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CPR II Exam 1 > Lecture 1: Vascular Pathology (Hillard) > Flashcards

Lecture 1: Vascular Pathology (Hillard) Flashcards

1
Q

At what level of the vasculature is blood pressure controlled?

A

Arterioles

  • primary site of physiologic changes to total peripheral resistance
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2
Q

What is an Arteriovenous Malformation and what 3 things is it caused by (R/P/N)?

What do large AVMs lead to?

A
  • tangle of worm-like arteries connecting to veins WITHOUT intervening capillaries (shunt); most congenital (M > F)

cause: rupture of aneurysm, penetrating injuries, or inflammatory necrosis (connects A to V)
- also SURGICAL –> hemodialysis/chemotherapy

  • large AVMs lead to HIGH-OUTPUT CARDIAC FAILURE
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3
Q

What is Berry Aneurysm and where does it most commonly occur?

What are two major risk factors of development?

A
  • abnormal focal dilation of artery due to media defect, usually in CIRCLE OF WILLIS (Anterior Cerebral A. branch point)

RF: hypertension and smoking

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4
Q

What 3 conditions can Berry Aneurysm be associated with (PKD/M/ED) and what does it cause clinically?

What does it feel like?

A
  • AD polycystic kidney disease, Marfans, Ehlers Danlos
  • most frequent cause of subarachnoid hemorrhage (“Worst headache of my life doctor”); repeat bleeding common (25-50% die w/rupture)
  • neck pain, vomiting, double vision, loss of consciousness, seizures
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5
Q

What is a Mycotic Aneurysm and what is it commonly caused by?

A
  • artery dilation due to vessel wall damage by infection
    cause: septic emboli from INFECTIVE ENDOCARDITIS, direct wall infection (circulating)

usually fairly rare

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6
Q

What is Fibromuscular Dysplasia?

What does it look like on angiography and what is a major complication it can cause?

What does it sound like?

A
  • focal, irregular medium/large artery thickening due to medial/intimal hyperplasia (“String of Beads” on angiography)
  • first degree relatives have inc. incidence (FEMALES) but not associated w/estrogen or oral contraceptives
  • affects RENAL ARTERIES –> Renal Artery Stenosis (activates RAAS; epigastric abdominal bruit)
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7
Q

What are 4 types of Vascular Abnormalities? (B/A/M/F)

A
  • Arteriovenous Fistula
  • Berry Aneurysm
  • Mycotic Aneurysm
  • Fibromuscular Dysplasia
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8
Q

What are 5 humoral constrictors of blood vessels (A/C/T/L/E) and what are 3 humoral dilators of blood vessels (P/K/N) that help determine Peripheral Resistance?

What is a neural constrictor and dilator of blood vessels that helps determine peripheral resistance?

A

C: angiotensin II, catecholamines, thromboxanes, leukotrienes, endothelin

D: prostaglandins, kinins, nitric oxide (NO)

Neural: Constrictor (alpha-adrenergic) and Dilator (beta-adrenergic)

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9
Q

What are 3 Blood Volume components and 2 Cardiac Factors that determine Cardiac Output?

A

BV: sodium, mineralcorticoids, ANP

CF: heart rate and contractility

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10
Q

What is the Renin-Angiotensin-Aldosterone System and what does it do?

What is the function of Atrial Natriuretic Peptide?

A
  • helps maintain blood pressure homeostasis
  • when BP is low, kidney releases RENIN (juxtoglomerular) that cleaves Angiotensinogen made by the liver, creating ANGIOTENSIN I
  • Angiotensin I gets converted to ANGIOTENSIN II by converting enzymes (ACE), allowing it to cause vasoconstriction of vessels, as well as causing adrenals to release more ALDOSTERONE (inc. Na/water reabsorption by kidneys), in order to inc. the BLOOD PRESSURE
  • ANP is released by the heart when there is too much volume; ANP vasodilates vessels and causes the kidneys to excrete sodium and water (DECREASES BLOOD PRESSURE)
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11
Q

What is the difference between Primary Hypertension and Secondary Hypertension?

What are 2 unmodifiable and 4 modifiable factors of Primary Hypertension?

