Chapter 9 Flashcards
Vascular disease most commonly involves what vessels?
arteries
Which type of narrowing/obstruction of the lumen of vessels with vascular disease is gradual? which is rapid?
gradual: atherosclerosis rapid: thromboembolism
what are the two general types of vascular disease?
- narrowing/obstruction of the lumen 2. weakening of vessel wall
what is arteriosclerosis?
hardening of arteries
what is atherosclerosis a subset of?
arteriosclerosis
what is an aneurysm?
dilation of a vascular wall
what is a thrombus? a common example of one?
BLOOD CLOT in a vessel. Ex: deep vein thrombosis (blood clot in leg, thigh, pelvis)
what is a varicosity?
dilation of a vein
What is the layers of the vascular structures throughout the CVS and what theyre made of?
- tunica intima: endothelia cells, internal elastic lamina 2. tunica media: smooth muscles, external elastic lamina 3. adventitia: CT, nerves, vessels
what supplies blood to the interior vascular wall (aka the tunica intima & inner portion of the tunica media) of the CVS?
diffusion of blood from the lumen
what supplies blood to the exterior vascular wall (aka outer tunica media & adventitia) of the CVS?
vasa vasorum
what is the vascular pathway?
Large elastic arteries –> medium muscular arteries –> small arteries –> arterioles –> capillary beds –> postcapillary venules –> collecting venules –> progressively larger veins
what in the vascular pathway controls blood pressure?
arterioles
what are postcapillary venules involved with?
edema and leukocyte diapedesis
where in the vascular pathway does gas exchange occur?
capillary beds
T/F: All vessels may spread disease?
true
which vascular structure is more prone to metastatic invasion?
veins
which vascular structures have valves?
veins
what vessels drain interstitial fluid?
lymphatic vessels
what’s another name for lymph nodes?
lymph follicles
what vessels are lined with endothelial cells?
ALL vessels
what is the MAIN feature of the lining of vessels? the other features?
main: non-thrombogenic interface other: regulates vasoreactivity & cell growth
what is endothelial activation? what’s it caused by?
pro-inflammatory response to trauma in vessels. caused by vascular lesions (HTN, diabetes, irradiation, infxn), thrombosis, atherosclerosis
are vascular anomalies typically symptomatic?
nope, most relevant during surgery
what are the three types of congenital vascular anomalies?
- berry aneurysms 2. arteriovenous fistula 3. fibromuscular dysplasia
what is a berry aneurysm?
dilation of CEREBRAL vessels rupture –> subdural hemorrhage
what is an arteriovenous fistula?
connection of arterial & venous systems, bypass capillaries
what is fibromuscular dysplasia?
local thickening of medium/lg artery walls –>ischemia non-atherosclerotic, non-inflammatory MC in young adult females
what population is fibromuscular dysplasia MC in?
young adult females
what is hypotension and its side effects?
<90/60 decreased perfusion, dysfunction
what is hypertension and its side effects?
> or equal to 140/80 damages vessels/organs atherosclerosis, hypertensive retinopathy
what determines blood pressure regulation?
- cardiac output (HR + stroke volume) 2. vascular resistance
what controls vascular tone & blood volume? (3 things)
- kidneys: sodium, renin-angiotensin system 2. adrenals: aldosterone 3. Heart: atrial natriuretic peptide (associated w stretching)
what happens, physiologically, when blood pressure increases?
stretches heart –> ANP is released 1. reduced sodium resorption 2. vasodilation
what happens, physiologically, when blood pressure decreases?
renin-angiotensin system kicks in 1. sodium resorption 2. vasoconstriction
what are 3 medicines used to control blood pressure?
ACE (angiotensin-converting enzyme) inhibitors, Angiotensin II receptor blockers diuretics (water pills)
what is the outlook for untreated patients with HTN?
50% die of ischemic heart disease (MI) or congestive heart failure (CHF) 1/3 will die of stroke
what’s the prevalence of HTN in the US?
25% of US adults
what is known as the ‘silent killer’?
insidious, asymptomatic HTN
T/F: is HTN MC idiopathic?
T: 95% idiopathic ‘essential HTN’ Increased vascular resistance, decreased sodium excretion
what race is most likely to be hypertensive?
african american
if you decrease your BP, you decrease your risk of what three conditions?
ischemic heart disease, congestive heart failure & stroke
what is malignant HTN? its prevalence? its symptoms?
>200/120 5% of all HTN cases lethal within 1-2 years causes: renal failure & retinal hemorrhage (papilledema)
what is the non-specific response of vascular walls to injury?
