Vascular Pathology Flashcards
1
Q
What are the 3 pathologic patterns of ARTERIOSCLEROSIS?
A
- ATHEROSCLEROSIS
- ARTERIOLOSCERLOSIS - “OLO” added
- MONCKEBERG MEDIAL SCLEROSIS
2
Q
What layer of the BV wall is thickened in ATHEROSCLEROSIS? Which sized vessels are most commonly affected?
A
INTIMA
Affects MEDIUM/LARGE sized vessels
3
Q
What sized BV does ARTERIOLOSCLEROSIS affect?
A
SMALL BV (arteriOLO - Arterioles)
4
Q
What is MONCKEBERG MEDIAL SCLEROSIS? What sized BV does it affect
A
Calcifications of the MEDIA Layer of the BV (MEDIUM SIZED ARTERIES)
5
Q
What is the predominant component of the INTIMAL PLAQUE in ATHEROSCLEROSIS?
A
Composed of mainly CHOLESTEROL
Necrotic Lipid Core = Cholesterol + Fibromuscular cap
Often with DYSTROPHIC CALCIFICATIONS
6
Q
What are the 4 most commonly involved arteries of ATHEROSCLEROSIS?
A
MEDIUM/LARGE BV:
“ICAP” - Atherosclerosis has a fibromuscular CAP
Internal Carotid + Coronary + Abdominal aorta + Popliteal
7
Q
What are the MODIFIABLE (4) risk factors of ATHEROSCLEROSIS?
A
HTN
HL - LDL increases risk, HDL decreases risk
SMOKING
DIABETES
8
Q
What are the 3 NON-MODIFIABLE risk factors of ATHEROSCLEROSIS?
A
AGE - Increasing age
GENDER - Males, post-menopausal females
GENETICS - FH is highly predictive of atherosclerosis
9
Q
**UW: Describe the pathogenesis of ATHEROSCLEROSIS (Minimally raised YELLOW SPOTS on inner surface)
A
STEP 1: DAMAGE to endothelium -> Lipids leak into INTIMA
STEP 2: FOAM CELLS/FATTY STREAK: LDL accumulation -> Lipids are oxidized and consumed by MACROPHAGES via scavenger receptors -> FOAM CELLS -> FATTY STREAKS
STEP 3: FIBROMUSCULAR CAP dvlm resulting in PLAQUE = Inflammation + Healing -> ECM deposition and SM proliferation + T cell recruitment -> COMPLEX ATHEROMAS
10
Q
ATHEROSCLEROSIS COMPLICATION 1: What complications (3) can result from >70% stenosis due to ATHEROSCLEROTIC PLAQUE?
A
- CORONARY ARTERY stenosis -> ANGINA
- POPLITEAL ARTERY stenosis -> PERIPHERAL VASCULAR DISEASE
- MESENTERIC ARTERY stenosis -> ISCHEMIC BOWEL DISEASE
11
Q
ATHEROSCLEROSIS COMPLICATION 2: Which complications (2) can result from ATHEROSCLEROSIS PLAQUE RUPTURE + thrombosis?
A
- CORONARY ARTERY plaque rupture + transmural thrombosis = MI
- MIDDLE CEREBRAL ARTERY plaque rupture + thrombosis = STROKE
12
Q
ATHEROSCLEROSIS COMPLICATION 3: What is the hallmark of ATHEROSCLEROTIC EMBOLI?
A
CHOLESTEROL CLEFTS in embolus that dislodges from the plaque
13
Q
ATHEROSCLEROSIS COMPLICATION 4: Describe the pathophysiology of how an ATHEROSCLEROTIC PLAQUE can result in an ANEURYSM (Eg. ABDOMINAL AORTA ANEURYSM).
A
ATHEROSCLEROTIC PLAQUE of intimal wall -> Blood carrying oxygen has a HARDER time diffusing across intima to media to adventitia -> BV wall (3 layers of live tissue) gets DEPRIVED of Oxygen -> Wall weakens -> Increases risk of ANEURYSM
14
Q
What are the 2 types of ARTERIOLOSCLEROSIS?
A
- HYALINE
2. HYPERPLASTIC
15
Q
What is visible upon microscopy of HYALINE ARTERIOSCLEROSIS?
