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Renal > 11 - Vascular Diseases and Chronic Kidney Disease > Flashcards

11 - Vascular Diseases and Chronic Kidney Disease Flashcards

1
Q

What are four renal vascular diseases?

A
  • Hypertensive nephrosclerosis
  • Renovascular HTN: renal artery atheroscleorsis, fibromusclar dysplasia
  • Atheroembolic disease
  • Thrombotic microangiopathy
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2
Q

What is hypertensive nephrosclerosis?

A

Chronic kidney disease in a pt with long-standing, poorly controlled HTN.

Typically evidence of other target organ damage as well - scarring of the kidney preventing normal filtering function.

Proteinuria often present.

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3
Q

What are morphological features hypertensive nephrosclerosis on gross and light microscopy?

A

Gross: normal to slightly small with finely granular subcapsular surface

LM: subcapsular glomerular sclerosis, tubular atrophy, initial fibrosis, arteriolar hyaline

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4
Q

What are morphological features of malignant HTN?

A

Mucoid intimal thickening (arteries)

Glomerular capillary wrinkling: constriction of afferent arteriole to avoid pounding from high BP

GBM duplication (similar to thrombotic microangiopathy (TMA))

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5
Q

What are causes of renovascular HTN?

A

Renal artery stenosis is a secondary cause of HTN with 2 main causes:

  • atheroscleorsis in older people
  • fibromuscular dysplasia in younger people, more commonly females

Trauma, dissection, extrinsic compression

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6
Q

What is the mechanism of HTN in renal artery stenosis?

A

Renin release converts angiotensinogen to angiotensin I.

ACE converts AngI to AngII, which causes vasoconstriction and aldosterone release.

This causes HTN.

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7
Q

In what pts should you suspect renal artery stenosis?

A
  • Early or late onset HTN
  • Difficult to control (many meds not helping)
  • Abdominal or flank bruit
  • Renal failure after starting ACE inhibitor (ACEs and ARBs treat chronic kidney fialure but can cause acute)
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8
Q

How do you dianose renal artery stenosis?

A
  • CT with contrast
  • MRA (MRI for BVs)
  • Renal arteriography
  • Doppler ultrasound
  • Captopril renogram
  • Renal vein renon sampling (renin will be high with unilateral stneosis)
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9
Q

What are the morphologic features of renal artery stenosis caused by atherosclerosis?

A
  • stenosis usually in proximal renal artery
  • Eccentric plaque with intimal fibrosis, cell debris, lipid and foam cells
  • Medial and adventitial fibrosis
  • Plaque may dissect of hemorrhage
  • Calcification may occur
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10
Q

What are the morphological changes of renal artery stenosis caused by fibromuscular dysplasia (FMD)?

A

Usually in younger women.

Intimal, medial, and adventitial forms.

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11
Q

What arteries are commonly effected by fibromuscular dysplasia (FMD)?

A

Renal artery: 60-75% (bilateral in 35%)

Cervicocranial arteries: 25-30%

Visceral arteries: 9%

Extremity arteries: 5%

Two vascular beds involved in up to 28%

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12
Q

What happens to vessel walls in the medial fibroplasia form of fibromuscular dysplasia (FMD)?

A
  • Alternating thinned media and thickening fibromuscular ridges
  • Forms string of beads appearance radiographically.
  • Beadining is larger than caliber of artery
  • Middle to distal artery
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13
Q

What is the treatment for renal artery stenosis?

A
  • Surgical revascularization
  • Angioplasty and stenting
  • Medical management only

You also need to fix implications: HTN

Stenosis itsenf needs surgical intervention

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14
Q

What are three thromboembolic diseases that impact the kidneys?

A
  1. Cortical infarcts
  2. Renal cholesterol microembolism synrome
  3. Thrombotic microangiopathy
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15
Q

What are morphological features of a cortical infarct?

A

Renal artery occlusion causing extensive parenchymal infarction.