A
  • ELEVATED BLOOD PRESSURE (“Silent Killer”) –> leads to End Organ Failure

Primary: 90-95% (idiopathic or essential HTN)
Unmod: inc. age, genetics (African American)
Modifiable: stress, obesity, inactivity, inc. salt

Secondary: 5-10% (causes by other disease process)
- kidney, endocrine, cardiovascular

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12
Q

What are 6 common causes of Secondary Hypertension? (PH/CS/P/RAS/CA/PKD)

A
  • Primary Hyperaldosteronism
  • Cushing Syndrome
  • Pheochromocytoma
  • Renal Artery Stenosis
  • Coarctation of Aorta
  • Polycystic Kidney Disease
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13
Q

How does Primary Hyperaldosteronism cause Secondary Hypertension?

What is the common feature of Primary Hyperaldosteronism?

A
  • idiopathic hyperaldosteronism (hyperplasia) or adenoma secrete inc. aldosterone, causing increased sodium reabsorption and increased potassium secretion
  • Hypertension with HYPOKALEMIA
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14
Q

What are 4 common causes of Cushing’s Syndrome and how does this patient present?

What is Cushing’s Syndrome associated with?

A
  • inc. cortisol production via pituitary tumor (inc. ACTH), adrenal tumor/hyperplasia, paraneoplastic tumor, or steroids
    pt: round face, inc. facial hair in women, stretch marks, weight gain in neck/back/belly
  • cause of Secondary Hypertension
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15
Q

How does Pheochromocytoma cause Secondary Hypertension?

How does a patient present and what test can be done to help confirm the diagnosis?

A
  • tumor of chromaffin cells in the adrenal medulla releases inc. epinephrine/norepinephrine causing inc. cardiac output and constricted blood vessels
  • tumor is golden brown and associated with MEN2

C: inc. BP, pounding headache/tremors/sweating

  • look for elevated metanephrines in URINE and PLASMA
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16
Q

How does Renal Artery Stenosis cause Secondary Hypertension?

What are two common causes of stenosis?

What noise does this condition make?

A
  • caused by atherosclerosis or fibromuscular dysplasia
  • hypertension due to activation of RAAS system (see dec. GFR, chronic kidney disease, inc. creatinine w/ischemia)

abdominal bruit (epigastric) that can radiate to the back

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17
Q

How does Secondary Hypertension due to Coarctation of the Aorta present?

What is a common finding of pts. with this condition?

A
  • hypertension caused by narrowing or constriction of the aorta (pts. usually have BICUSPID AORTIC VALVE)
  • will present with HYPERTENSION in upper extremities and HYPOTENSION in lower extremities
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18
Q

What do untreated hypertensive patients usually die from?

What is a common eye finding of patients with hypertension?

A
  • 1/2 die from ischemic heart disease or congestive heart failure, while another 1/3 die from stroke
  • pt. with hypertension can have retinopathy with arteriovenous nicking and flame-shaped hemorrhages
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19
Q

What is the difference between Hyaline Arteriosclerosis and Hyperplastic Arteriosclerosis?

A

Hyaline: due to CHRONIC hypertension

  • inc. SM synthesis and C3 protein across endothel.
  • pink thickening of walls –> downstream ischemia

Hyperplastic: due to SEVERE hypertension

  • SM forms concentric lamellations (“onion skin”)
  • basement membrane thickens/reduplicates
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20
Q

What are Hypertensive Crisis and Hypertensive Emergency?

A

Crisis: rapid inc. in BP > 180-200/120 (ACUTE)

Emergency: hypertensive crisis with END ORGAN DAMAGE

  • renal failure, encephalopathy, papilledema
  • retinal hemorrhage, acute heart failure
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21
Q

What is Arteriosclerosis and what are its 3 types?

A
  • hardening of the arteries (inc. thickness, dec. elasticity)
  1. Arteriolosclerosis: hyaline/hyperplastic
    • downstream ischemia (small A and arterioles)
  2. Atherosclerosis: hardening with plaque formation
    • stenosis/occlusion and aneurysm
  3. Monckeberg Medial Sclerosis
    • age related degenerative process (no clinical)
    • muscular artery calcifications
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22
Q

What is the number 1 cause of mortality in the United States?

A

Myocardial Infarction (almost 1/4 of all deaths in the United States) –> due to atherosclerosis

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23
Q

Atherosclerotic Risk

What conditions increase and decrease the amounts of LDL and HDL in a patient?