- endothelial injury/dysfxn 2. smooth muscle cell recruitment 3. growth of smooth muscle cell & ECM 4. irreversible intimal thickening (vessel stenosis)**
what happens to vessel walls with aging?
tunica intima thickens and becomes harder rarely clinically significant
dystrophic calcification
Mönckenberg medial sclerosis
Fibromuscular dysplasia
Hyaline arteriolosclerosis
Hyperplastic arteriolosclerosis
Malignant Hypertension: papilledema
polyarteritis nodosa
strawberry tongue
Kawasaki disease
Thromboangiitis obliterans
Buerger disease
what causes hyaline arteriolosclerosis? what happens to the arteries?
benign HTN –> chronic hemodynamic stress
prolonged DM
luminal narrowing
pink hyaline
increased ECM
what causes hyperplastic arteriolosclerosis?
severe HTN
luminal narrowing –> onionskin appearance
kidneys are most sensitive
what is arteriolosclerosis?
arteriosclerosis of small arteries/arterioles
possible ischemic injury (HTN, diabetes)
what are the different types of arteriosclerosis?
arteriolosclerosis
Monckenberg medial sclerosis
atherosclerosis
what is Monckenberg medial sclerosis?
calcium within arteries –> tunica media
dystrophic calcification
no stenosis
NOT clinically significant
MC > 50 years old = ELDERLY
details about atherosclerosis
atheroma/plaque
STENOSIS
rupture
thrombosis
Heart, brain, GI, kidneys, legs
T/F: 99% of arteriosclerosis is atherosclerosis?
True
dystrophic calcification
Monckenberg medial sclerosis
What is the #1 cause of morbidity & mortality in US?
Atherosclerosis
CAD, MI, carotid atherosclerosis, stroke
what are atheromas? why are they important?
associated with atherosclerosis
- plaque build up on the inside of artery walls, protrude into the lumen, decrease flow, block diffusion of blood to the middle of the blood vessel
- prone to rupture –> massive thrombosis
- weakens tunica media –> risk for aneurysm
what are foam cells?
fat-laden macrophages
associated with atheromatous plaque
how much occlusion must occur for there to be coronary artery disease?
70% occlusion of coronary arteries
what is the ‘response to injury’ hypothesis?
chronic endothelial injury –> inflammation –> atherosclerosis
at what areas, branch points or straight-aways, is atherosclerosis most likely to occur? why?
branch points because there’s more turbulence
does dyslipidemia cause atherosclerosis?
yes, it is increased cholesterol
does atherosclerosis weaken the vessel wall?
yes, and if the wall ruptures, it is a thrombosis
which plaque is more likely to rupture, one with a thick fibrous cap or thin fibrous cap?
thin fibrous cap
true aneurysm vs. false aneurysm
true: all 3 layers of a vessel, heart wall
false: defect in a vascular wall; extravascular hematoma
what is a dissection?
blood enters the arterial wall
dissects layers of the vessel
hematoma
where do abdominal aortic aneurysm’s occur most commonly?
located between the renal & common iliac arteries
what part of the vessel degenerates and dies with abdominal aortic aneurysms?
ECM and tunica media
which gender is more likely to acquire an AAA?
men
is an AAA a contraindication for adjusting?
yes
percentages for likelihood of an AAA rupturing depending upon their size:
< or equal to 4 cm :
4-5 cm:
5-6 cm:
>6 cm:
< or equal to 4 cm: very rare
4-5 cm: 1% per year
5-6 cm: 11% per year
>6 cm: 25% per year
what percent of ruptured AAA are fatal?
50%
what’s the smallest an AAA can be?
5 cm or larger is an AAA
what is an aortic dissection?
blood splays apart the laminar planes of the media to form a blood-filled channel inside the aortic wall
what is the major risk factors for aortic dissections?
HTN*** 90% of cases
older males (40-60)
adolescents with CT disorders (marfan, Ehlers-Danlos, Wilson)
what unlikely condition helps protect against aortic dissections?
atherosclerosis
symptoms of an aortic dissection
sudden & severe tearing or stabbing pain in the
anterior chest, projects posterior and radiates inferior
what is the most common & most severe type of aortic dissection? were does it occur? what is the other type?
most common & severe: Type A/proximal/DeBakey I & II– ascending aorta
other type: Type B/distal/DeBakey III – distal to left subclavian A
what is vasculitis and in what vessels is it most common?
inflammation of the vascular wall, local vessel destruction
MC in small arteries
Aortic dissection types
First and Second: Type A/Proximal = most common & severe
third: Type B/distal
what are the three causes of vasculitis?
- infectious: vascular invasion = Hep B
- non-infectious: immune mediated, ADRs = SLE, penicillin
- etc: irradiation, trauma
what is the most common vasculitis in older adults (>50 years)?
giant cell arteritis/temporal arteritis
what arteries are involved in giant cell arteritis?
