Pathoma Cardio / Vascular High Yield Flashcards
What types of vessels are affected in medium-vessel vasculitidies?
Muscular arteries -> medium-sized vessels
What is responsible for the appearance of the vessels in polyarteritis nodosa? Which vessels are not involved?
Beads on a string appearance -> aneurysmal dilatations due to weakening of the wall from new lesions with FIBRINOID NECROSIS (malignant HTN), as well as old lesions which are the “string” due to fibrosis.
What vessels are involved / not involved in polyarteritis nodosa?
All vessels of the body except pulmonary arteries will be involved
- > can even result in skin manifestations such as livedo reticularis / palpable purpura
- > renal and neurologic damage is quite common
- > also involves the muscles and joints often (myositis / arthritis) #457
What is the treatment for polyarteritis nodosa?
Corticosteroids, cyclophosphamide
-> fatal if not treated
What is the other name for Kawasaki disease and who tends to get it? What is the characteristic ocular finding?
Mucocutaneous lymph node syndrome
Tends to occur in children <4 years old, especially Asians
Ocular finding - conjunctival injection WITHOUT purulent discharge
-similar to leptospirosis
What is the mnemonic for Kawasaki disease?
CRASH and burn (your Kawasaki motorcycle)
Conjunctival injection Rash - (toxic erythema of some kind) Adenopathy - cervical nodes Strawberry tongue Hand-foot changes -> erythematous rash (think of holding the motorcycle with your hands and feet as in pathoma)
burn - Fever
What medium vessel vasculitis is especially associated with Raynaud phenomenon?
Buerger disease - thromboangiitis obliterans
-> this is the one associated with smoking
What are the three C’s of Wecener’s (Wegener / Granulomatosis with polyangiitis)?
C distribution - nasopharynx, lungs, kidneys
C-anca
Cyclophosphamide / corticosteroids is the treatment
What at the three key findings of Wegener’s?
Small vessel NECROTIZING granulomatous inflammation
Upper respiratory tract - sinusitis, nasal mucosal ulceration
Lungs - hemoptysis, cough, dyspnea
Renal - severe nephritic syndrome due to pauci-immune (Type III) RPGN
What will CXR show in Wegener’s?
Large nodular densities due to small vessel vasculitis and necrotizing giant cell inflammation?
How does Microscopic polyangiitis differ from Wegener’s?
- Necrotizing vasculitis but NO granulomas - most similar to polyarteritis nodosa, but all lesions will be in the same stage.
- No nasopharyngeal involvement
- Palpable purpura is generally present - leukocytoclastic vasculitis
- p-ANCA is present instead of c-ANCA
Why might you confuse microscopic polyangiitis with Churgg-Strauss?
Both of these are p-ANCA positive, and commonly involve the kidneys -> RPGN
What are the key defining differences of Churgg-Strauss and what is it also called?
Eosinophilic GRANULOMAtosis with polyangiiitis
- > will have granulomas (vs MP)
- > associated with asthma / sinusitis
- > peripheral neuropathy / foot drop is common
- > associated with IgE / eosinophilia
What makes purpura palpable vs not palpable?
- > important cuz purpura just means there is vasculitis bleeding into the skin
- > Palpable implies there is inflammation associated with it
i.e. Henoch-Schonlein purpura
What are the modifiable risk factors for atherosclerosis?
- Smoking
- Diabetes
- HTN
- Hypercholesterolemia
What are the nonmodifiable risk factors for atherosclerosis?
- Advancing age
- Male sex / postmenopausal female - estrogen is protective
- Genetics - multifactorial
How much stenosis is needed before you get complications of atherosclerosis?
> 70%
What arteries does atherosclerosis affect and what happens if you get it in your popliteal or mesenteric arteries?
Large / medium sized arteries
Popliteal - Peripheral vascular disease
Mesenteric - Ischemic bowel disease
What is fibroelastic hyperplasia?
A condition occurring in the larger vessels of the kidney (i.e. arcuate arteries) due to longstanding HTN, in benign nephrosclerosis
-> intimal thickening and reduplication of IEL. Basically a lot like hyaline arteriolosclerosis but of larger arteries. Intimal thickening is not due to lipids so it can’t be called atherosclerosis.
What is seen microscopically in the kidney in benign nephrosclerosis? What does this progress to?
Scarred glomeruli and atrophic tubules due to progressive fibrosis from decreased renal bloodflow secondary to hyaline arteriolosclerosis (due to diabetes / longstanding benign HTN allowing proteins to leak into the intima).
Progresses to chronic renal failure due to scarring and reduced RBF
Where does the calcification occur in Monckeberg calcific stenosis and what is the clinical significance?
Think Monckeberg MEDIAL calcific stenosis
- > calcification within the tunica media which does not reduce luminal caliber and is thus insignificant
- > significance is that calcification may show up on mammography and be confused with comedocarcinoma -> just notice that it has a vascular pattern to distinguish
Where does aortic dissection typically occur and why is HTN the most important cause?
Occurs in the first 10 cm of the aorta which is under high stress. You need weakening of the tunica media for this to occur.
Media is particularly thick in the first 10 cm. In HTN, hyaline arteriolosclerosis of the vasa vasorum occurs -> poor blood supply to the media -> atrophy and weakness of the media
Why does tree-barking occur in thoracic aneurysm? What is a major complication?
Reduplication of the intima when the media is weakened by plasma-cell obliterative endarteritis of vasa vasorum by syphilis
Major complication - dilation of aortic valve root - aortic valve insufficiency
When is an abdominal aortic aneurysm at risk for rupture?
When >5cm in diameter
Will Kaposi sarcoma blanch? Why or why not?
No, because althought it is a tumor of endothelial cells, they are not true functioning blood vessels (vs strawberry hemangioma)
What explains ST elevation vs ST depression?
ST depression - angina - reversibly injured subendocardium does not reach as positive of a value during ventricular depolarization -> current flows from epicardium to subendocardium -> ST depression.
ST elevation - transmural infarction - only the endocardium directly touching the ventricular lumen is alive -> only part to fully depolarize. Charge flows from injured endocardium to necrotic epicardium.
What is the cause of unstable angina vs prinzmetal angina?
Unstable angina - Thrombotic occlusion of coronary artery which is INCOMPLETE -> no infarction
Prinzmetal angina - ST elevation due to COMPLETE occlusion of artery due to vasospasm
When does Prinzmetal angina cause MI?
Like any other cause of MI -> complete occlusion of coronary artery for >20 min
What branch of the right main coronary artery supplies the heart areas of right dominant hearts? Where would this come from otherwise?
Posterior descending coronary artery
- > supplies posterior 1/3 of IV septum and inferior walls of left ventricle
- > also supplies AV node and posteromedial papillary muscle
-> otherwise this would come from left circumflex artery
What areas does the left anterior descending artery supply?
- Anterior wall of LV
- Anterior 2/3 of interventricular septum
- Anterior LV papillary muscle (dual supply with circumflex)
- Anterolateral wall
What does the left circumflex artery supply?
- Posterolateral LV
2. Anterior LV papillary muscle (dual supply with LAD)
How do you differentiate between unstable angina and NSTEMI? What is the differential cause of them?
Unstable angina: Acute coronary syndrome without myocardial necrosis
NSTEMI: Acute coronary syndrome with myocardial necrosis -> cardiac markers (troponins) will be elevated
-> caused by ischemia lasting longer than 20 minutes, will not be a full occlusion of the coronary artery (would be a STEMI otherwise since epicardium would be affected)