A

LDL

  • inc: animal products, trans fats (fried, snacks) - BAD
  • dec: soluble fiber, statins

HDL

  • inc: exercise and moderate alcohol
  • dec: obesity and smoking
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24
Q

What are the 5 conditions needed to have Metabolic Syndrome (O/T/H/BP/IR)

What does Metabolic Syndrome put patients at inc. risk of developing?

A
  • abdominal obesity, inc. triglycerides, dec. HDL, high BP, insulin resistance
  • need at least 3 of the 5

inc. risk of atherosclerosis

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25
Q

How are cigarette smoking, Diabetes Mellitus, hyperhomocysteinemia, and C-reactive protein related to Atherosclerotic Risk?

A

CS: doubles risk of ischemic heart disease

DM: doubles chance of myocardial infarction

HHC: inc. levels correlate w/inc. coronary atherosclerosis, peripheral vascular disease, stroke

CRP: measure of inflammation, inc. by IL-6
- inc. correlates with inc. cardiovascular risk

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26
Q

What does an atherosclerotic plaque look like on imaging?

A
  • narrowed lumen with a fibrous cap over a cholesterol core (plaque)
  • plaque forms on the internal elastic lamina (will be on the outside of the plaque)
  • calcifications and neovascularization can be noted as the vessel tries to get alternate blood flow
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27
Q

How do Atherosclerotic Plaques develop?

A
  • LDL enters the intima due to endothelial injury (chronic damage) and is taken up by the macrophages that are trying to help repair the vessel, becoming foam cells
  • foam cells cannot get rid of the lipids; they release inc. cytokines to bring more macrophages as a fatty core of necrosis forms
  • smooth muscles proliferate around these areas to help try and repair the damage to the vessel; recruited by growth signals sent from the macrophages
28
Q

Atherosclerotic Plaque Development

What are 3 common growth factors that cause smooth muscle proliferation and collagen deposition?

A
  • PDGF (released by platelets, MO, endothelial cells, SM)
  • Fibroblast growth factor
  • TGF-alpha
29
Q

What are the 5 most commonly affected arteries do to atherosclerotic plaques?

A

LOWER ABDOMINAL AORTA, coronary arteries, popliteal arteries, internal carotid arteries, Circle of Willis

30
Q

What are 3 clinical outcomes of atherosclerotic plaque formation?

A
  1. aneurysm and rupture
    • acute plaque rupture = most dangerous problem
  2. occlusion by thrombus
  3. critical stenosis
    • when 70% dec. in cross-sectional area

all can cause end-organ damage

31
Q

What is a “True” aneurysm, “False” aneurysm, and arterial dissection?

A

True: intact (thinned) muscular wall at site of dilation

False: defect through wall of vessel communicating with extravascular hematoma (“pulsating”)

Dissection: blood enters defect in arterial wall and tunnels between its layers

these can RUPTURE, leading to catastrophic problems

32
Q

What are Marfan Syndrome and Ehlers Danlos Syndrome?

What are pts. with these diseases at inc. risk of developing?

A

MS: FBN1 fibrillin gene mutation (inc. TGF-b –> elastic tissue weakening)

  • tall, long fingers, subluxation, mitral valve prolapse
  • inc. risk of aortic aneurysm and dissection

EDS: mutation in collagen (abnormal wound healing)

  • hyperelastic, fragile skin; subluxation, mitral prolapse
  • inc. risk of aortic dissection (colon/cornea rupture)
33
Q

What is Tertiary Syphillis and what does it put patients at higher risk of developing?

A
  • STI caused by spirochete T. pallidum presenting >5 yrs after primary infection (chancre lesion)
  • causes neurosyphillis, gummas (inflammatory lesions), and CV problems; classic “Treebark” appearance of aorta (rough, pitted aorta w/calcifications)
  • inc. risk of obliterative endarteritis of vasa vasorum causing thoracic aneurysm; aortic valve regurgitation can also occur
34
Q

What is primary risk factor for the development of an Abdominal Aortic Aneurysm and where does it commonly develop?

