Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BioScience I > Cardiovascular disease ppt > Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

atherosclerosis primarily effects what type of arteries?

A

elastic/muscular arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

symptomatic atherosclerotic disease most often involves the arteries supplying what organs

A
  1. Heart
  2. Brain
  3. kidneys
  4. LE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

the major consequences of atherosclerosis are

A
  1. MI
  2. Cerebral infarction
  3. Aortic Aneurysm
  4. PVD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

where does atherosclerosis start?

A

endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

what begins the cycle of atherosclerosis

A

vascular injury in the endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

overall atherosclersosis in an intimal disease but causes damage where?

A

medial (from aneurysmal dilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what Cariac problems are associated with atherosclerosis?

(the cariac sequelae)

A

Acute coronary syndrome

AMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

with atherosclerosis what causes the AMI

A
  • physiology-thrombus, supplt/demand, mirco emboli
  • remodeling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are problems associated with atherosclerosis is the carotids?

A
  1. Bruit
  2. TIA
  3. CVA
  4. Amaurosis fugax (visoin loss)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what happens to the morphology of the heart from CHF

A

LV dilation/hypertrophy

LA dilation=a fib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what occurs in the kidneys from left sided CHF

A
  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)

,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Left atrial dilation > ___ = diastolic function

A

4cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what occurs in neurological system as a result of Left sided HF

A
  1. in far advanced CHF, cerebral hypoxia may give rise to HYPOXIC ENCEPHALOPATHY
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Clinical manifestations of hypoxic encephalopathy

A
  1. irritability
  2. loss of attention span
  3. restlessness
  4. stupor
  5. coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the #1 cause of RHF

A

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. .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the #1 isolated cause of RHF

A

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. .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the major morphologicalthat differ from LHF and clinnical effects of PURE RHF

A
  1. pulmonary congestion is minimal,
  2. engorgement of the systemic and portal venous systems may be pronounced.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

morphology of the heart with RHF (2)

A
  1. Hypertrophy and dilation of RV
  2. poss septal hypertrophy/bulging
33
Q

RHF effects of Hepatic system

A
  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
Q

RHF effects of the renal system

A
  1. Congestion

leading to greater fluid retention, peripheral edema, and more pronounced azotemia

35
Q

RHF effects of the neurological system

A
  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
Q

RHF effects of tissues

A
  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
Q

just some info to think about, how this r/t real life

A

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
Q

***********

know aneurysm

A

just know the following

39
Q

aortic aneurysms is caused by what

A
  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
Q

where are most Aortic aneurysm found

A
  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
Q

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!!)

A
  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
Q

difference bt true and false aneurysms

A
  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
Q

3 different shapes of aneurysms

A
  1. sacular
  2. cylindroid
  3. fusiform
44
Q

explian each type of aneurysm

A
  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
Q

define aneurysm

A

aneurysm is a localized abnormal dilation of a blood vessel or the wall of the heart

46
Q

define true aneurysm

A

When an aneurysm is bounded by arterial wall components or the attenuated wall of the heart, it is called a true aneurysm

47
Q

define false aneurysm

A

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
Q

Causes a mycotic aneurysm?

Possiable complications?

how may they origionate (3)?

A
  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
Q

what is the main bacteria that causes mycotic AAA

A
  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
Q

what are inflamatory AAA characterized by

A
  1. dense periaortic fibrosis containing an abundent, inflammatory reaction rich lymphocytes and plasma cells with many macrophages and ften giant cells
51
Q

what is important ablout mural thrombus

A
  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
Q

people generally associate aortic dissections with the actual ripping and tearing of the aorto open. but what really is an aortic dissection

A

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
Q

what is a huge difference b/t aneurysms and dissections?

A

*** 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
Q

what pt’s do Aortic dissections usually occur in?

A
  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
Q

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

what is the moct common tissua finding in Aortic dissection?

A

cystic medial degeneration

56
Q

Pathophysiology of aortic dissection

A
  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
Q

if the dissection extends into other vessels what can occur

A

thrombus

58
Q

if the dissection extends into the root what can occur

A

AV dysfunction

59
Q

pt’s with marfan syndrome are autosomal dominant, they have mutatinos in the ___1____ gene that leads to __2___ __2__

A
  1. fibrillin gene
  2. annuloaortic ectasia
60
Q

According to the book

Aortic dissections are generally classified into two types

(per his slides is defined as the stanford classification)

A
  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
Q

Aortic dissectins are also classified by the debakey classifications decribe it!

A
  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
Q

what is peripheral venous insufficiency

A

impeded forward flow of venous blood

63
Q

what is the sequelae of peripheral venous insufficiency

3 main things

A
  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
Q

90% of all DVTs are where?

where are other places the can occur

A
  • deep leg veins

others- pelvic, dural sinuses

65
Q

DVTs have what type of onset

A

insidious

66
Q

s/s of DVTs (3)

A
  1. unilateral edema
  2. pain
  3. homans sign
67
Q

what can occur from DVTs

A
  • embolic episode (PE)
68
Q

Main defining characteristics of Peripheral VENOUS Insufficiency?

(basically what you will see)

A
  1. Stasis Dermatitis
  2. Venous Ulcer
69
Q

s/s of Stasis dermatitis for peripheral venous insufficiency

(4)

A
  • Hyperpigmentation
  • dermal sclerosis
  • dilation of superficial veins
  • erythema
70
Q

what are 4 s/s of Venous ulcers

A
  • Melleolar area
  • superficial, irregular
  • maderate to heavy drainage
  • stasis dermatitis

WET

71
Q

S/S of arterial Ulcers from PAD (3)

A
  • over bony pressure points
  • deep, circular, well demarcated
  • dry necrosis
72
Q

SVC syndrome is R/t what 2 things

A
  • neolasms
  • aneurysms
73
Q

what causes SVC syndrome

A

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
Q

what is raynauds syndrome

A
  • 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
Q

what is Kawasaki disease

A
  • 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
Q

3 inflammatory arterial diseases

A
  1. temporal
  2. kawasaki
  3. takayasu
77
Q

what is temporal arterialitis

A
  • 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
Q

what is takayasu arteritis

A
  • Vasculitis of the medium and larger arteries
  • characterized by occular disturbancs and marked weakening of the pulses in the upper extremities
  • PULSLESSNESS DISEASE
79
Q

fuck it !!!!!!!!!!! we got this boyd bitch!!

A

and his noodle arms

BioScience I (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions