol/fibrous cap
  • May rupture may progress
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10
Q

************************

4 key stages

of atherosclerosis?

and name what is going on with each

A
  1. Intimal thickening- proteoglycan matrix/ xanthoma
  2. Pathologic intimal thickening- fatty pools-no necrosis
  3. Fibrous cap atheroma- lipid rich necrotic core, macrophage infiltration. late = stenosis r/t hemorrhage/ healing/layers
  4. Thin Fibrous cap- majorly vulnerable, major macrophage infiltration
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11
Q

3 main risk of advanced lesions of atherosclerosis

A
  1. patchy or massive calcification( norrow and brittle)
  2. focal rupture/ ulceration (highly thrombogenic)
  3. superimposed thrombus (aneurysmal dilation)
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12
Q

overall atherosclersosis in an intimal disease but causes damage where?

A

medial (from aneurysmal dilation)

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13
Q

what Cariac problems are associated with atherosclerosis?

(the cariac sequelae)

A

Acute coronary syndrome

AMI

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14
Q

the cardiac sequelae of atherosclerosis r/t ACS/AMI can result in what 3 things

A
  1. dysrhythmia
  2. CHF/cardiogenic shock
  3. Arrest/death
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15
Q

with atherosclerosis what causes the AMI

A
  • physiology-thrombus, supplt/demand, mirco emboli
  • remodeling
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16
Q

what are risk factors that increase mortality r/t AMI from atherosclerosis

A
  1. Age (40-60 increases 5 fold)
  2. Cariogenic shock
  3. papillary muscle rupture
  4. STEMI vs NSTEMI
  5. recurrent AMI
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17
Q

what are problems associated with atherosclerosis is the carotids?

A
  1. Bruit
  2. TIA
  3. CVA
  4. Amaurosis fugax (visoin loss)
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18
Q

what problems can occur from atherosclerosis in the peripheral?

A
  1. Intermittent claudication (cramping/aching/fatique/discomfort) (reproducible with exertion/ relieved with rest)
  2. Critical limb ischemia (acute or chronic) ( unrelenting rest pain/ ulcers/gangrene)
  3. Mesenteric Ischemia
  4. HTN
  5. Any organ system
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19
Q

4 primary causes of CHF

A
  1. systolic or diastolic (both) dysfunction
  2. HTN
  3. Aortic/ mitral valvular disease
  4. Non-ischemic mypcardial disease
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20
Q

what happens to the morphology of the heart from CHF

A

LV dilation/hypertrophy

LA dilation=a fib

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21
Q

left-sided heart failure is most often caused by

From book clarifying last cards

A
  1. Ischemic heart disease
  2. HTN
  3. Aortic and Mitral valve disease
  4. Non-ischemic myocardial disease
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22
Q

Clarification from book

Morphology of the heart from CHF

Left sided

A
  1. LVH
  2. hypertrophy and fibrosis of myocardium
  3. secondary enlargement of Left atrium which causes A-fib and thus increased risk for clots
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23
Q

what occurs in the lungs due to CHF (Left sided),

A
  1. Pressure increases in the pulm veins mounts and is transmitted retrograde to the cappillaries and arteries
  2. results in pulm congestion (pulm edema)
  3. —-eventually RHF
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24
Q

what are clinical manifestations of Pulmonary edema from left sided heart faliure