A
  • ATHEROSCLEROSIS is the major risk factor for Abdominal Aortic Aneurysm (occurs more in smokers and older men > 50 yo)
  • commonly develops BELOW renal arteries but ABOVE aortic bifurcation (contains bland laminated mural thrombus)
35
Q

What is the difference between an Asymptomatic and Symptomatic Abdominal Aortic Aneurysm?

A

Asymptomatic: majority of cases
- pulsatile abdominal mass with radiology findings

Symptomatic: nonruptured = pain in abdomen and back (MISDIAGNOSIS) or RUPTURE = severe acute pain, pulsatile mass, HYPOTENSION

surgical bypass considered when diameter > 5 cm

36
Q

What is the Inflammatory-type Abdominal Aortic Aneurysm?

A
  • fibroinflammatory infiltrate due to IgG4 antibodies and circulating plasma cells
  • see with pancreatitis and Primary Sclerosing Cholangitis

responds well to steroid therapy

37
Q

What is the most important risk factor for Thoracic Aortic Aneurysms and what do they cause clinically?

A
  • HYPERTENSION is the most important risk factor (also syphilic aortitis, connective tissue disease, and large vessel vasculitis)
    clinical: breathing difficulties, dysphagia, and cough (due to compression and encroachment of structures)
38
Q

What are the two most common causes of Aortic Dissection and what is the classic triad they present with?

A

causes: Hypertension (men 40-60) and connective tissue diseases
- intimal tearing w/blood filled channels

Triad: thoracic pain, pulse abnormalities, mediastinal widening on X-RAY (pain radiates to back and down as dissection progresses)

39
Q

What is the most common dissection of the aorta?

A

DeBakey 1 - proximal to left common carotid artery

  • most common; more prone to rupture
  • Debakey 2 - only ascending thoracic aorta
  • both are TYPE A dissections

Debakey 3 - Type B; only descending aorta
- can handle with medical management

40
Q

What is Giant Cell (Temporal) Arteritis?

What antibodies are associated with it?

What is a serious complication of this vasculitis?

A
  • Most Common vasculitis of older adults (F > 50 yo)
    • large to small vessels (temporal/vertebral/ophthalmic)
    • headache, facial pain, fever
  • T-cell mediated autoimmune response (intimal thickening w/granuloma) with anti-endothelial and anti-SM Abs
  • can cause VISION LOSS –> diagnosis early to prevent permanent issues (get TEMPORAL Artery BIOPSY)
41
Q

What is Takayasu Arteritis?

What does it cause clinically?

A
  • granulomatous autoimmune vasculitis of Large and Medium arteries (thickening of aorta and major branch vessels - pulmonary, coronary, renal)
    • mononuclear infiltrate with giant cells
  • see in F < 50 yo with WEAKENING of upper extremity PULSES and OCULAR DISTURBANCES (+/- fatigue, HTN, fever, dec. weight)
42
Q

What is Polyarteritis Nodosa (PAN)?

What is it commonly associated with and how does it classically present?

Where is it most commonly found and where is it never found?

A
  • systemic vasculitis of small to medium vessels (young adults due to immune-mediated complex)
    • see fibrinoid necrosis
    • necrotizing, segmental at BRANCH POINTS
  • associated with HEPATITIS B INFECTION
  • involves RENAL VESSELS > heart > liver > GI and presents with RAPIDLY ACCELERATING HTN (can be FATAL); peripheral neuritis/myalgias, bloody stools

SPARES PULMONARY VESSELS

43
Q

What is Kawasaki Disease?

How do pts present? (F/ST/EPS/GR)

A
  • arteritis of Large to Medium vessels (CORONARY ARTERY) in infancy/early childhood (MI in young kid)
  • caused by infectious trigger –> activated T Cells and macrophages
  • presents with febrile illness, “strawberry tongue”, conjunctivitis, and erythema of palms/soles
    • also genital rash
44
Q

What is Churg-Strauss Syndrome?

What ANCA is it associated with?

A
  • small vessel necrotizing vasculitis w/ASTHMA, HYPEREOSINOPHILIA, LUNG INFILTRATES
  • palpable purpura, GI tract bleeds, renal disease (many organ systems can be involved)
  • heart is involved in 60% of pts. and can cause cardiomyopathy/myocarditis (1/2 of deaths)
  • MPO-ANCA (less than 1/2 have ANCA)
45
Q

What is Granulomatous w/Polyangiitis (Wegner’s Granulomatosis)?

