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Systems Path 1 > Vascular System > Flashcards

Vascular System Flashcards

1
Q

What causes HTN?

A

95% idiopathic: “essential HTN”

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2
Q

What positive affects are noted with a decrease in BP?

A

Deacreased risk of IHD, CHF, and stroke

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3
Q

Malignant HTN is considered thus by what BP range?

A

200/120: lethal within 2 years

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4
Q

What is early malignant HTN?

A

Papilledema, retinal hemorrhage

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5
Q

What is late malignatn HTN?

A

Renal failure

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6
Q

What is vascular injury?

A

Non-specific (stereotypical) response. Trauma, infxn, inflammation, immune reaciton

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7
Q

What are examples of endothelial activation?

A

Thrombosis, atherosclerosis

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8
Q

What are the 4 stages of vascular wall response to injury?

A

Endothelial injury/ dystunction
Smooth muscle cell recruitment
Growth of smooth muscle cell adn ECM
Irreversible intimal thickening (vessel stenosis = tissue ischemia)

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9
Q

What are the characteristics of arteriosclerosis?

A

“Hardening of the arteries”. Arterial thickening, deacersed elasticity

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10
Q

What is arterioLOsclerosis?

A

Small arteries/arterioles hardening (not arteriosclerosis). Possible ischemic injry (HTN, diabetes)

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11
Q

What is Monckeberg medial sclerosis?

A

Ca++ within tunica media. No stenosis: not clinically significant Age related, >50 years old.

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12
Q

What is the MC type of arteriosclerosis?

A

Atherosclerosis.

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13
Q

What are some features of arteriosclerosis?

A

Atheromas (plaques). Stenosis, aneurysm, dissection, thrombosis. Heart (CAD), brain, intestines, kidneys, legs.

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14
Q

What are some characteristics of hyaline arteriolosclerosis?

A

Benign HTN (chronic hemodynamic stress)
Prolonged DM
Luminal narrowing
Pink hyaline, Increased ECM

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15
Q

What are some characteristics of hyperplastic arteriolosclerosis?

A

Severe HTN
Luminal narrowing
“Onionskin appearance”
Kidney are most sensitive

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16
Q

What are some features of monckeberg medial sclerosis?

A

Dystrophic calcification
Idiopathic
Affects elderly
Incidental Dx: x-ray mammogram

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17
Q

99% of arteriosclerosis is….

A

Artherosclerosis

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18
Q

What is the #1 cause of morbidity and mortality in the US?

A

Atherosclerosis. CAD, MI, carotid atherosclerosis, stroke

Atheromas.

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19
Q

Where do atheromas protrude into?

A

Lumen, deacreasing flow (vascular stenosis)

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20
Q

Atheromas are prone to rupture, what happens with thsi?

A

Massive thrombosis,. Macrophages, lipids (foam cells), Ca++, dibris, MC cause of MI

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21
Q

What do atheromas weaken?

A

Tunic media -> aneurysm risk

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22
Q

What are foam cells?

A

Fat-laden macrophages

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23
Q

What do foam cells cause?

A

Possible blood flow obstuction (ischemia). CAD = 70% occlusion of coronary arteries

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24
Q

What are some hemodynamic distrubances that can cause atherosclerosis?

A

Turbulence.

Branch points or turbulent areas

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25
Q

What does chronic endothelial injury lead to?

A

Atherosclerosis

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26
Q

What are addtl risk factors for atherosclerosis?

A

Family Hx, increased age, males. Dyslipidemia, smoking, HTN, DM, stress, inflammation (C-reative protein), inactiity

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27
Q

What are the risk factors for MI?

A

Hyperlipidemia, HTN, smoking. Multiplicative: 2 of the risk factors = 4x risk, all 3 = 7x risk

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28
Q

What is metabolic syndrome?

A

Central obesity, HTN, insulin resistance, dyslipidemia, hypercoagulability/pro-inflammatory state (adipokines). Risk for cardiovascular disease

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29
Q

What are the consequences of atherosclerosis?

A

Stroke, AAA
MI, CHF
Peripheral vascular disease (PVD) -> gangrene

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30
Q

What is an aneurysm?

A

Local vascular dilations (ballooning).

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31
Q

What are some complications associated with an aneuryism?

A

Stasis -> thromboembolism

Thinned wall -> rupture/hemorrhage

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32
Q

What is a true aneurysm?

A

All 3 layers of a vessel of heart wall. Saccular aneurysm (one sided bulge), Fusiform aneurysm (both sides bulge)

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33
Q

What is a false aneurysm?

