• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/86

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

86 Cards in this Set

  • Front
  • Back
what is arteriosclerosis?
- "hardening of the arteries" secondary to arterial wall thickening
what is arteriolosclerosis?
what diseases are assoc w/ it?
is there a pathological lumen narrowing?
- basically arteriosclerosis process but specific to small arteries & arterioles
- assoc w/ HTN & diabetes mellitus
- of coarse there is
what is medial calcific sclerosis?
is there a pathological lumen narrowing?
- calcification of media
- nope, not this time
what is another name for medial calcific sclerosis?
Monckeberg sclerosis
what is atherosclerosis?
is there a pathological lumen narrowing?
- basically arteriosclerosis process but specific to med to large arteries
- fo sho there is
where do you see changes in the intima of large to med sized arteries?
atherosclerosis
what do the lesions in artherosclerosis look like?
- atheromas (raised lesion) or plaques
- the lesions are lipid deposits in the intima covered by a fibrous cap
what are 3 complications of atherosclerosis?
- atheromas or plaques protrude in to lumen and...
- can obstruct-->ischemia-->MI
- can rupture-->thrombosis
- can weaken underlying media-->aneurysm
what are the risk factors for atherosclerosis?

(hint: 4 nonmodifiable and 5 modifiable)
NON-MODIFIABLE
- inc age
- male
- family hx
- genetic disorder
MODIFIABLE
- Hyperlipidemia (inc LDL)
- HTN
- ciggs
- diabetes
- C-reactive protein & inflamm
What kind of change do you observe in the intima of atherosclerotic arteries?
What is earliest sign in intima suggesting atherosclerosis?
- yellowish discoloration (fat) or white lesions (collagen fibrous cap)
- first sign is fatty yellow streaks w/n intima
atherosclerosis pathogenesis list?
(just have basic understanding of these)
- chronic endothelial injury
- accum of lipoproteins (LDL) w/n lumen
- monocyte adhesion to endothelium
- plt adhesion
- factor release
- SM cell proliferation (can secrete collagen which accum)
- ECM prod
- lipid accum in cells
if in the thoracic aorta, where do atherosclerotic plaques/lesions generally hang out?
-(in the dorsal part) often around intercostal artery projections
collagen depostion in atherosclerosis causes what?
- a raised intima into lumen (fibrous caps)
where is common site for plaque buildup in abdominal aorta leading to thrombus or aneurysm?
- right before bifurcation of iliac arteries
are plaques more commonly found in the thoracic aorta or the abdominal aorta?
- abdominal aorta
- both the dorsal & ventral parts
- numerous plagues can be found
- plaques more prone to ulcerate
what would happen if a thrombus in abdominal aorta right before bifurcation of iliac arteries embolized?
- it would probably move to leg and become lodged in an artery causing ishemia, possibly gangrene
what does an aneurysm look like pathologically?
- wide, cracked valleys
- causing a weakening or thinning of media
If the pathogenesis of an aneurysm were as follows, where would you expect the location of the aneurysm?
1. atherosclerosis-->
2. syphilis-->
3. dissecting secondary to cystic medial nedcrosis-->
4. congenital (Berry)-->
1. abdominal aorta
2. thoracic aorta
3. variable but prob in thoracic aorta
4. cerebral arteries
most likely epidemiology of AAA (abdominal aorta aneurysm)?
>50 male
most common site of AAA?
- below renal arteries & above bifurcation
2 types of morphology for AAA? which is more common?
Fusiform - diffuse elongated widening in arterial wall (most common)
Saccular - outpouching of portion of wall (less artery involved)
3 complications of aneurysm?
- obstruction
- rupture
- embolism
what would kidney look like if wasnt receiving enough blood due to arteriolosclerosis? what could have caused this?
- kidney surface would not be smooth. it would look granular
- HTN
Thoracic Aortic Aneurysm morphology?
- Saccular (spherical outpouching)
- obliterative endarteritis
- patchy loss of elastic fibers in media
- wrinkling "tree bark" of intima
3 complications of Thoracic Aortic Aneurysm?
- aortic valvular ring dilatation
- aortic insufficiency
- congenital heart failure
Thoracic Aortic Aneurysms common in?
- ascending aorta
- aortic arch
what are the 2 etiologies & epidemiology of Aortic Dissection?