What ANCA is associated with it?

A
  • small to medium vessel necrotizing granulomatous vasculitis of RESPIRATORY TRACT (+/- necrotizing renal pathology)
  • T Cell mediated hypersensitivity in 40 yo MALES
  • PR3-ANCA (c-ANCA)
46
Q

What is Microscopic Polyangiitis?

What ANCA is it associated with?

A
  • necrotizing vasculitis of small vessels (capillaries and venules too)
  • uniform stage of disease that affects ANY organ system and have NO significant deposition of immunoglobulin
  • MPO-ANCA
47
Q

What is Behcet’s Disease and what is its triad?

What genetic marker is it associated with?

What finding is required for diagnosis?

A
  • small to medium vessel vasculitis with triad: oral aphthous ulcers, genital ulcers, uveitis (can present with arthritis too)
  • associated with HLA-B51
  • vasculitis is NEUTROPHILIC (neutrophils REQUIRED for diagnosis)
48
Q

What is Buerger Disease (Thromboangiitis Obliterans)?

Who is this commonly seen in?

A
  • segmental vasculitis of small and medium vessels of TIBIAL and RADIAL arteries (hands and feet)
  • acute/chronic inflammation w/luminal necrosis and granulomatous inflammation in HEAVY SMOKERS < 35 yo (toxic rxn to cigarette process)
  • thrombosis –> vascular insufficiency –> ulceration and gangrene

starts as Raynauds phenomenon –> intermittent claudication

49
Q

What is the difference between Primary and Secondary Raynauds phenomenon?

A

Primary: symmetric involvement in young women; episodic w/spontaneous remission

Secondary: asymmetric involvement due to SLE, scleroderma, or Buerger Disease (worsens with time)

proximal vasodilation, central vasoconstriction, distal cyanosis

50
Q

What 3 things (VM/TH/S) cause Myocardial Vessel Vasospasm and what is Takotsubo Cardiomyopathy?

A
  • excessive vasoconstriction due to high lvls of vasomediators (cocaine, caffeine, pheochromocytoma), elevated thyroid hormones, autoantibodies/T Cells (SCLERODERMA)
  • TC = “Broken Heart Syndrome” due to emotional stress –> surge of catecholamines (enlarged left ventricle)
51
Q

What are Varicose Veins?

A
  • abnormally dilated and twisted veins leading to stasis, congestion, edema, ischemia of overlying skin (STASIS DERMATITIS)
  • poor wound healing and superimposed infection
52
Q

What is Portal Hypertension and what 4 findings does it lead to development of?

A
  • venous hypertension due to cirrhosis
  • causes esophageal varices, splenomegaly, hemorrhoids (rectum), and caput medusae (distended superficial epigastric veins)
53
Q

Superior Vena Cava Syndrome vs Inferior Vena Cava Syndrome

A

S: due to compression/invasion of neoplasms (lung carcinoma or lymphoma)

  • marked dilation of veins of head/neck
  • respiratory distress, facial swelling (bending over)

I: due to hepatocellular carcinoma, renal cell carcinoma, thrombosis (DVT)

  • marked LE edema
  • distension of superficial lower abdominal veins
54
Q

What is Thrombophlebitis?

What is the most serious potential consequence?

A
  • venous thrombosis and inflammation usually in deep veins of LEGS
    • due to inactivity, hypercoagulable states, tumor
  • presents w/edema, cyanosis, erythema, pain

PULMONARY EMBOLISM is most serious potential consequence

55
Q

Lymphangitis vs Lymphedema

What is Peau d’ orange?

A

Lymphangitis: inflammation of lymphatic channels

  • due to group A beta-hemolytic strep
  • red, painful, SubQ streaks
  • lymphadenitis = painful enlarged LNs (draining)

Lymphedema: congenital defect (primary) and blockage of normal lymphatics (secondary)
- malignant tumor, surgical procedure

Peau d’ orange - draining lymphatics of skin overlying skin of breast cancer filled with tumor cells

56
Q

What is the difference between Nevus Simplex, Port-Wine Stain, and Sturge-Weber Syndrome?