A
Pink hyaline thickening of vascular wall (proteins leaking into BV wall)
16
Q
***What are the 2 most common causes of HYALINE ARTERIOSCLEROSIS?
A
BENIGN HTN - High pressure pushes proteins into wall
DIABETES - Nonenzymatic glycosylation of BM -> Leaky BV -> Protein leaks in -> Hyaline arteriolosclerosis
17
Q
Describe the pathophysiology of how ARTERIOLOSCLEROSIS can progress to CHRONIC RENAL FAILURE.
A
ARTERIOSCLEROSIS -> Protein leakage into BV wall and thickening -> REDUCED caliber of RENAL AFFERENT ARTERIOLE -> End-organ [kidney] ischemia -> GLOMERULAR SCARRING = ARTERIOLONEPHROSCLEROSIS -> Can ultimately progress to CHRONIC RENAL FAILURE
18
Q
Describe what is seen in the gross appearance of a kidney that has been affected by ARTERIOLOSCLEROSIS (Renal afferent arteriole).
A
Shrunken kidneys - Due to arterionephrosclerosis (glomerular scarring)
Scarring on surface of kidney (CORTEX)
19
Q
ONION SKIN APPEARANCE of a BV
A
HYPERPLASTIC ARTERIOLOSCLEROSIS - Due to Smooth muscle hyperplasia decreasing the blood flow to end organ
20
Q
What is the most common cause of HYPERPLASTIC ARTERIOLOSCLEROSIS?
A
MALIGNANT HTN: Super high bp -> SM responds by excessive proliferation in attempt to CONTAIN that high BP
21
Q
What are two pathologies that you see FIBRINOID NECROSIS (=death of vessel wall)?
A
MALIGNANT HTN + VASCULITIS
22
Q
**What is the GROSS APPEARANCE of the kidney that has been affected by HYPERPLASTIC ARTERIOLOSCLEROSIS?
A
**FLEA BITTEN KIDNEY - Due to ACUTE RENAL FAILURE that precipitated from reduced vessel caliber with end-organ ischemia -> Pin point hemorrhages on the surface of kidney
23
Q
FIBRINOID NECROSIS (death of BV wall) + FLEA BITTEN SURFACE OF KIDNEY = what type of arteriosclerosis? What is the most common cause?
A
HYPERPLASTIC ARTERIOLOSCLEROSIS
Most common cause = MALIGNANT HTN
24
Q
How is MONCKEBERG MEDIAL CALCIFIC SCLEROSIS generally discovered?
A
NON-OBSTRUCTIVE as in Atherosclerosis or arteriolosclerosis - Therefore NOT clinically significant
Detected as INCIDENTAL finding on X-RAY or MAMMOGRAPHY
25
PIPE STEM APPEARANCE of CALCIFICATIONS ON X-RAY in the pattern of the vessels
MONCKEBERG MEDIAL CALCIFIC SCLEROSIS
26
What layers of the BV wall are affected by an AORTIC DISSECTION?
TEAR through the Media INTIMA
| BLOOD DISSECTS through media of aortic wall
27
What are the 2 requirements of an AORTIC DISSECTION?
1. HIGH STRESS: Occurs at the proximal 10cm of the aorta (ARCH or ASCENDING AORTA)
2. PRE-EXISTING WEAKNESS OF TUNICA MEDIA: HTN is most common cause of media weakness
28
How does HTN result in WEAKNESS of TUNICA MEDIA (1 of 2 requirements of AORTIC DISSECTION)?
HTN -> Hyaline arteriolosclerosis of VASO VASORUM supplying the outer half of the BV wall -> Reduced luminal caliber -> Decrease blood flow to outer half -> SMOOTH MUSCLE (MEDIA) ATROPHY = weakness
29
What are 2 other less common congenital causes of that result in WEAKNESS of TUNICA MEDIA (1 of 2 requirements of AORTIC ANEURYSM)?