1. HTN [90%] - (40-60 yo. men)
2. Conn Tiss abnormality - (younger)
---> due to Marfan Syn
---> due to cystic medial degeneration
where do most aortic dissections begin? where can they appear?
- ascending aorta
- basically anywhere in aorta
Aortic Dissection morphology?
intima tear-->blood into media-->extends proximally & distally
2 main complications of Aortic Dissection?
1. massive catastophic hemmorhage (hemothorax)
2. rupture into pericardium (cardiac tamponade)
is Aortic Dissection assoc w/ atherosclerosis?
-hell no, aortic dissection is normally thoracic region where as atherosclerosis is normally in abdominal aorta
most common site of Berry aneurysm?
anterior communicating artery
a berry aneurysm rupture is assoc w/?
subarrachnoid hemorrhage
there is a higher incidence of of berry aneurysms in what type of pt?
one w/ polycystic kidney dx
what is vasculitis?
- inflamm of vessel walls
sx of vasculitis?
fever, myalgia, arthralgias, malaise
causes of vasculitis?
- immune mediated or direct invasion by pathogen
- can be infectious or non-infectious
examples of non-infectious vasculitis? (list abs you would expect to find)
1. SLE (antiDNA ab)
2. Wegener (antineutrophil cyto ab)
3. Kawasaki (antiendothelial cell ab)
4. Giant cell (Temporal) arteritis
Takayasu arteritis
Polyarteritis nodosa
list features of Giant cell (Temporal) arteritis
- Most Common vasculitis!!!!!
- seen in pts >50
- chronic granulomatous inflamm
- major target is small arteries, like temporal artery in head
- aorta---NOT common site
sx of Giant cell (temporal) arteritis?
- fever, fatigue, weight loss
- HA w/ facial pain
- abrupt optical sx
pathology of Giant cell (temporal) arteritis?
- nodular intimal thickenings-->lumen stenosis & thrombosis
- granulomatous inflamm of inner media
- lymphos and multinucleated giant cells
- very edmatous intima
- fragmentation of internal elastic lamina
Takayasu Arteritis info
- aka "pulseless dx" due to weak pulse in upper extremeties
- can also lead to blindeness
- granulomatous
- med-large arteries
- young females
Takayasu Arteritis pathology
- aortic arch w/ narrowing of assoc great arteries
- patchy medial necrosis
- adventitial inflamm
- collagenous scarring of arterial wall
Polyarteritis nodosa info
- med vessels
- spares very small vessels (venules, arterioles, capillaries)
- EPISODIC
- HEPATITIS B ang present (30%)
sx of Polyarteritis nodosa
- malaise, fever, weight loss
- abdominal pain
- melena (blood in stool)
pathology of Polyarteritis nodosa
- acute or chronic
- many inflamm cells
- FIBRINOID NECROSIS
-Lung & Glomeruli sparred
sx of Kawasaki dx?
(aka Mucocutaneous Lymph Node Syn)
- Calor
- Cerival lymphadenopathy
- Conjuctiva erosion
- Coronary Artery aneurysm
- Convalescent desquamation
- strawberry tongue
Kawasaki dx info
- 80% in pts <4
- fibrinoid less than PAN
what causes Hypersensitivity Leukocytoclastic Vasculitis?
- immunologic rxn to antigen
- antigens often (aspirin, penicillin, thiazide diuretics, strep, staph, hepatitis, TB)
what type of vessels are affected in Hypersensitivity Leukocytoclastic Vasculitis?
- arterioles, capillaries, venules (small vessels only)
what would you see histologically for Hypersensitivity Leukocytoclastic Vasculitis?
- LEUKOCYTOCLASTIC (fragmented WBCs)
- nuclear debris from neutros
- fibrinoid necrosis
what are the sx of Hypersensitivity Leukocytoclastic Vasculitis?
- cutaneous vasculitis
- PALPABLE PURPURA in lower extremities
- common in LUNG (hemoptysis) & GLOMERULI (hematuria)
which dx is common in lung and glomeruli?
which dx spares these 2 sites?
- Hypersensitivity Leukocytoclastic Vasculitis
- Polyarteritis nodosa
what is Churg-Strauss syndrome and where does it occur?
- systemic vasculits
- basically everywhere except kidney
what does Churg-Strauss syndrome look like histologically?