A

NS: simple birth mark, most common vascular ectasia
- forehead, eyelid, nose –> most regress

PWS: progressive ectasia of vascular plexus
- rare; persists into adulthood

SWS: trigeminal nerve facial port-wine nevi

  • mental retardation, seizures, hemiplegia, glaucoma
  • leptomeningeal capillary-venous malformation
  • skull radio-opacities
57
Q

Vascular Telangiectasia vs Hereditary Hemorrhagic Telangiectasia

A

TV: permanent dilation of small vessels/capillaries

  • Spider Telangiectasia: radial red lines around center
  • face/neck/chest (inc. circulating estrogen)

HHT = Osler-Weber-Rendu Disease

  • auto dominant mutation in TGF-b signal pathway
  • telangiectasia of organs and mucous membranes
  • nosebleeds, GI, hematuria (depends on location)
58
Q

Hemangioma

What is the difference between Capillary, Congenital, Cavernous, and Pyogenic Hemangiomas?

A
  • common benign vascular tumor (inc. blood vessels filled with blood);

Capillary: red spot, most common, mucosa/viscera
Congenital: at birth, usually regresses; “Strawberry”
Cavernous: indistinct border, more likely to bleed
- usually deeper; associated w/Von Hippel Lindau
Pyogenic: rapidly growing, often in oral mucosa
- type of cavernous hemangioma
- seen in gingiva of pregnant women

59
Q

What is a Glomus Tumor?

Where are they most commonly located?

A
  • mesenchymal tumor composed of modified SM arising from glomus body (responsible for thermoregulation)
  • usually located SUBUNGALLY (bluish tumor); is painful especially with change in temperature or tactile stimulation
  • well-circumscribed, bland tumor that is rarely malignant
60
Q

What is Lymphangioma?

What is the difference between Simple (Capillary) and Cavernous (Cystic) lymphangiomas?

When is Cavernous lymphangioma typically seen?

A
  • benign, lymphatic neoplasm (no RBCs in lumen)

S: around head/neck, axillary predilection

C: neck/axilla of kids; LARGE, massively dilated lymphatic space (fail to communicate with veins)

  • seen in Turner’s Syndrome (F 45 XO)
  • also Downs/Klinefelters –> hard to resect
61
Q

What is Bacillary Angiomatosis?

What is used for visualization?

A
  • reactive vascular proliferation to Gram (-) Bartonella bacilli in IMMUNOCOMPROMISED pts (HIV/transplant)
  • benign lesion with red papules
  • use Warthin Silver Stain to visualizes bacteria and treat with antibiotics
62
Q

What is Kaposi Sarcoma and how does it progress physically?

A
  • angioproliferative disorder caused by HHV-8 (double stranded) creating erythematous nodules
  • starts as macule (dilated channels, small hyperchomatic nuclei) –> plaque (infiltrative spindle cells with irregular vascular channels) –> Tumor/Nodule (nodular spindle cell mass)
63
Q

Kaposi Sarcoma

What is the difference between Classic, Endemic, Iatrogenic, and AIDS-associated forms?

A

C: sporadic, usually LE; indolent
- Mediterranean, Middle-Eastern, Eastern European M

E: African children < 10 yo; LN and cutaneous

I: T cell immunosuppression in transplant pts.
- Calcineurin

A: MOST COMMON IN US; disseminated/aggressive
- most common type of AIDS related malignancy

64
Q

What is an Angiosarcoma and what are 3 risk factors related to the Liver development?

What are two other risk factors for development of angiosarcoma?

What is a common genetic marker of disease?

A
  • malignant vascular tumor that is locally invasive and frequently metastasizes (poorly defined vessels lined by endothelial cells w/ATYPIA)

Liver: arsenic, thorotrast, and PVC production

  • also arises from lymphadema w/axillary node dissection = lymphangiosarcoma; also RADIATION for carcinoma

check for CD31 and CD34 cells!

65
Q

What is Balloon Angioplasty and Vascular Grafting?

A

BA: balloon that can compress plaque in vessels; used with stents (mesh wiring, usually drug-eluting) to help open up vasculature (drugs block thrombosis)

  • balloons can cause plaque rupture
  • stents can cause immediate thrombosis

VG: either synthetic or autologous; replacement of vessel or bypass of occluded vessel

  • ONLY USED in LARGE VESSEL applications
  • ex: Coronary Artery Graft or AAA stent graft

CPR II Exam 1 (15 decks)

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