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Term 4 > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

What is considered malignant hypertension?

A

BP of 200/120 with end organ damage (retinopathy)

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2
Q

how does malignant hypertension cause retinopathy?

A
  • HTN -> increase hydrostatic pressure -> delicate retino blood vessels - > damage arterioles & leakage into retina area -> retinopathy
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3
Q

Hypertensive Encephalopathy

A
  • Severe HTN -> lethargy, seizures, cortical blindness, and coma
  • lethargy occurs due to the damage of organs
  • seizures and coma due to damage of brain
  • Cortical blindness due to retinopathy
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4
Q

Hypertensive thrombotic Microangiopathy

A
  • increase HTN -> hemolysis -> thrombocytopenia
  • due to vascular wall damage -> clotting
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5
Q

What are two complications associated with HTN and atherosclerosis?

A

kidney -> renal failure, nephrosclerosis
Heart -> LVF, Ischemic heart disease

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6
Q

How does HTN affect the blood vessels?

A
  1. Accelerate Atherosclerosis
  2. Degenerative changes in M/L arteries (damage)
  3. Small vessel changes such as hyaline arteriosclerosis and hyperplastic arteriolosclerosis
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7
Q

Hyaline Arteriolosclerosis

A

Chronic HTN-> hemodynamic stress -> plasma protein leakage and SM matrix production -> deposits of pink hyaline -> thickening of walls -> narrowing lumen of vessel -> impairment of blood flow and ischemic changes.

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8
Q

Hyperplastic Arteriolosclerosis

A

Sudden increase in BP (malignant) -> thickening of Basement membrane (PAS positive) -> smooth cell hyperplasia -> concentric lamination “onion skin” with luminal narrowing -> accompanied by fibrinoid necrosis -> organ BV is supplying will have decrase BF and begin necrosis.

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9
Q

How is the kidney affected by HTN?

A
  • Hyaline Arteriolosclerosis -> benign
  • Hyperplastic arteriolosclerosis -> necrosis -> malignant nephrosclerosis
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10
Q

How does HTN affect the brain?

A

Hyaline & Hyperplastic arteriolosclerosis can cause intraparenchymal hemorrhages.

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11
Q

How does HTN affect the retina?

A

hyperplastic arteriolosclerosis -> cotton wool spots
due to infarct.

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12
Q

What is pulmonary HTN?

A
  • high BP in BV carrying supply to lungs
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13
Q

When do we see pulmonary HTN?

A

Heart Failure, Congenital heart disease, valvular disorders, lung diseases

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14
Q

What changes in BV would be see in pulmonary HTN?

A
  • Fibrotic intimal thickening
  • medial hyperplasia
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15
Q

Systemic Left Sided hypertensive heart disease

A
  • Left ventricular hypertrophy w/o other CVD
  • Hx of HTN in over organs
  • HTN -> LVH -> Ischemic Heart Disease -> LVF
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16
Q

Isolated Pulmonary Right sided HTN heart disease

A
  • AKA “Cor Pulmonale”
  • RV and RA hypertrophy
  • Pulmonary HTN -> RVF due to back presssure -> Cor pulmonale
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17
Q

what causes Acute Cor Pulmonale?

A
  • Massive pulmonary embolism -> RV dilated but no hypertrophy
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18
Q

what causes Chronic Acute Pulmonale?

A
  • COPD
  • pulmonary fibrosis, cystic fibrosis, obesity
  • RV hypertrophy, RA hypertrophy w/ dilation
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19
Q

What are causes for secondary HTN?

A
  • renal -> Glomerulonephritis, Renal Artery Stenosis
  • Endocrine -> Cushing disease, OCP, thyrotoxicosis
  • Vascular -> Coarctation of aorta, polyarteritis nodosa, aortic insufficiency
  • Neurogenic -> intracranial pressure, Polyneuritis
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20
Q

What is an aneurysm?

A
  • abnormal dilation of an artery of heart
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21
Q

How do we classify an aneurysm?

A
  • True involves all the layers of the vessel
  • can be either saccular or fusiform
  • False is a defect in the wall -> hematoma takes place in extravascular place. “pulsating hematoma”
22
Q

What are common causes of Aneurysms?

A
  • Atherosclerotic
  • Syphilitic
  • Mycotic
  • Vasculitic
  • Congenital
  • Iatrogenic
23
Q

Pathogenesis of Aneurysms

A
  • Dysfunctional CT synthesis + CT degradation -> loss of SMC
  • “cystic medial degeneration”
  • loss of SMC and loss of elastic fibers -> loose walls -> bubble -> aneurysm
24
Q

Abdominal Aortic Aneurysm

A
  • Atherosclerotic plaques that cause ischemia of the inner media
  • the plaques increase the absorption distance leading to decrease BF
  • creates thinner walls
25
Q

Ascending Aortic Aneurysm

A
  • HTN causes narrowing of lumen of Vasa Vasorum
  • Ischemia of outer media
  • leads to loss of SMC and aortic degeneration
26
Q

Cystic medial degeneration

A
  • increase in destoryed elastin
  • also areas with no elastin, resemble cystic spaces
27
Q

Signs & Symptoms of AAA

A
  • Most likely male
  • Above 50 usually
  • Smokers
  • discovered as a abdominal mass stimulating a tumor
  • Ruptures into peritoneal cavity or retroperitoneal tissue; possibly fatal
  • obstruction will cause downstream tissue ischemia injury
28
Q

What is seen in the tertiary stage of syphillis?