- granulomatous inflamm w/ intense eosinophilia proliferation
- fibrinoid necrosis narrowing vessel lumen
lab result for Churg-Strauss syndrome?
- eosinophilia
- pANCA present 67%
what is the major target for Wegener Granulomatosis?
- LUNG
what is the triad assoc w/ Wegener Granulomatosis?
1. acute necrotizing granulomas of U/L resp tract
2. necrotizing or granulomatous vasculitis
3. focal necrotizing glomerulonephritis
who gets Wegener Granulomatosis?
- usually 40-50 yo males
what is the gross representation of Wegener Granulomatosis?
- persistent pnuemonitis w/ bilateral inflitrates w/ cavitation (like TB)
labs for Wegener Granulomatosis?
- cANCA 95%
does Wegener Granulomatosis have renal involvement? give 2 sx of Wegener Granulomatosis?
- yes
- also chronic sinusitis and mucosal ulcers of pharynx
what is Thromboangiitis Obliterans (Beurger dx)? where is it commonly located?
- a segmental, thrombosing, acute & chronic vascular inflamm-->leading to vascular insufficiency
- primarily in extremities (tibial, radial arteries)
sx of Thromboangiitis Obliterans (Beurger dx)?
- cold sensitivity (reynauds)
- very severe ULCERS of fingers, toes, feet
- painful even at rest
what is thought to cause Thromboangiitis Obliterans (Beurger dx)?
smoking in young people, <35 yo
Infectious vasculitis culprits?
1.bacterial-->
2.rickettsial-->
3.spirochetal-->
4. fungal-->
5. viral-->
1. neisseria
2. RMSF
3. syphilis
4. aspergilosis, mucor (mold genus found in often in soil)
5. herpes zoster
what cells are targeted by rickettsial related vasculitis?
what is a sign of rickettsial vasculitis?
- endothelial cells (inflamm & hemorrhage)
- HEMORRHAGIC RASH
where does aspergillosis attack?
what is result?
- vessel walls
- often in lung tiss, causes arterial thrombosis & infarction
Varicose veins are caused by?
--->vein dilatation--->incompetent valves-->venous stasis and pedal edema--> prolonged intraluminal press
what complications can you see w/ Varicose veins?
- stasis dermatitis & ulceration of overlying skin
T/F varicose veins are noncontributory to pulmonary thromboembuli?
True
where does thrombophlebitis occur?
deep leg veins
what is the clinical picture leading to a DVT?
- cardiac failure
- prego
- obese
- pt on bed rest w/ prolonged immobilization
what sign can help diagnose thrombophlebitis?
- Homan sign (dorsiflexion of foot)
- get edema and pain over affected veins
what is the most common vascular tumor? is it malignant?
- Hemangioma (capillary type specifically)
- no its benign ALWAYS
what is a hemangioma? where do they occur?
- vascular tumor consisting of inc # of blood filled vessels
- can be localized or involve large segment of body
- they can be superficial (skin) or internal (liver)
what are the 2 types of Hemangioma?
1. Cavernous type
2. Capillary type
Capillary Hemangioma
- skin, lips, subcutaneous tiss
- NOT encapsulated but very well circumscribed
- LARGEST SINGLE TYPE OF VASCULAR TUMOR
- can appear in juveniles and newborns but they usually regress by age 7
Cavernous Hemangioma
- less dilated vessels
- less cricumscribed
- no inflamm cell invasion
- see blood filled thin walled vessels
- usually involve deep tiss
--->usually found accidentally on autopsy
Glomus Tumor (Glomangioma) benign? where? what?
- BENIGN but painful
- found on digit often under fingernail
- smooth muscle cells of glomus body see specialized arteriovenous anastomosis
what is the gross representation of Kaposi sarcoma?
- red to purple patches consisting of dilated blood vessels (often feet in non HIV assoc)
- may appear as raised plaques
(((think tom hanks in Philadelphia)))
histology of Kaposis?
- SPINDLE CELLS, slit spaces
Kaposi's is most commonly assoc w/?
HIV
---but it doesnt have to be
what kind of tumor is an Angiosarcoma?
-MALIGNANT
- involving endothelial cells
How do you get hepatic angiosarcoma?
carcinogenic exposure
--->thorotrast, arsenic, polyvinyl choride
are cells in Angiosarcoma well differentiated or highly anaplastic?
can be either