MARFAN SYNDROME
| EHLER DANLOS SYNDROME
30
Cardiac Pathologies associated with MARFAN [defect in fibrillin]/EHLER DANLOS SYNDROME [defect in collagen]
1. MVP
2. CYSTIC MEDIAL AORTIC DEGENERATION -> AORTIC DISSECTION (Tunica media contains HIGH amounts of ELASTIC connective tissue)
3. THORACIC AORTA ANEURYSM (Weakness of entire BV wall -> Predisposes to dvlm of aneurysm)
31
What is the most common cause of death in pts with an AORTIC DISSECTION?
PERICARDIAL TAMPONADE
32
What are the 3 complications of an AORTIC DISSECTION?
1. END ORGAN ISCHEMIA (KIDNEY - acute renal failure): Blood from aneurysm flows FORWARD and compresses onto the renal artery
2. PERICARDIAL TAMPONADE: Blood from aneurysm flows BACKWARD and compresses the heart
3. Rupture with FATAL HEMORRHAGE into MEDIASTINUM
33
What is the ONE requirement of an ANEURYSM?
Weakness in the AORTIC WALL
34
What is the classic cause of THORACIC AORTIC ANEURYSM. Describe the pathophysiology.
TERTIARY SYPHILIS
Endarteritis of VASOVASORUM -> Reduced luminal caliber -> Decreased blood flow -> Atrophy of BV wall -> WEAKNESS of BV WALL (1 of 1 requirement of an aneurysm)
35
What is the most common complication of a THORACIC AORTA ANEURYSM? What are the 2 less common complications?
1. AORTIC REGURGITATION**: Due to Aneurysm creating an aortic root dilation -> Stretches the aortic valve -> Insufficiency
2. DYSPHAGIA or DYSPNEA: Due to compression of mediastinal structures (Airway, esophagus)
3. THROMBUS/EMBOLUS: Balloon-like dilation -> Turbulent flow instead of laminar flow -> Activates COAG cascade
36
TREE BARK APPEARANCE OF AORTA is associated with which pathology?
TERTIARY SYPHILIS resulting in endarteritis of vasovasorum -> Scarring/fibrosis of BV wall -> THORACIC AORTA ANEURYSM -> Aortic regurgitation
Tree bark = Scarring and fibrosis of aorta
37
Where is the most common location of an ABDOMINAL AORTA ANEURSYM?
Distal to RENAL ARTERIES, proximal to ABDOMINAL AORTA BIFURCATION
38
What is the most common cause of AAA? Who is the typical, classical pt?
ATHEROSCLEROSIS
| Typical pt = risk factors of atherosclerosis (MALE SMOKER >60yo with HTN, HL)
39
When the pulsatile abdominal mass of an ABDOMINAL AORTIC ANEURYSM grows with time, it eventually becomes >5cm in diameter. What is the main complication and clinical presentation at this point?
FEAR OF ANEURYSM RUPTURE
Clinical Presentation = 1. HYPOTENSION (Rupture resulting in bleeding and shock) + 2. PULSATILE MASS (Feel blood coursing through) + 3. FLANK PAIN
40
Infant presents with a BENIGN TUMOR comprised of BV on the face. What is the Tx of choice for this pt?
Pt has a HEMANGIOMA. NO SURGICAL resection that would result in a scar bec it often regresses during childhood.
41
What is another common location of a HEMANGIOMA?
LIVER + SKIN
42
How does one differentiate between a HEMANGIOMA of the skin and a PURPURA.
Pressing down on the HEMANGIOMA: YES BLANCHING because it is a tumor of the BV
Pressing down on the PURPURA: NO BLANCHING because there is actual bleeding in the skin
43
What is a malignant proliferation of ENDOTHELIAL CELLS that is HIGHLY AGGRESSIVE?
ANGIOSARCOMA
44
What tissues does a HEMANGIOSARCOMA most commonly involve?
SKIN
LIVER
BREAST
45
What are 3 RISK FACTORS of a LIVER ANGIOSARCOMA?
POLYVINYL CHLORIDE
ARSENIC
THOROTRAST
46
Would pressing on a KAPOSI SARCOMA result in BLANCHING?
NO, would NOT result in blanching (as in a HEMANGIOMA)
Because it is a proliferation of ENDOTHELIAL CELLS that are NOT BV yet (Blood is simply interspersed within channels of skin)
47
Which virus drives KAPOSI SARCOMA (Low grade malignant tumor proliferation of endothelial cells)? Which 3 pt populations does it most commonly affect?