A

Defect in a vascular wall, extravascular hematoma. Communicates with lumen = pulsatile

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34
Q

Where do true aneurysms happen?

A

Aortic arch
Abdominal aorta
Iliac arteries

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35
Q

What are risk factors for aneurysms?

A

HTN/atherosclerosis: ischemia of tunica media

Marfan syndrome, Ehlers-Danlos syndrome

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36
Q

What is an abdominal aortic aneurysm (AAA)?

A

Dilation of > 50% of normal.

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37
Q

Where is the MC location for AAA?

A

Between renal and common iliac arteries

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38
Q

What are some features that facilitate AAA?

A

Degeneration and necrosis of media and ECM. Inflammation: macrophages, MMPSs
Decreased diffusion: thinning of wall

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39
Q

What are some risk factors for AAA?

A

Males, smoking, >50 years, caucasian, familial Hx. of AAA, atherosclerosis, HTN

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40
Q

With is the Dx for AAA?

A

Ultrasounds or CT

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41
Q

T/F

People with AAAs are okay to be adjusted

A

True,

Being extremely cautious with any HV adjusting.

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42
Q

What can be obstructed in an AAA considering the aorta

A

Kidneys, spinal cord, G.I., legs. Mass effect: may compress ureters.

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43
Q

If an AAA produces emboli, what is a great risk factor?

A

Tissue infarct

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44
Q

What happens in AAA with rupture?

A

Hemorrhage

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45
Q

T/F

90% of AAA are Fatal

A

False,

Only 50% are fatal

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46
Q

What is an aortic dissection?

A

Blood enters the arterial wall “blood splays apart the laminar planes of the media to for a blood-filled channel inside the artic wall”

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47
Q

What are 2 types of aortic dissections?

A

Massive hemorrhage

Pericardial tamponade

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48
Q

What is the major risk factor for aortic dissection?

A

HTN: major risk factor, 90% of cases. Male 40-60 years. Adolescents/young adults with CT disorders (Marfans, Ehler-Danlos, Wilson disease)

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49
Q

T/F

Aortic dissection is commonly found in conjunction with substantial atherosclerosis

A

False,

Rare in presence of substantial athersclerosis (act as somewhat of a protection).

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50
Q

What is Wilson disease?

A

Autosomal recessive. Abnormal copper ion transpiration. Excessive copper accumulation.

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51
Q

What organs are affected by Wilson disease?

A

Liver: steatohepatitis
Brain: psychosis, parkinsonism
Eye: Kayser-Fleischer ring

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52
Q

What is pain like with aortic dissections?

A

Sudden & severe “treaing or stabbing”. Anterior chest, projects posteriorly between scapulae. Inferior radiation: progressive dissection.

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53
Q

What is a DDx for aortic dissections?

A

MI

54
Q

What are complications associated with aortic dissections?

A

Depends on location

Type A: proximal
Type B: distal

55
Q

What is vasculitis (vasculidites)

A

Inflammation of vascular wall
Local vessel destruction
MC in small arteries
Fever, malaise, myalgia, arthralgia, fatigue

56
Q

What is infectious vasculitis?

A

Vascular invasion (e.g. Hep B)

57
Q

What is non-infectious vasculitis?

A

Immune-mediated, ADRs. (e.g. SLE, penicillin)

58
Q

What is are a few ancillary causes of vasculitis?

A

Irradiation, trauma (physical, chemical)

59
Q

What is giant cell (temporal) arteritis?

A

MC vasculitis in older adults (> 50 years). Idiopathic, T cells, autoimmun ehypothesis

60
Q

What vessels are involved in giant cell (temporal arteritis)?

A

Large and small arteries of head, patchy involvement (may involve an artery and not another very close to it)

  1. Temporal artery
  2. Ophthalmic artery: 50% diplopia/sudden blindness
  3. Vertebral artery & aorta (giant cell aortitis)
61
Q

What are some features of giant cell (temporal) arteritis?

A

Facial pain, HA, pyrexia, vision distrubance. Granulomatous inflammation

62
Q

What is the tx for giant cell (temporal) arteritis?

A

Corticosteroids

63
Q

What is Takayasu arteritis?

A

“pulseless disease”. Granulomatous vasculitis (autoimmune hypothesis). Pronounced narrowing of lumen (aortic arch, branches off aortic arch,

64
Q

What arteries are involved in Takayasu arteries?