A
  1. Dyspnea ( earliest and cardinal sign)
  2. orthopnea
  3. Paroxysmal nocturnal dyspnea
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25
what occurs in the kidneys from left sided CHF
1. The decreased CO causes decreased Renal pefusion 2. this activated the RAAS causing restention of Na+ and H2O 3. leading to worsening of Pulmonary edema 4. this compensatory reaction is countereacted by the release of ANP through atrial dilatio 5. which acts to decrease ecessive blood volume 6. If kidney perfusion becomes severe the impaired excretion of nitrogenoys products may cause azotemia (in this instance azotemia) ,
26
Left atrial dilation \> ___ = diastolic function
4cm
27
what occurs in neurological system as a result of Left sided HF
1. in far advanced CHF, cerebral hypoxia may give rise to HYPOXIC ENCEPHALOPATHY
28
Clinical manifestations of hypoxic encephalopathy
1. irritability 2. loss of attention span 3. restlessness 4. stupor 5. coma
29
what is the #1 cause of RHF
LHF usually it is a secondary consequence of left-sided heart failure because any increase in pressure in the pulmonary circulation incidental to left-sided heart failure inevitably produces an increased burden on the right side of the heart. The causes of right-sided heart failure must then include all those that induce left-sided heart failure (Kumar 563) Kumar, Vinay. Robbins & Cotran Pathologic Basis of Disease, 7th Edition. Saunders Book Company, 082004. .
30
what is the #1 isolated cause of RHF
Severe pulm HTN pure right-sided heart failure most often occurs with chronic severe pulmonary hypertension and thus is called cor pulmonale. In this condition, the right ventricle is burdened by a pressure workload due to increased resistance within the pulmonary circulation. Hypertrophy and dilation are generally confined to the right ventricle and atrium, although bulging of the ventricular septum to the left can cause dysfunction of the left ventricle (Kumar 563) Kumar, Vinay. Robbins & Cotran Pathologic Basis of Disease, 7th Edition. Saunders Book Company, 082004. .
31
what are the major morphologicalthat differ from LHF and clinnical effects of PURE RHF
1. pulmonary congestion is minimal, 2. engorgement of the systemic and portal venous systems may be pronounced.
32
morphology of the heart with RHF (2)
1. Hypertrophy and dilation of RV 2. poss septal hypertrophy/bulging
33
RHF effects of Hepatic system
1. Congestive hepatomegaly 2. Cardiac sclerosis/ cirrosis (the central areas can become fibrotic, creating so-called cardiac sclerosis or cardiac cirrhosis) 3. Portal HTN (ascites, varices) 4. congestive slenomegaly
34
RHF effects of the renal system
1. Congestion leading to greater fluid retention, peripheral edema, and more pronounced azotemia
35
RHF effects of the neurological system
1. Encephalopathy symptoms essentially identical to those described in left-sided heart failure may occur, representing venous congestion and hypoxia of the central nervous system
36
RHF effects of tissues
1. Peripheral edema/ anasarca, 2. pleural/pericardial effusions Peripheral edema of dependent portions of the body, especially ankle (pedal) and pretibial edema, is a hallmark of right-sided heart failure. In chronically bedridden patients, the edema may be primarily presacral. Generalized massive edema is called anasarca.
37
just some info to think about, how this r/t real life
the symptoms of pure left-sided heart failure are largely due to pulmonary congestion and edema. In contrast, in right-sided heart failure, respiratory symptoms may be absent or quite insignificant, and there is a systemic (and portal) venous congestive syndrome, with hepatic and splenic enlargement, peripheral edema, pleural effusion, and ascites. In many cases of chronic cardiac decompensation, however, the patient presents with the picture of biventricular CHF, encompassing the clinical syndromes of both right-sided and left-sided heart failure.
38
\*\*\*\*\*\*\*\*\*\*\* know aneurysm
just know the following
39
aortic aneurysms is caused by what
1. Atherosclerosis (plaque in the intima and damage to the media Atherosclerosis, the most frequent etiology of aneurysms, causes arterial wall thinning through medial destruction secondary to plaque that originates in the intima.
40
where are most Aortic aneurysm found
1. Usually in the abdominal aorta (but anywhere) Atherosclerotic aneurysms occur most frequently in the abdominal aorta (abdominal aortic aneurysm, often abbreviated AAA), but the common iliac arteries, the arch, and descending parts of the thoracic aorta can be involved
41
what is pathogenesis causes of AA (not anesthesia assistances they have no pathogenesis causes they were placed here by inadequate uneducated fucktards of anesthesiologist who are afraid of our superior knowledge and skills not only r/t anesthesia but also skills with bare knuckle hand to face combat!!)
1. Familial/genetic There is a genetic susceptibility to AAA beyond the genetic predisposition to atherosclerosis or hypertension. For example, as discussed subsequently in the section on Marfan syndrome and aortic dissection, genetic defects in a connective tissue component responsible for the strength of the aorta can themselves produce aneurysms and dissections. Recent attention has focused on an altered balance of collagen degradation and synthesis mediated by local inflammatory infiltrates and the destructive proteolytic enzymes they produce and regulate
