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CPR Exam 2 > Chapter 20.3 Vascular Diseases > Flashcards

Chapter 20.3 Vascular Diseases Flashcards

1
Q

Renal vascular diseases can be categorized in what ways?

A
  1. Small vessel disease
  2. Large vessel disease
  3. Thrombotic microangiopathies
  4. Other
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2
Q

Nephrosclerosis, commonly assx with _____, is defined by prescense of varying degrees of

A

Nephrosclerosis, commonly assx with HTN, is defined by prescene of varying degrees of

  • glomerulsclerosis
  • interstitial fibrosis and tubular atrophy
  • arteriosclerosis
  • arteriolosclerosis
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3
Q

In nephrosclerosis, what happens as the lumen narrows?

A
  • contributes to glomerulosclerosis (global and segmental), which can cause interstitial fibrosis and tubular atrophy.
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4
Q

What is Benign Nephrosclerosis.

A
  • Hyaline sclerosis of the renal arterioles and small arteries d/t benign HTN=> multi-focal ischemia of kidney parenchyma that the sclerotic vessels supply
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5
Q

Is Benign Nephrosclerosis is a general process or a specific Dx?

A

General process

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6
Q

Benign Nephrosclerosis is strongly associated with _________

and it will occur more in who?

A
  1. HTN
  2. Blacks, increasing age and DM
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7
Q

What 2 microscopic processes occur in benign nephrosclerosis?

A
  • Medial and intimal thickening (fibroelastic hyperplasia) due to hemodynamic changes, aging => narrowing of lumen
  • Hyaline protein depositions in arteriolar walls (hyaline arteriolosclerosis) => homogenous and eosinophillic thickening
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8
Q

How does the cortical surface of the kidney appear in Benign Nephrosclerosis?

A
  • Granular, leather appearance due to scarring and shrinking => causing a reduction in cortical mass
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9
Q

Ischemia that occurs in Benign Nephrosclerosis causes what?

A
  • patchy ischemic atrophy of tubules and glomeruli
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10
Q

Benign nephrosclerosis can progress to what?

A
  • glomerulosclerosis
  • chronic tubulointerstitial injury (tubular atrophy & interstitial fibrosis)
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11
Q

Does Benign nephrosclerosis cause renal failure/renal insufficiecy.

A

No. Obny in 3 cases:

  1. African-Americans
  2. Severe HTN
  3. Diabetic Nephropathy
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12
Q

Malignant Nephrosclerosis typically occurs most often in whom?

A

Younger men, black

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13
Q
  • Malignant Nephrosclerosis is a renal disease with typical arterial changes associated with ______________
A

Malignant or accelerated HTN

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14
Q

What type of HTN is a clinical syndrome and a medical emergency?

A

Malignant HTN

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15
Q

What is the pathogenesis of malignant HTN?

A
  1. Injured endothelium (d/t hemodynamic changes) => ↑ permeability to fibrinogen and plasma proteins,
  2. => Irreversible endothelial injury => focal vascular cell death and platelet deposition
  3. This will lead to:
    1. fibrinoid necrosis of arterioles and small arteries,
    2. activation of platelets and coagulation factors causing intravascular hemorrhage** and **thombosis
  4. Fibrinoid necrosis leads to hyperplastic arteriolitis/onion skinning (malignant arteriolar sclerosis), causes
    • Ischemic kidneys d/t lumen narrowing.
      • RAAS => Elevated plasma renin
    • This creates a self-perpetuating cycle of damage and HTN
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16
Q

What do we see as a result of the fibrinoid necrosis and hyaline arteriolitis seen in malignant nephrosclerosis?

A

Ischemic kidneys and high plasma renin

  • Lumen narrowing causes ischemic kidneys
  • + RAASs ==> high plasma renin
    *
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17
Q

High plasma renin results in what in Malignant Nephrosclerosis?

A

self-perpetuating cycle of damage and HTN

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18
Q

What are the morphological manifestations of malignant HTN.

A

Malignant arteriolosclerosis/malignant nephrosclerosis

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19
Q

How does the cortical surface of the kidney appear in Malignant Nephrosclerosis?

A

“Flea-bitten”; small, pinpoint petechial hemorrhages

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20
Q

What are the histological manifestation of malignant nephrosclerosis?

A
  1. Fibrinoid necrosis of arterioles
  2. Hyperplastic arteriolitis (collagen + proteoglycans and plasma proteins), indicative of renal failure
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21
Q

The full-blown syndrome of Malignant HTN is characterized by what BP, and other serious clinical manifestations?

A
  • BP: >180/>120,
  • Papilledema,
  • Retinal hemorrhages,
  • Encephalopathy
  • CV abnormalities
  • Renal failure
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22
Q

Early symptoms of Malignant HTN are due to what?

A

↑ ICP

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23
Q

Large vessel disease: Unilateral renal artery stenosis causes ____________ and is important to recognize. Why?

A
  • Unilateral renal artery stenosis causes 2-5% of HTN cases and is important to recognize because it is curable by surgery.
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24
Q

Renal artery stenosis is a cause of _____ due to what?

A

HTN

Due to an increasing production of renin from an ischemic kidney

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25
Q

What perpetuates HTN in renal artery stenosis?

A

Accumulation of Na+

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26
Q

Renal artery stenosis is most commonly due to what?

A

1. Atherosclerosis (70%)

2. Fibromuscular dysplasia (medial** (most common), intimal and adventitial hyperplasia)

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27
Q

Atherosclerosis is more common in

A
  1. Men
  2. Increasing age
  3. DM
28
Q

Which cause of renal artery stenosis is more often seen in younger age groups (3rd-4th decades) and is more common in woman?

A

Fibromuscular dysplasia of the renal artery

29
Q

Which cause of renal artery stenosis is more often seen in older people?

A

atherosclerosis;

30
Q

What is the classic appearance on arteriography of renal artery stenosis due to fibromuscular dysplasia?

A

“String of beads”

31
Q

In general pts w/ renal artery stenosis present clinically similar to what other disorder?

How can it be diagnosed?

A
  • Resemble those w/ essential HTN
  • Occasionally bruit can be heard over kidney on ausculation (rare)
  • High renin levels, response to ACE inhibitors, renal scans, and IV pyelography may all aid in Dx
  • Need arteriography to localize stenotic lesion
32
Q

What is the arteriolosclerosis like in the ischemic kidney in renal artery stenosis vs. non-ischemic (functional) kidney?

A
  • Ischemic kidney: decrease size and show signs of diffuse ischemic necrosis
  • Contralateral kidney (healthy) may show more severe arteriolosclerosis, depending on severity of the HTN!

*Think the ischemic kidney w/ stenosis is essentially shut off from the blood supply, while the functional kidney is getting rocked by extremely high/persistent BP

33
Q

What are the 2 important thrombotic microangiopathies?

A
    1. HUS (Hemolytic-uremic syndrome)
    1. TTP (thrombotic thrombocytopenic purpura)
34
Q

Thrombotic microangiopathy are a diverse set of conditions that all lead to

A
  • Insults that cause excessive activation of platelets, forming thrombi in capillaries and arterioles in various tissue beds, including the kidneys.
35
Q

What are the 3 major findings in the Thrombotic Microangiopathies (HUS and TTP)?

A
  • Thrombi in capillaries and arterioles
  • Microangiopathic hemolytic anemia
  • Thrombocytopenia (low platelet count)**** (big clue in a question stem!)
36
Q

Thrombocytopenia that occurs in HUS and TTP causes what?

A
  1. Results in flow abnormalities that shear red cells
  2. Causes microangiopathic hemolytic anemia and microvascular occlusions
  3. Causes ischemia and organ dysfunction.
37
Q

The primary cause/inciting event that causes thrombi formation in HUS differs from TTP how as far as pathogenesis?

A
  • HUS = injury to endothelial cells and platelet activation ==> intravascular thrombosis
  • TTP = platelet activation –> aggregation
38
Q

What are triggers of injury to endothelial cells?

A
  1. bacterial toxins
  2. cytokines
  3. viruses
  4. certain meds
  5. anti-endothelial antibodies
39
Q

In HUS, what is a result of damage to the endothelial cells?

A
  1. Decrease prostaglandin I2 and NO, which inhibit aggregation of platelets
  2. Increased endothelin, which causes vasoconstriction
40
Q

What is the trigger for platelet activation and thrombosis in typical HUS vs. atypical HUS?

A
  • Typical HUS - Shiga-like toxin (from E.coli) after eating food
  • Atypical HUS - inherited mutation of proteins that cause excessive activation of complement
41
Q

Typical HUS is associated with what synonyms?

A

1. Epidemic

2. Classic

3. Diarrhea +

42
Q

Atypical HUS is associated with what synonyms?

A
  • Non-epidemic
  • Diarrhea negative
43
Q

Who is most often affected by Typical HUS?

How is this form treated/managed and prognosis?

A
  • Children
  • Renal failure is managed w/ dialysis and most pts recover normal renal function within weeks
  • Long-term prognosis is variable due to renal damage
44
Q

What are the 2 common inherited mutations which cause Atypical HUS?

A
  1. factor H mutation
  2. Factor I and CD46 mutation
45
Q

Besides inherited mutations, what else can cause Atypical HUS?

A
  • Antiphospholipid syndrome, either 1° or 2° to SLE
  • Pregnancy –> postpartum renal failure
  • Vascular diseases of kidney: systemic sclerosis and malignant HTN
  • Chemotherapy and immunosupprants
  • Irradiation of kidney
46
Q

What has a worse prognosis: Typical or Atypical HUS?

A

Atypical, due to underlying conditions

47
Q

Thrombotic Thrombocytopenic Purpura (TTP) is classically manifested by what pentad, what is the dominant feature?

A

1) Neurological sx’s = Dominant feature
2) Fever
3) Microangiopathic hemolytic anemia
4) Thrombocytopenia
5) Renal failure

48
Q

TTP and Atypical HUS both appear more commonly in adults, occassionally having similar sx’s. How are they distinguished from one another?

A

Atypical has of normal ADAMTS13 in plasma

49
Q

TTP is associated with inherited or acquired deficiencies in what?

The most common cause is due to what?

A
  • ADAMTS13 = negative regulator of vWF, which forms large multimers of vWF => activate platelets
  • Inhibitory autoantibodies against ADAMTS13 = MOST COMMON!
50
Q

Who is most often affected by TTP and it typically presents before what age?

A
  • Woman
  • Presents before 40 yo
51
Q

What is the course of TTP and treatment?

A
  • Relapsing and remitting course
  • Plasma exchange to remove autoAB to ADAMTS13
52
Q

Light microscopy of chronicdisease associated with atypical HUS/TTP will show what?

A
  • Mildy HYPERcellular glomeruli
  • Thickened capillary walls
  • Splitting/reduplication of BM (“tram-tracks”)
  • “Onion-skinning” of arterial walls
53
Q

What are the morphological characteristics seen on micrcoscopy in both HUS/TTP?

Which arteries will show necrosis? (quiz question!)

A
  • In acute, active dz, the kidney shows patchy or diffuse CORTICAL necrosis and subscapular petechiae
  • Thrombi occluded glomerular capillaries
  • Mesangiolysis
  • Interlobular arteries w/ fibrinoid necrosis of wall and occlusive thrombi
54
Q

When is life stress related to atherosclerosis?

A

When pt has unhealthy coping mechanisms

55
Q

Bilateral renal artery disease (aka atherosclerotic ischemic renal disease) is a common cause of what in older individuals?

A

Chronic ischemia w/ renal insufficiency, sometimes w/o HTN

56
Q

How is bilateral renal artery disease definitively diagnosed?

Treatment?

A
  • Arteriography

- Surgical revascularization

57
Q

Atheroembolic renal disease is caused by what?

Most often seen in whom and when?

A
  • Fragments of atheromatous plaques from aorta or renal artery embolize into intrarenal vessels,
  • Most commonly in older adults w/ severe atherosclerosis, esp. following surgery on AAA repaire, aortography, or intra-aortic cannulization
58
Q

What occurs when atheroembolism throws?

A

to a sudden obstruction of blood flow in the renal artery or their main segmental branches and to ischemia of kidney => infarction w/ renal dysfunction of failure

59
Q

Hemorrhagic renal infarcts are due to what?

A

renal vein thrombosis

60
Q

What is the most common cause of renal infarct?

A

Embolism from mural thrombus on left side of heart

61
Q

Renal infarct occurs when what?

A
  • Decreased blood flow (25% of CO)
  • End-organ vascular supply
  • Lack of collateral circulation
62
Q

What are OTHER sources of emboli leading to renal infarcts?

A
    • Mural thrombosis from left atrium/ventricle due to MI
    • Vegetative endocarditis
    • Aortic aneurysms
    • Aortic atherosclerosis
63
Q

Due to the lack of collateral blood supply, how do renal infarcts appear morphologically?

Shape?

A
  • Sharply demarcated, pale, yellow-white areas of coagulative necrosis
  • Wedge-shaped
64
Q
  • Sickle Cell Nephropathy is seen both the disease and can manifest with sickle trait as well.
    • ​What are the sx?
A
  1. Hematuria
  2. Hyposthenuria
  3. 30% will have sub-nephrotic proteinuria
65
Q

How does sickle cell nephropathy alter the kidney?

A
  1. Patchy papillary necrosis
  2. Cortex is pale d/t diffuse ischemic
  3. Vascular disruption
66
Q
  • Diffuse Cortical Necrosis is what?
  • Caused by?
  • Can lead to?
A
  • Coagulative necrosis of both glomeruli and tubules
  • Obstetic MRGENCIES, septic shock, surgery complications
  • Systemic hypoperfusion or hypoxia

CPR Exam 2 (29 decks)

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