A

Aortitis

29
Q

What is pathogenesis of syphilitic Aneurysm?

A

Spirochete -> inflammatory response -> obliterative endarteritis of vasa vasorum in aorta -> narrowing of VV lumen -> ischemic injury to elastic tunica in aorta -> media destruction and weakening -> chronic inflammation, scarring

  • obliterative endarteritis is inflammation of inner lining of BV causing obstruction
30
Q

What structural changes occur in syphilitic Aneurysms?

A
  • Chronic inflammation -> fibrosis -> tree bark appearance -> wrinkling can occur due to atherosclerosis, lead to narrowing of coronary ostia -> aortic valve dilation -> valve insufficiency -> hypertrophy of left ventricle -> Cor Bovinum “Cow heart”
31
Q

Where does a syphilitic Aneurysm usually take place?

A

Thoracic aorta

32
Q

Where do Aneurysms due to Marfans syndrome usually take place?

A

Ascending Aorta or arch of aorta due to the highest pressure and decrease of elastic tissue in area

33
Q

What is mutation and inheritance of Marfans syndrome?

A

Autosomal Dominant
Fibrillin 1 mutation

34
Q

What is etiopathogenesis of aneurysm due to marfan syndrome?

A
  • decrease in fibrillin-1 ->incompetent elastic fibers -> aneurysms, aortic dissection, valve lesions
35
Q

what are skeletal abnormalities of Marfan’s patients?

A
  • elongated axial bones
  • lower body is longer
  • long thin extremities
  • ocular ciliary body is rich in fibrillin resulting in subluxation
36
Q

Where are Berry aneurysms located?

A

Circle of Willis -> Anterior Cerebral Artery

37
Q

What is the genetic mutation associated with Berry Aneuryms?

A

Autosomal dominant polycystic kidney disease

38
Q

Pathogenesis of Berry Aneurysm

A
  • the arterial media is weakened at birth already, but no aneurysm is present
  • clinically silent until ruptured
  • can rupture whenever but usually during increased cranial pressure (orgasm or stool straining) -> subarachnoid hemorrhage -> severe headache, coma
39
Q

What is a mycotic aneurysm?

A
  • Not true aneurysm
  • Weakened and ruptured vessel wall due to microbial infection
40
Q

Pathogenesis of mycotic aneurysm

A

dislodged septic embolism -> *causes BV wall damage -> causes rupture -> hemorrhage and abscess at site

  • due to infective endocarditis, which is bacterial infection of BV or heart or valve
  • small and clinically silent
  • mycotic is a misnomer bc they thought it was initially by a fungal infection
41
Q

What is an Aortic Dissection?

A
  • is a false aneurysm
  • seperation of the layers of media due to weakening from blood filled channels within the aorta
  • between the middle and outer third of aortic wall
42
Q

who is most susceptible to an aortic dissection?

A
  • males
  • 40-60 years old
  • antecedent hypertension
  • younger patients with syndromic diseases (marfans)
43
Q

Pathogenesis of Aortic Dissection

A
  • Hypertension
  • Marfans or Ehler Danlos
44
Q

How are Aortic dissections classified?

A

DeBakey Classification (I, II, or III)

45
Q

Type A Dissections, proximal lesion, Debakey 1/2

A
  • More common in ascending aorta
  • high mortality
  • need rapid treatment
46
Q

Type B Dissections, distal lesions, Debakey 3

A
  • Descending aorta distal to left subclavian artery
  • can be managed conservatively
47
Q

What are clinical symptoms of Aortic dissection?

A
  • sudden excruciating pain
  • starts in anterior chest
  • radiating to back between scapulae
  • absent weak pulse
  • confused with MI
48
Q

What is the most common cause of death from a aortic dissection?

A

rupture and bleeding into the pericardial, pleural, or peritoneal cavities

49
Q

Complications with Aortic dissection

A
  • retrograde dissection into aortic root->disrupts aortic valve
  • cardiac tamponade or aortic insufficiency -> with blood
  • extension into great arteries of neck or various other arteries -> vascular obstruction -> ischemia
  • EX: if dissection reaches coronary arteries -> MI or dissection reaches spinal arteries transverse myelitis
50
Q

What is a Double barreled Aorta?

A

When a dissecting hematoma reenters the lumen of aorta through a second distal intimal tear, this creates a second vascular channel within the media

This channel becomes endothelialized forming a chronic dissection

Term 4 (5 decks)

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