- temporal artery
2. ophthalmic artery: 50%, involves EYES (diplopia & permanent blindness)
- vertebral artery & aorta
what kind of inflammation is found with giant cell arteritis/temporal arteritis?
granulomatous inflammation
what is hypothesized to cause giant cell arteritis, polyarteritis nodosa and takayasu arteritis?
autoimmune hypothesis
granulomatous vasculitis is aka
takayasu arteritis
what arteries are affected in takayasu arteritis/granulomatous vasculitis?
aortic arch
branches off the aortic arch
what is known as the ‘pulseless disease’?
takayasu arteritis
radial & carotid arteries
what sense does takayasu arteritis affect?
eyesight
what age group does granulomatous vasculitis affect?
<50 years***
what arteries does polyarteritis nodosa affect?
system-wide small & medium-sized arteriesa
what arteries avoid damage with polyarteritis nodosa?
pulmonary arteries
what causes polyarteritis nodosa?
1/3: chronic hep B viral infection
2/3: idiopathic, autoimmune hypothesis
what age group is affected by polyarteritis nodosa? what are the symptoms?
MC in young adults
symptoms: episodic, diffuse myalgia & peripheral neuritis, end-organ damage
renal A: rapid increase in blood pressure
G.I. A: abdominal pain, bloody stools
what is the pediatric vasculitis?
Kawasaki disease; 80% <4 years
what percentage of Kawasaki disease has cardiovascular involvement?
20%
what determines the prognosis of Kawasaki disease?
the severity of CAD, if present
no CAD = full recovery
>50% of aneurysms resolve within 2 years
what is the ‘hallmark’ of Kawasaki disease?
acute/persistant fever that doesn’t respond to ibuprofen or acetaminophen
what vasculitis is hypothesized to be a type IV hypersensitivity?
Kawasaki disease
what is the main sign of Kawasaki disease? how is it treated?
sign: strawberry tongue
Tx: aspirin, steroids, CABG (coronary artery bypass graft)
what type of vasculitis is a type II hypersensitivity?
Wegener granulomatosis, necrotising vasculitis
what organs does Wegeners granulomatosis effect? what changes occur?
kidneys and upper & lower respiratory tracts
- granulomas
- systemic vasculitis – small & medium arteries
- glomerulonephritis
what population is effected by Wegners granulomatosis?
middle age males
what is the prognosis for untreated Wegener granulomatosis?
lethal after 1 year (80%)
What is effected with Thromboangiitis obliterans/Buerger disease?
medium-sized arteries
feet (tibial A) & hands (radial A)
who is effected by thromboangiitis obliterans/Buerger disease?
Heavy tobacco smokers
Males, 25-35 years
signs/symptoms of Buerger disease?
pain at rest
Raynaud phenomenon
Vascular claudication (pain that goes away after you stop moving)
ulcerations & gangrene
**woman on the video**
what is Raynaud phenomenon? who does it occur in? primary v. secondary?
exaggerated arteriole vasoconsriction
MC in females
primary: cold & emotional
secondary: atherosclerosis, Buerger disease, lupus, scleroderma
What three diseases make up 90% of venous diseases?
- varicose veins
- phlebothrombosis: NO previous inflammation
3. thrombophlebitis: Follows inflammation
Details about Thrombophlebitis
DVTs = 90% of all cases
localized cyanosis or erythema
what cancers are associated with superior vena cava syndrome? inferior vena cava syndrome?
SVC syndrome: bronchogenic carcinoma & mediastinal lymphoma
IVC syndrome: hepatocellular carcinoma & renal cell carcinoma
primary vs. secondary lymphadema
primary: congenital lymphatic abnormalities; milroy disease, hypoplasia/agenesis of lymph vessels
secondary: obstruction of previously normal lymph vessels; neoplasia, infection, thrombosis, fibrosis
what are 2 signs of chronic lymphedema?
Peau d’orange
brawny induration (hardening of skin)
are vascular tumors most commonly malignant or benign?
benign
details about hemangiomas
common benign
increase in local capillary growth
superficial tissues
enlarge after birth –> most self-resolve by age 7
details about kaposi sarcoma
malignancy of lymphatic endothelial cells
HHV-8
defining disease of AIDS
MC in lower extremity
details about angiosarcoma
malignant endothelial neoplasia
extremely variable
if anaplastic –> poor prognosis
MC older adults
widely spread –> MC skin, breast, liver
long latency period
what 2 vessels are commonly used for vascular grafts?
- great saphenous vein: 50% at 10 years
- internal mammary artery: 90% at 10 years
what is the most common type of arteriolosclerosis?
hyaline
what is the MC arteriosclerosis?
atherosclerosis