HHV-8
48
What is a malignant proliferation of ENDOTHELIAL CELLS that is HIGHLY AGGRESSIVE?
ANGIOSARCOMA
49
What tissues does a HEMANGIOSARCOMA most commonly involve?
SKIN
LIVER
BREAST
50
What are 3 RISK FACTORS of a LIVER ANGIOSARCOMA?
POLYVINYL CHLORIDE
ARSENIC
THOROTRAST
51
Would pressing on a KAPOSI SARCOMA result in BLANCHING?
NO, would NOT result in blanching (as in a HEMANGIOMA)
Because it is a proliferation of ENDOTHELIAL CELLS that are NOT BV yet (Blood is simply interspersed within channels of skin)
52
Which virus drives KAPOSI SARCOMA (Low grade malignant tumor proliferation of endothelial cells)? Which 3 pt populations does it most commonly affect?
HHV-8
3 pt populations -
1. OLDER EASTERN EUROPEAN MALES: Tx = surgical removal of tumor localized to skin
2. AIDS: Tx = anti-retroviral agents (To boost immune system and increase CD4 ct)
3. Tx Recipients: Tx = decrease immunosuppression
53
What are the 2 possible clinical presentations of VASCULITIS?
1. NON-SPECIFIC Sx of inflammation (fever, weight loss, myalgia)
2. END-ORGAN ISCHEMIA: Vasculitis -> Inflammation and damage of endothelial cells -> Tissue fibrosis -> LUMINAL NARROWING + THROMBOSIS (due to exposed sub-endothelial collagen)
54
What are the 2 types of LARGE VESSEL VASCULITISES?
1. TEMPORAL (GIANT CELL) ARTERITIS
| 2. TAKAYASU ARTERITIS
55
GIANT CELL ARTERITIS: Who is the classic typical pt affected by GIANT CELL ARTERITIS?
FEMALE age>50yo
56
GIANT CELL ARTERITIS: Which vessels can possibly be inflamed in GIANT CELL TEMPORAL ARTERITIS? What are the associated clinical sx with each vessel?
Branches of the CAROTID ARTERY
1. TEMPORAL ARTERY - Headache
2. OPHTHALMIC ARTERY - Visual disturbances
3. ARTERIES SUPPLYING JAW MUSCLES - Jaw claudication
57
GIANT CELL ARTERITIS: What is POLYMYALGIA RHEUMATICA?
Pts with GIANT CELL ARTERITIS who have FLU-like sx + MYALGIA
NECK, TORSO, SHOULDER, PELVIC GIRDLE PAIN + MORNING STIFFNESS
58
GIANT CELL ARTERITIS: What is the marker of inflammation with GIANT CELL ARTERITIS?
ESR >150
59
GIANT CELL ARTERITIS: What is seen on BIOPSY of a GIANT CELL TEMPORAL ARTERITIS?
1. GRANULOMATOUS INFLAMMATION: Giant cells + Epithelioid histiocytes [macrophages] + Lymphocytes
2. INTIMAL FIBROSIS (post-inflammation healing)
60
To diagnose GIANT CELL ARTERITIS, is it safe to look at one portion of the vessel? If the biopsy comes out negative, can I r/o GIANT CELL ARTERITIS?
It is NOT safe to look at only portion of the vessel. Lesions of GIANT CELL ARTERITIS are SEGMENTAL - 1) Need to take out a LONG segment of the vessel and 2) Need to look at ALL parts of the vessel under the microscope
NO, can NOT rule out with a negative biopsy bec it just means that the segment you might have taken out for biopsy doesn't contain the lesion
61
If GIANT CELL ARTERITIS is suspected, what is the IMMEDIATE TREATMENT (even before diagnosis is confirmed)? What is the reason?
CORTICOSTEROIDS immediately
| Due to high risk of BLINDNESS without Tx (endothelial damage of ophthalmic artery is irreversible)
62
TAKAYASU ARTERITIS: Who is the typical pt affected?