42
difference bt true and false aneurysms
1. True aneurysm. The wall bulges outward and may be attenuated but is intact. 2. False aneurysm. The wall is ruptured, and there is a collection of blood (hematoma) that is bounded externally by adherent extravascular tissues.
43
3 different shapes of aneurysms
1. sacular 2. cylindroid 3. fusiform
44
explian each type of aneurysm
1. Saccular- usually spherical( involving only a portion of the vessel wall and very in sizes 5-20 cm, often completly or partially filled by thrombus 2. Fusiform- very in diameter up to 20 cm, may involve the entire ascending and transferse portions of aortic arch, or large segments of abdominal aorta or iliacs ( no shape specifics) 3.
45
define aneurysm
aneurysm is a localized abnormal dilation of a blood vessel or the wall of the heart
46
define true aneurysm
When an aneurysm is bounded by arterial wall components or the attenuated wall of the heart, it is called a true aneurysm
47
define false aneurysm
a false aneurysm (also called pseudoaneurysm) is a breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space (“pulsating hematoma”).
48
Causes a mycotic aneurysm? Possiable complications? how may they origionate (3)?
1. Infection of a major artery that weakens its wall gives rise to mycotic aneurysm. 2. Thrombosis and rupture are possible complications. 3. Mycotic aneurysms may originate either (1) from embolization and arrest of a septic embolus at some point within a vessel, usually as a complication of infective endocarditis; (2) as an extension of an adjacent suppurative process (3) by circulating organisms directly infecting the arterial wall
49
what is the main bacteria that causes mycotic AAA
1. Salmonella gastroenteritis Mycotic abdominal aortic aneurysms are atherosclerotic AAAs that have become infected by lodgment of circulating organisms in the wall, particularly in bacteremia from a primary Salmonella gastroenteritis. In such cases, suppuration can further destroy the media, potentiating rapid dilation and rupture
50
what are inflamatory AAA characterized by
1. dense periaortic fibrosis containing an abundent, inflammatory reaction rich lymphocytes and plasma cells with many macrophages and ften giant cells
51
what is important ablout mural thrombus
1. the aneurysm and the nearby aorta often contain atheromatous ulcers covered by granular mural thrombi, prime sites for the formation of atheroemboli that may lodge in the vessels of the kidneys or lower extremities. 2. Additionally, a thrombus frequently fills at least part of the dilated segment. Occasionally the aneurysm may affect the origins of the renal and superior or inferior mesenteric arteries, either by producing direct pressure on these vessels or by narrowing or occluding their ostia with mural thrombi. Not infrequently, AAAs are accompanied by smaller fusiform or saccular dilations of the iliac arteries.
52
people generally associate aortic dissections with the actual ripping and tearing of the aorto open. but what really is an aortic dissection
seperating og the layers Aortic dissection is a catastrophic illness characterized by dissection of blood between and along the laminar planes of the media, with the formation of a blood-filled channel within the aortic wall (Fig. 11–20), which often ruptures outward, causing massive hemorrhage
53
what is a huge difference b/t aneurysms and dissections?
\*\*\* not associated with dilation\*\*\* In contrast to atherosclerotic and syphilitic aneurysms, aortic dissection may or may not be associated with marked dilatation of the aorta. For this reason, the older term “dissecting aneurysm” is discouraged.
54
what pt's do Aortic dissections usually occur in?
1. HTN 2. Connective tissue abnormality 3. Complications post arterial cannulation/CPB 4. pregnancy (PIH) Aortic dissection occurs principally in two groups of patients: More than 90% of dissections occur in men between the ages of 40 and 60 with antecedent _hypertension_. The second major group of patients, usually younger, has a systemic or localized abnormality of connective tissue that affects the aorta (e.g., _Marfan syndrome,_ discussed in Chapter 5). Dissection can also be iatrogenic, as a complication of _arterial cannulation_ (e.g., during diagnostic catheterization or cardiopulmonary bypass). Rarely, for unknown reasons, dissection of the aorta or its branches, including the coronary arteries, occurs during or _following pregnancy_. ***_Dissection is unusual in the face of substantial atherosclerosis or other cause of medial scarring such as syphilis_***
55
\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\*\* what is the moct common tissua finding in Aortic dissection?
cystic medial degeneration
56
Pathophysiology of aortic dissection