A

Places where pulses are checked: radial, carotid, renal, pulmonary

65
Q

What are some symtpoms/features of Takayasu arteritis?

A

Fatigue, fever, weight loss, pulmonary HTN

66
Q

What is an example of the variety of neuro defects with Takayasu arteritis?

A

Visual disturbances (not as much as in temporal arteritis).

67
Q

What age group is indicated in takayasu arteritis?

A

Younger individuals

68
Q

What is polyarteritis nodosa (PAN)?

A

System-wide vasculitis, transmural necrosis (small and medium sized arteries).

69
Q

What does PAN do to the vessels it affects?

A

Weakens walls -> aneurysm, hemorrhage, or ulceration. Tissue atrophy, ischemia, or infarction.

70
Q

What tissues are MC affected by PAN?

A

Kidneys, viscera, heart, liver, GI (avoids pulmonary arteries oddly).

71
Q

What are symptoms of PAN?

A

Episodic, widespread, constitutional. Weigth loss, fatigue, fever, malaise.

72
Q

What age groups are MC affected by PAN?

A

Any age, but MC in young adults.

73
Q

1/3 of anyone with PAN will have…

A

Chronic Hep B infxn (HBV antigen)

74
Q

2/3 of anyone with PAN will ahve…

A

Idiopathic, automimmune hypothesis

75
Q

How are myalgia and peripheral neuritis inolved in PAN?

A

Diffuse, motor defects

76
Q

What artery is affected by PAN and causes rapid increase in BP (renovascular HTN)?

A

Renal artery

77
Q

If someone has PAN and has abdominal pain, bloody stools (frank/obvious), what is happening?

A

PAN affecting GI arteries

78
Q

What is the prognosis of PAN if untreated?

A

Fatal

79
Q

What is the Tx for PAN?

A

Corticosteroids: 90% cure

80
Q

What kind of dermatological features can be noted with PAN?

A

Widespread vascular lesions.

Segmental fibrinoid necrosis and thrombosis (biopsy)

81
Q

What is kawasaki disease?

A

Pediatric vasculitis (80%

82
Q

What % involvement is cardiovascular issues apart of kawasaki disease?

A

20%

83
Q

What is the description of the damage of kawasaki disease?

A

Aneurysm or thromubs -> MI

84
Q

T/F

Kawasaki disease is self limiting?

A

True

85
Q

What determines the prognosis of Kawasaki?

A

Severity of CAD

86
Q

Who recovers full from Kawasaki disease?

A

Patients without CAD

87
Q

What tends to happen more often than not with aneurysms in kawasaki disease?

A

> 50% resolve within 2 years.

88
Q

What is the cause of Kawaski diease?

A

Idiopathic, hypothesized type IV hypersens. Genetics + viral antigens. Rare, asian descent, males.

89
Q

What is the hallmark of Kawasaki disease?

A

Actue/persistant fever. No response to ibuprofen or acetaminophen

90
Q

What are some features of kawasaki disase?

A

Conjunctivitis, swollen extemities, cervical lymphadenopathy, desquamation of extremitites (de-squamous cell-ing), strawberry tongue (oral erythema)

91
Q

What are the treatments for Kawasaki disease?

A

Aspirin, corticosteroids, CABG

92
Q

What is Wegener granulomatosis?

A

Type II hypersensitivity. Necroptizing vasculitis -> ischemia

93
Q

What is primarily involved with Wegener granulomatosis?

A

Kidneys, and upper/lower respiratory tracts: nose, nose/sinuses, trachea, lung

94
Q

What are 3 major features of Wegener granulomatosis?

A

Granulomas
Sytemic vasculitis: small/medium arteries
Glomerulonephritis

95
Q

What is the age group MC affected by Wegener granulomatosis?

A

Middle-aged (40- years old), males

96
Q

What are some secondary features of Wegener granulomatosis?

A 
Bilateral pneumonitis (95%0, couch, chest pain, hemoptysis, dyspnea
Chronic sinusitis (90%)
97
Q

What are some issue with renal disease associated with Wegener’s granulomatosis?

A

Hematuria, proteinuria, possible renal failure

98
Q

What are some nasopharyngeal issues associated with Wegeners?

A

Inflammation/ulcers (75%). Rhinitis, sinusisits, nose bleeds

99
Q

What is Thromboangiitis obliterans (Buerger disease)?

A

Medium-sized arteries. Inflammation, thrombosis -> vascular insufficiency.

100
Q

What arteries are MC affected by Thromboangiitis obliterans?