Unlike GIANT CELL TEMPORAL ARTERITIS (>50yo females), TAKAYASU
63
TAKAYASU ARTERITIS: What is seen on biopsy of TAKAYASU ARTERITIS?
Granulomatous vasculitis - Same as GIANT CELL ARTERITIS [epithelioid histiocytes + giant cells + lymphocytic rim]
64
TAKAYASU ARTERITIS: What vessel is affected?
AORTA ARCH at branch points
65
TAKAYASU ARTERITIS: How do you differentiate TAKAYASU ARTERITIS with GIANT CELL ARTERITIS (2)?
TAKAYASU : 50yo females, 2. Affects branches of carotid artery (temporal, ophthalmic, jaw muscles)
66
TAKAYASU ARTERITIS: Why is TAKAYASU ARTERITIS sometimes called PULSELESS DISEASE?
Because of UE Claudication (Weak/Absent pulse)
67
TAKAYASU ARTERITIS: Similar to GIANT CELL ARTERITIS, what is the clinical presentation of TAKAYASU ARTERITIS? What is the inflammatory marker? What is the Tx?
CLINICAL PRESENTATION: Visual, neurologic deficits, UE claudication + Non-specific systemic signs (fever, myalgia, headaches)
ESR >150
Tx = CORTICOSTEROIDS
68
What arteries are involved in MEDIUM-VESSEL VASCULITIS?
MUSCULAR ARTERIES (Eg. Renal artery)
69
Name the 3 types of MEDIUM VESSEL VASCULITIS.
1. POLYARTERITIS NODOSA
2. KAWASAKI
3. BUERGER
70
POLYARTERITIS NODOSA: Which MUSCULAR arteries are involved with PAN and what are the associated Sx?
RENAL ARTERY: HTN
MESENTERIC ARTERY: Abdominal Pain + Melena
INTERNAL CAROTID ARTERY: Neurologic deficits
+ Skin lesions
71
POLYARTERITIS NODOSA: All organs can basically be involved with PAN, except for which organ?
LUNGS
72
POLYARTERITIS NODOSA: Which infection is most commonly associated with PAN? How can this be confirmed?
HEPATITIS B
| +HBsAg
73
POLYARTERITIS NODOSA: What is the histological change on biopsy associated with PAN? Which other pathology do you also see this process?
FIBRINOID NECROSIS: Lots of PINK in the BV wall
| Also seen with MALIGNANT HTN resulting in HYPERPLASTIC ARTERIOLOSCEROSIS
74
STRING OF PEARLS APPEARANCE ON IMAGING (that is NOT FIBROMUSCULAR DYSPLASIA). Why do you this string of pearls?
POLYARTERITIS NODOSA - See string of pearls based on stage of lesion
EARLY STAGE LESION (STRINGS)= Transmural inflammation + Fibrinoid necrosis
LATE STAGE LESION (PEARLS) = Post-inflammation healing with fibrosis = NODULES/NODES on arteries
75
POLYARTERITIS NODOSA: What complication do you have an increased risk of due to the fibrotic nodules that form on the affected muscular arteries?
WEAKENED BV WALL -> Increased risk of ANEURYSMS
76
POLYARTERITIS NODOSA: What is the Tx (2) of POLYARTERITIS NODOSA?
CORTICOSTEROIDS + CYCLOPHOSPHAMIDE
77
KAWASAKI DISEASE: Who is the typical pt affected with KAWASAKI disease?
Asian child
78
KAWASAKI DISEASE: Think of a kid on a motorcycle putting hands on handles, and HR racing. What is the typical presentation?
```
VERY NON-SPECIFIC: Almost seems like a VIRAL infection
FEVER
CONJUNCTIVITIS
ERYTHEMATOUS RASH ON PALMS AND SOLES
ENLARGED CERVICAL LYMPH NODES
```
79
KAWASAKI DISEASE: What is the most commonly involved artery? What are the two possible complications?
CORONARY ARTERY
COMPLICATION 1: MI - Vasculitis of coronary artery -> Exposure of subenodethlial collagen -> Activation of coagulation cascade -> Transmural ischemia due to thrombus
COMPLICATION 2: ANEURYSM with rupture - Due to weakened BV wall post-vasculitis
80
When a baby presents with viral infection-like symptoms what is the Tx that you must absolutely avoid? To prevent which pathology?
ASA
| To prevent REYES SYNDROME
81
KAWASAKI DISEASE: What is the Tx? What is the mechanism?
1 .ASA - Selective inhibition of COX-1 -> Selective decreases of TXA2 (normally facilitating PLT aggregation) -> Decreases thrombus formation in coronary artery
2. IVIG
82
BUERGER DISEASE: What is the most common association with BUERGER DISEASE? Thus what is the Tx?
SMOKING - Highest association with BUERGER DISEASE (Medium vessel vasculitis)
Tx = SMOKING CESSATION
83
BUERGER DISEASE: Which organs are most commonly involved?
NECROTIZING VASCULITIS of the DIGITS
84
BUERGER DISEASE: What is the typical clinical presentation of BUERGER DISEASE?
ULCERATION + GANGRENE + AUTO-AMPUTATION OF FINGERS/TOES + RAYNAUD
85
What types of vessels are affected with SMALL VESSEL VASCULITIS? Name the 4 types of SMALL VESSEL VASCULITIS.
ARTERIOLES, CAPILLARIES, VENULES
| 4 types: WEGENER GRANULOMATOSIS, MICROSCOPIC POLYANGIITIS, CHURG-STRAUSS SYNDROME, HENOCH-SCHONLEIN PURPURA
86
WEGENER GRANULOMATOSIS: Think WECENER GRANULOMATOSIS - What are the 3 most commonly involved organs? Name the associated Sx
NASOPHARYNX - SINUSITIS + NASOPHARYNGEAL ULCERATION
LUNG - Hemoptysis + Bilateral Lung Nodular Infiltrates
KIDNEYS - Hematuria due to RPGN (rapid progressive glomerulonephritis)
87
WEGENER GRANULOMATOSIS: Who is the typical pt affected?
MIDDLE AGED MALES
88
WEGENER GRANULOMATOSIS: What is the typical marker that correlates with disease activity?
C-ANCA
| THINK "C"
89
WEGENER GRANULOMATOSIS: What is the Tx?
Think C
| CYCLOPHOSPHAMIDE + CORTICOSTEROIDS
90
WEGENER GRANULOMATOSIS: What is the classic histological finding on biopsy?
NECROTIZING GRANULOMAS + Surrounding NECROTIZING VASULITIS
91
MICROSCOPIC POLYANGIITIS: Which organs does Microscopic polyangiitis preferentially involve?
INVOLVES MULTIPLE ORGANS, but particularly affects LUNG + KIDNEY
92
MICROSCOPIC POLYANGIITIS: Is similar to WEGENER GRAULOMATOSIS with 3 exceptions
[Hint: 1 clinical sx, 1 biopsy finding, 1 diagnostic test finding]
MICROSCOPIC POLYANGIITIS: NO nasopharyngeal involvement (sinusitis/nasopharyngeal ulcers), NO GRANULOMAS, P-ANCA correlating with disease activity
WEGENER: YES nasopharyngeal involvement, YES granulomas, c-ANCA not p-ANCA correlating with disease activity
93
What is the Tx of MICROSCOPIC POLYANGIITIS? Are relapses common or uncommon?
Same as WEGENER GRANULOMATOSIS - CORTICOSTEROIDS + CYCLOPHOSPHAMIDE, relapses are common
94
CHURG-STRAUSS SYNDROME: What is the common diagnostic test finding between MICROSCOPIC POLYANGIITIS and CHURG-STRAUSS?
p-ANCA
95
CHURG-STRAUSS SYNDROME: Name 3 distinguishing features between CHURG-STRAUSS and MICROSCOPIC POLYANGIITIS.
[Hint: 1 PMH key note, 2 biopsy findings]
1. CHURG-STRAUSS: History of ASTHMA, whereas microscopic polyangiitis does NOT
2. CHURG-STRAUSS: YES granulomas (MPA - no granulomas) + Peripheral EOSINOPHILIA (MPA - no eosinophils)
96
What is the most common vasculitis in children?
