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Internal Medicine > Chapter 272 - Renovascular Disease > Flashcards

Chapter 272 - Renovascular Disease Flashcards

1
Q

Vascular disorders that commonly

threaten the blood supply of the kidney

A

large-vessel atherosclerosis,

fibromuscular diseases, and embolic disorders

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2
Q

predictive of

systemic atherosclerotic disease events.

A

Rates of urinary albumin excretion (UAE)

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3
Q

reduces UAE and risk of cardiovascular events

A

statins

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4
Q

causes of Large-vessel renal artery occlusive disease

A

extrinsic
compression of the vessel, intimal dissection, fibromuscular dysplasia
(FMD), atherosclerotic disease (most common)

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5
Q

considered a specifically treatable

“secondary” cause of hypertension.

A

renal artery stenosis

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6
Q

common and often has only minor hemodynamic

effects

A

Renal artery stenosis

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7
Q

reported in 3–5% of normal subjects presenting

as potential kidney donors without hypertension

A

FMD

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8
Q

It may present clinically
with hypertension in younger individuals (between age 15 and
50), most often women

A

FMD

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9
Q

does not often threaten kidney function,
but sometimes produces total occlusion and can be associated with
renal artery aneurysms

A

FMD

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10
Q

common in the general population (6.8% of a community-based
sample above age 65).

The prevalence increases with age and for
patients with other vascular conditions such as coronary artery disease
(18–23%) and/or peripheral aortic or lower extremity disease (>30%).

A

Atherosclerotic renal artery stenosis (ARAS)

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11
Q

It appears to slow these rates of total occlusion in ARAS and
improve clinical outcomes

A

Intensive treatment of arterial

blood pressure and statin therapy

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12
Q

results of Critical levels of stenosis

A

reduction in perfusion pressure
that activates the renin-angiotensin system, reduces sodium excretion,
and activates sympathetic adrenergic pathways

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13
Q

characterized by angiotensin dependence in the
early stages, widely varying pressures, loss of circadian blood pressure
(BP) rhythms, and accelerated target organ injury, including left
ventricular hypertrophy and renal fibrosis

A

systemic hypertension

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14
Q

treatment of renovascular HPN

A

agents that block the renin-angiotensin system and
other drugs that modify these pressor pathways

restoration of renal blood flow by either endovascular or surgical
revascularization

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15
Q

tend to affect both the post-stenotic
and contralateral kidneys, reducing overall glomerular filtration rate
(GFR) in ARAS.

A

ARAS and systemic hypertension

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16
Q

When kidney function is threatened by large-vessel

disease primarily

A

ischemic nephropathy

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17
Q

Moderately

reduced blood flow that develops gradually

A

reduced GFR and limited oxygen consumption with preserved tissue
oxygenation

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18
Q

what happens with more advanced disease in ARAS and systemic HPN

A

reductions

in cortical perfusion and frank tissue hypoxia develop

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19
Q

It develops in patients with other risk factors for atherosclerosis
and is commonly superimposed upon preexisting small-vessel
disease in the kidney resulting from hypertension, aging, and diabetes.

A

ARAS

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20
Q

Nearly 85% of patients considered for renal revascularization have
what stage and what rate of GFR

A

stage 3–5 chronic kidney disease (CKD) with GFR <60 mL/min per
1.73 m2

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21
Q

strong predictor of morbidity- and
mortality-related cardiovascular events, independent of whether renal
revascularization is undertaken.
Diagnostic approaches to renal

A

presence of ARAS

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22
Q

Levels of renin activity are therefore subjected to what?

A

timing,

the effects of drugs, and sodium intake

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23
Q

Renal artery velocities by Doppler
ultrasound _____ generally predict hemodynamically important
lesions (>60% vessel lumen occlusion)

A

> 200 cm/s

although some treatment trials
require velocity >300 cm/s to avoid false positives

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24
Q

has predictive value regarding the viability of the kidney

It remains operator- and institution-dependent

A

renal resistive

index

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25
Q

has a strong negative predictive value when

entirely normal.

A

Captopril-enhanced

renography

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26
Q

less
often used, as gadolinium contrast has been associated with nephrogenic
systemic fibrosis

A

Magnetic resonance angiography (MRA)

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27
Q

provides excellent vascular images

and functional assessment, but carries a small risk of contrast toxicity.

A

Contrast-enhanced computed tomography

(CT) with vascular reconstruction

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28
Q

treatment for patients with FMD that are commonly
younger females with otherwise normal vessels and a long life
expectancy

A

percutaneous renal

artery angioplasty

29
Q

Medical therapy for Renal Artery Stenosis

A

blockade of the renin-angiotensin
system, attainment of goal BPs, cessation of tobacco, statins, and
aspirin

30
Q

Follow-up requires surveillance for progressive occlusion criteria??

A

worsening renal function and/or loss of BP control

31
Q

often reserved for patients failing

medical therapy or developing additional complications

A

Renal revascularization

32
Q

major complications in renal revascularization

A

renal artery dissection, capsular perforation, hemorrhage,

and occasional atheroembolic disease

33
Q

can be catastrophic and accelerate both hypertension

and kidney failure, precisely the events that revascularization is intended to prevent

A

atheroembolic

disease

34
Q

they are more likely to recover function after restoring blood flow

A

Patients with rapid loss of kidney
function, sometimes associated with antihypertensive drug therapy,
or with vascular disease affecting the entire functioning kidney
mass

35
Q

treatment for hypertension is refractory to effective therapy

A

revascularization

36
Q

arise most frequently as a result of cholesterol
crystals breaking free of atherosclerotic vascular plaque and lodging
in downstream microvessels.

A

Emboli to the kidneys

37
Q

suspected in >3% of elderly subjects

with end-stage renal disease (ESRD) and is likely underdiagnosed

A

Atheroembolic renal disease

38
Q

risk factors for atheroembolic renal disease

A

males with a history of diabetes, hypertension,

and ischemic cardiac disease

39
Q

precipitating events in atheroembolic renal disease

A

angiography,
vascular surgery, anticoagulation with heparin, thrombolytic
therapy, or trauma

40
Q

days where clinical manifestations of this syndrome (atheroembolic disease) commonly
develop

A

between 1 and 14 days

41
Q

Systemic embolic disease manifestations

A

fever, abdominal pain, and weight loss

42
Q

cutaneous manifestations of systemic embolic disease

A

livedo reticularis and localized toe gangrene

43
Q

require dialytic support

A

Progressive renal failure

44
Q

laboratory findings of systemic embolic disease

A

rising creatinine, transient eosinophilia (60–80%), elevated sedimentation rate, and hypocomplementemia

45
Q

Definitive diagnosis for systemic embolic disease

A

kidney biopsy demonstrating microvessel occlusion with

cholesterol crystals that leave a “cleft” in the vessel

46
Q

can lead to

declining renal function and hypertension

A

Thrombotic occlusion of renal vessels or branch arteries

47
Q

causes of thrombosis

A

local vessel abnormalities, such as local

dissection, trauma, or inflammatory vasculitis

48
Q

patchy, transient areas of infarctions

A

segmental

arteriolar mediolysis

49
Q

distant embolic events that causes thromboembolic renal disease

A

left atrium in patients
with atrial fibrillation

fat emboli originating from traumatized
tissue, most commonly large bone fractures

50
Q

Cardiac sources that causes thromboembolic renal disease

A

vegetations from subacute bacterial endocarditis

venous circulation if right-to-left
shunting - patent foramen ovale

51
Q

Clinical manifestations of acute arterial thrombosis

A

flank pain,

fever, leukocytosis, nausea, and vomiting

52
Q

sign of kidney infarction

A

lactate dehydrogenase (LDH) rise to extreme levels

53
Q

sign of kidney infarction, both kidneys affected

A

renal function will decline precipitously with

a drop in urine output

54
Q

Diagnosis of

renal infarction

A

vascular imaging with MRI, CT

angiography, or arteriography

55
Q

Options for interventions of newly detected arterial occlusion

A

surgical reconstruction, anticoagulation, thrombolytic therapy,
endovascular procedures, antihypertensive
drug therapy

56
Q

treatment for unilateral disease - arterial dissection with thrombosis

A

supportive care

with anticoagulation

57
Q

It is potentially

catastrophic, producing anuric renal failure

A

Acute, bilateral occlusion of kidney

58
Q

rapidly progressive
BP elevations with target organ injury including retinal hemorrhages,
encephalopathy, and declining kidney function.

A

“Malignant” Hypertension

note: mortality rates in excess of 50% over 6–12 months

59
Q

Postmortem studies of such
patients identified vascular lesions, with breakdown of the vessel wall, deposition of eosinophilic material
including fibrin, and a perivascular cellular infiltrate.

A

fibrinoid necrosis

60
Q

separate lesion
was identified in the larger interlobular arteries in many patients
with hyperplastic proliferation of the vascular wall cellular elements,
deposition of collagen, and separation of layers

A

“onionskin” lesion.

61
Q

It can led

to obliteration of glomeruli and loss of tubular structures.

A

fibrinoid necrosis

62
Q

mainstay of therapy for malignant

hypertension

A

Antihypertensive therapy

63
Q

It most commonly
develops in patients with treated hypertension who neglect to take
medications or who may use vasospastic drugs, such as cocaine

A

Malignant hypertension

64
Q

findings in renal abnormalities

A

rising serum creatinine
hematuria and proteinuria

biochemical findings:
evidence of hemolysis (anemia, schistocytes, and reticulocytosis) and
changes associated with kidney failure.

65
Q

African-American males

A

more likely to develop rapidly progressive hypertension and kidney
failure than are whites in the United States

66
Q

type of Genetic polymorphisms common in the African-American population
predispose to subtle focal sclerosing glomerular disease, with severe
hypertension developing at younger ages secondary to renal disease
in this instance

A

APOL1

67
Q

lesser degrees of hypertension induce less severe, but prevalent,
changes in kidney vessels and loss of kidney function

large portion of patients reaching ESRD without a specific etiologic
diagnosis are assigned the designation

A

hypertensive nephrosclerosis

68
Q

Pathologic examination for hypertensive nephrosclerosis

A

afferent arteriolar
thickening with deposition of homogeneous eosinophilic material
(hyaline arteriolosclerosis) associated with narrowing of vascular
lumina

69
Q

Clinical manifestations of hypertensive nephrosclerosis

A 
retinal vessel changes associated
with hypertension (arteriolar narrowing, arteriovenous crossing
changes), left ventricular hypertrophy, and elevated BP

Internal Medicine (3 decks)

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