A

Feet (tibial artery), hands (radial artery))

101
Q

Who is most at risk for Thromboangiitis obliterans?

A

Heavy tobacco smokers: endothelial damage. Relieved with abstinence

102
Q

What is MC affected by thromboangiitis obliterans?

A

Males, age 25-35 years

103
Q

What kind of symptoms associated with ischemia is found in thromboangiitis obliterans?

A

Painful extremities, cyanosis/cold. Ulcerations, gangrene.

104
Q

What are some symptoms of thromboangiitis obliterans?

A

Pain at rest
Exercise -> vascular claudication
Ulcerations and gangrene (amputation)
Possible Raynaud phenomenon.

105
Q

What is raynaud phenomenon?

A

Exaggerated arteriole vasoconstriction. Pallor and cyanosis. Extremities: fingers, toes (nose, earlobes, lips).

106
Q

T/F

Raynauds is a serious condition

A

False

Benign condition. Unless it’s chronic which can produce tissue atrophy - skin, CT, muscles.

107
Q

When does raynaud onset?

A

Adolescent/young adults, MC in females

108
Q

What is primary raynauds?

A

Cold and emotional, 5% of US

109
Q

What is secondary raynauds?

A

Atherosclerosis, Buerger disease, Lupus (SLE), scleroderma, atherosclerosis

110
Q

What is takotsubo cardiomyopathy?

A

“Broken heart syndrome” or “cardiac raynaud” or “stress cardiomyopathy”. Extreme psychological stress causing increased catecholamine production which may affect the coronary arteries, stimulating vasospasm increasing heart rate and contractility. Fatal arrythmia (V-fib). Possible cardiac ischemia -> MI

111
Q

What is a veinous thrombosis?

A

Blood clot formation

112
Q

What is a phlebitis?

A

Vein inflammation

113
Q

What are the three conditions that make up 90% of venous diseases?

A
  1. Varicose veings
  2. Phlebothrombosis: venous thrombosis without previous inflammation (rare)
  3. Thrombophlebitis: venous thrombosis following inflammation (MC used term)
114
Q

What are vericose veins?

A

Superficial veins: dilated and tortuous (Legs MC). INcreased intraluminal pressure. Dilation -> incompetent valves.

115
Q

What are some features of vericose veins?

A

Congestion/edema, pain, thrombosis, ulceration.

116
Q

What are some risks for vericose veings?

A

Obesity, genetics, pregnancy. MC a cosmetic concern

117
Q

T/F

Vericose veins are high risk for the production of emboli?

A

False

No real association

118
Q

What is thrombophlebitis?

A

Thrombosis and inflammation lOCALIZED CYANOSIS/ERYTHEMA, EDEMA, PAIN.

119
Q

What is the major risk for thrombophlebitis?

A

Immobilization

120
Q

Are DVTs involved in throbophlebitis?

A

DVTs (90% of all cases)

121
Q

What are some other risks for throbophlebitis?

A

Recent surgery, pregnancy, obesity, immobilization, O.C., CHF, genetics

122
Q

What is often produced with thrombophlebitis that causes fatality?

A

Possible pulmonary embolism. May be the 1st indication of thrombophlebitis

123
Q

What is superior vena cava syndrome?

A

Compression or invasion of SVC. Bronchogenic carcinoma, mediastinal lymphoma congesting UE veings: edema (head, neck, arms)

124
Q

What is inferior vena cava syndrome?

A

Compression or invasion of IVC
Hepatocellular carcinoma, renal cell carcinoma
Congestion of LE veins: edema, proteinuria

125
Q

What is lymphedema?

A

Rare. Obstruction -> tissue expansion. Lymphatic obstuction -> inflammation.

126
Q

What is primary congenital lymphatic abnormalities

A

Milroy disease (inherited). Hypoplasia or agenesis of lymph vessels

127
Q

What is secondary obstruction of normal lymph vessels?

A

Neoplasia, infxn (filariasis), thrombosis, ribrosis (surgery)

128
Q

What is Peau d’organge?

A

“Skin of an orange” acute lymphedema

129
Q

What is the long-term consequence of lymphedema?

A

Brawny induration (hardening of the edemic tissues).

130
Q

What tissues do vascular tumors originate from?

A

Endothelial cells
Connective tissue or vessels
MC benign

131
Q

What is the MC benign vascular tumor?

A

Hemangioma

132
Q

Occasionaly vascular tumors can be farily aggressive. What is the condition called?

A

Kaposi sarcoma

Systems Path 1 (9 decks)

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