1. intimal tear into (NOT THROUGH) the media 2. usually laminar spread (middle and outer third) 3. poss re-rupture into aorta- new luman 4. rupture and death In spontaneous dissection, an intimal tear that is presumably the origin extends into but not through the media of the ascending aorta, usually within 10 cm of the aortic valve (Fig. 11–20A). Such tears are typically transverse or oblique, 1 to 5 cm in length, with sharp but jagged edges. The dissection can extend along the aorta proximally toward the heart as well as distally, sometimes all the way into the iliac and femoral arteries. The dissecting hematoma spreads characteristically along the laminar planes of the aorta, usually between the middle and outer thirds (Fig. 11–20B). It often ruptures out, causing massive hemorrhage. In some instances, the blood reruptures into the lumen of the aorta, producing a second or distal intimal tear and a new vascular channel within the media of the aortic wall (to produce a “double-barreled aorta” with a “false channel”). In the course of time, false channels may become endothelialized (“chronic dissection”
57
if the dissection extends into other vessels what can occur
thrombus
58
if the dissection extends into the root what can occur
AV dysfunction
59
pt's with marfan syndrome are autosomal dominant, they have mutatinos in the \_\_\_1\_\_\_\_ gene that leads to \_\_2\_\_\_ \_\_2\_\_
1. fibrillin gene 2. annuloaortic ectasia
60
According to the book Aortic dissections are generally classified into two types (per his slides is defined as the stanford classification)
1. Type A: involves the Ascending portion or both ascending and descending aorta (these are more common and more serious and damaging) 2. Type B: distal lesions not involving the ascending part and begining distal to the subclavian artery \*\*\*\* A = Ascending \*\*\* B= Below
61
Aortic dissectins are also classified by the debakey classifications decribe it!
1. Type A: from root down 2. Type B: Root only (stops there) 3. Type C: distal LSC 4. Type D: type A but with multiple tears
62
what is peripheral venous insufficiency
impeded forward flow of venous blood
63
what is the sequelae of peripheral venous insufficiency 3 main things
1. Varicose veins-usuually surerficial, dilated, tortuous vellses, valvular dysfunction 2. peripheral edema- from orthostatic, hydrostatic and lymphatic pressures 3. predisposes to thrombosis- b/c of HF, neoplasms, obesity, immobility
64
90% of all DVTs are where? where are other places the can occur
* deep leg veins others- pelvic, dural sinuses
65
DVTs have what type of onset
insidious
66
s/s of DVTs (3)
1. unilateral edema 2. pain 3. homans sign
67
what can occur from DVTs
* embolic episode (PE)
68
Main defining characteristics of Peripheral VENOUS Insufficiency? (basically what you will see)
1. Stasis Dermatitis 2. Venous Ulcer
69
s/s of Stasis dermatitis for peripheral venous insufficiency (4)
* Hyperpigmentation * dermal sclerosis * dilation of superficial veins * erythema
70
what are 4 s/s of Venous ulcers
* Melleolar area * superficial, irregular * maderate to heavy drainage * stasis dermatitis WET
71
S/S of arterial Ulcers from PAD (3)
* over bony pressure points * deep, circular, well demarcated * dry necrosis
72
SVC syndrome is R/t what 2 things
* neolasms * aneurysms
73
what causes SVC syndrome
obstruction of SVC everything above mass becomes edematous dialtion of all proximal veins poss pulmonary veins The superior vena caval syndrome is usually caused by neoplasms that compress or invade the superior vena cava, most commonly a primary bronchogenic carcinoma or mediastinal lymphoma. The consequent obstruction produces a distinctive clinical complex manifested by dusky cyanosis and marked dilation of the veins of the head, neck, and arms. Commonly the pulmonary vessels are also compressed, inducing respiratory distress
74
what is raynauds syndrome
* Exaggerated vasomotor response Raynaud phenomenon refers to paroxysmal pallor or cyanosis of the digits of the hands or feet and, infrequently, the tips of the nose or ears (acral parts) owing to cold-induced vasoconstriction of the digital arteries, precapillary arterioles, and cutaneous arteriovenous shunts \*\*\*\* interesting \*\*\*\*\*the fingers change color in the sequence white—blue—red In contrast to uncomplicated, or primary, Raynaud phenomenon, **_secondary Raynaud phenomenon_** refers to arterial insufficiency of the extremities caused by various conditions, including SLE, systemic sclerosis (scleroderma), atherosclerosis, or Buerger disease (see above).
75
what is Kawasaki disease
* Arteritis that often involves the coroary arteries, usually in young children and infants * associated with mucocutaneous lymph node syndrome---manifested by fever, conjunctival and oral erythema and erosion, edema of hands and feet, erythemia of palms and soles, a skin rash and enlargment of cervical lymph nodes
76
3 inflammatory arterial diseases
1. temporal 2. kawasaki 3. takayasu
77
what is temporal arterialitis
* most common in older individuals and rare before age 50 * Symptoms are either only vague and constitutional—fever, fatigue, weight loss—without localizing signs or symptoms, or facial pain or headache, often most intense along the course of the superficial temporal artery, which may be painful to palpation. * More serious are ocular symptoms
78
what is takayasu arteritis
* Vasculitis of the medium and larger arteries * characterized by occular disturbancs and marked weakening of the pulses in the upper extremities * PULSLESSNESS DISEASE
79
fuck it !!!!!!!!!!! we got this boyd bitch!!
and his noodle arms