HENOCH SCHONLEIN PURPURA (HSP) in children = SMALL VESSEL VASCULITIS
97
HSP: What is the pathophysiology of HSP? What infection does this commonly follow?
IgA deposits
| UPPER RESPIRATORY INFECTION
98
HENOCH SCHONLEIN PURPURA (HSP): What are the 3 typical presentations of HSP? Which is the most likely to occur?
1. IgA NEPHROPATHY = most likely - Presents with HEMATURIA
2. PALPABLE purpura along buttocks and legs - PALPABLE (other purpuras are NOT palpable, whereas HSP ones are due to the INFLAMMATION along the vasculitis)
3. GI PAIN + BLEEDING
99
**UWorld: What is the most common cause of death in MARFAN SYNDROME pts? What is the second most common cause of death?
AORTA DISSECTION = most common cause
Heart failure secondary to MVP or Aortic regurgitation
100
**UWorld: Segmental vasculitis EXTENDING INTO contiguous veins and nerves is characteristic and unique to which vasculitis?
BUERGER'S DISEASE
101
**UWorld: Lipid intimal plaques that bulge into the arterial lumen is characteristic of what pathology?
ATHEROSCLEROSIS
102
**UWorld: Onion-like concentric thickening of arteriolar walls as a reuslt of LAMINATED SMC and reduplicated BM is characteristic of what pathology?
HYPERPLASTIC ARTERIOLOSCERLOSIS (From MALIGNANT HTN)
Malignant HTN = DIASTOLIC PRESSURES >120-130
Presents with HEADACHE, RENAL FAILURE, PAPILLEDEMA (medical emergency)
103
**UWorld: Granulomatous inflammation of the MEDIA is characteristic of what pathology?
TERMPORAL (GIANT CELL) ARTERITIS = most common form
OTHERS: TAKAYASU
WEGNER'S, CHURG-STRAUSS
104
**UWorld: Fibrinoid necrosis (Death of BV) = Which 2 pathologies?
Fibrinoid Necrosis + TRANSMURAL INFLAMMATION of arterial wall = Which of the 2?
1. HYPERPLASTIC ARTERIOLOSCLEROSIS (malignant HTN Diastolic BP>120-130)
2. POLYARTERITIS NODOSA - Fibrinoid necrosis + Transmural inflammation of arterial wall = STRING OF PEARLS
105
**UW: Large FRIABLE vegetations on valve cusps + DESTRUCTION = ?
INFECTIVE ENDOCARDITIS
106
**UW: Diffuse FIBROUS THICKENING + Distortion of leaflets + COMMISSURAL FUSION at leaflet edges + Narrowing of orifice = ?
CHRONIC RHEUMATIC FEVER
107
**UW: Which vasculitis has most common association with an MI and/or coronary aneurysm?
KAWASAKI
108
**UW: Describe the pathogenesis of ATHEROSCLEROSIS (Minimally raised YELLOW SPOTS on inner surface)
STEP 1: DAMAGE to endothelium -> Lipids leak into INTIMA
STEP 2: FOAM CELLS/FATTY STREAK: LDL accumulation -> Lipids are oxidized and consumed by MACROPHAGES via scavenger receptors -> FOAM CELLS -> FATTY STREAKS
STEP 3: FIBROMUSCULAR CAP dvlm resulting in PLAQUE = Inflammation + Healing -> ECM deposition and SM proliferation + T cell recruitment -> COMPLEX ATHEROMAS
109
**UW: High fevers, strawberry tongue, perioral erythema/fissuring, periungual desquamation, swollen lymph nodes, red eyes
KAWASAKI DISEASE
110
**UW: TRIAD: JOINT PAIN + LE/BUTTOCK purpura + HEMATURIA
| + Occasional abdominal pain
HSP
IgA-mediated HSR vasculitis
Renal pathology is same as IgA NEPHROPATHY (BERGER) = MESANGIAL proliferation + CRESCENT formation
HSP = PALPABLE PURPURA + RENAL DISEASE (HEMATURIA) + ARTHRALGIA/ARTHRITIS
111
**UW: Fibrinoid necrosis (3 pathologies)
MALIGNANT HTN + VASCULITIS + SERUM SICKNESS (e.g. mAb treatments + Igs - Type III HSR)