Smaller branch: wedge-shaped infarct causing pale hyperemic border, coag necrosis, and hemorrhage and acute inflammation at edge (from damaged tissue)

Fibrotic (later)

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16
Q

What is atheroembolic disease and when can it occur?

A

Disruption of atherosclerotic plaques can cause acute and subacute renal failure.

Occurs after procudes that disrupt plaques in the aorta, leading to a shower of cholesterol emboli that lodge in renal microvasculature.

17
Q

What are some manifestations of emboli?

A

Acute renal failure, bowel infarction, digital infarction, stroke.

Eosinophils can be seen in the blood or urine.

18
Q

What is seen in the body when someone has a cholesterol atheroemboli?

A

Any sized artery can be affected; cholesterol clefts seen in artery lumen. Usually see cellular reaction around it.

May see parenchymal infarct distally.

Eosinophilia may be related to activation of C5a which is chemotactic for eosinophils.

19
Q

What aresome outcomes of atheroembolic disease?

A
  • Stabolized or normal renal funciton in mild, iso.ated cases
  • Chronic, progressive deterioration in renal function in subacute cases
  • End-stage renal disease in severe cases
  • Permanent dialysis may be necessary
20
Q

What is thrombotic microangiopathy characterized by?

A

Thrombosis in capillaries and arterioles causing:

  • Microangiopathoic hemolytic anemia
  • Thrombocytopenia
  • Renal failure

Hemolytic uremic syndrome

Thrombotic thrombocuytopenic purpura (TTP)

21
Q

What is the pathogenesis of thrombotic microangiopathy?

A

Endothelial injury (from HTN) and activation causes intravascular thrombosis.

Platelet aggregation: vascular obstruction and vasoconstriction.

Hemolytic uremic syndrome: often occur after intestinal infection with E. coli 0157:H7; can also be caused by shiga toxin

22
Q

What effect does thrombotic microangiopathy (TMA) have on the glomerulus? What can cause TMA?

A

TMA - capillary loops have pink deposits on biopsy of fibrin and platelet plugs. No urine can go down to tubules. No renal function.

Anything that can damage your endothelium can cause this - exp malignant HTN.

23
Q

Renal artery stenosis can be cause by _____ or ______. How does it clinically present?

A

Atherosclerosis or FMD.

Presents as resistant HTN or kidney dysfunciton (often after ACE-I or ARB).

24
Q

What is chronic kidney diease?

A

Progressive irreversible renal insufficiency that develops over months to years.

May ultimately lead to end-stage renal disease where the kidneys no longer function to maintain life (GFR <10 ml/min)

25
Q

What are the main caues of chronic kidney disease?

A

Diabetes (catepillar on a leaf, ruins filtration in the kidney over time - irreversible)

HTN

Glomerulonephritis (unless diagnosed and treated)

Cystic diseases (like polycystic kidney disease)

26
Q

What gross changes are seen in chronic kidney disease? What can cause these changes?

A

Kidney size usually reduced from scarring - but not always

Normal or large kidneys may be seen with:

  • diabetes
  • amyloidosis
  • HIV
  • cystic kidney disease
27
Q

What are consequences of chronic kidney disease?

A

Anemia: decreased erythropoietin production, occurs below GFR of 60 ml/min. Epo comes from spceial fibroblasts located between the cortex and the medulla (juxtamedullary fibroblasts)

HTN

  • Secondary hyperparathyroidism: excessive PTH exretion. Decreased renal synthesis of 1,25-dihydroxy-D3 an decreased phosphate excretion from damaged kidneys leads to hypocalcemia, hyperphosphatemia, and renal osteodystrophy (from leaching the bone of calcium).
28
Q

What other findings can be seen with chornic kidney disease?

A
  • Metabolic acidosis: decreased secretion of ammonium and retention of phosphates and sulfates (cannot get acid out due to kidney damage)
  • Hyperkalemia: can’t get rid of K
  • Inability to maintain Na and H2O balance
  • Coagulopathy - platelet dysfunction
  • Sensorimotor neuropathy
29
Q

What are physical symptoms of chornic uremia from chronic kidney disease?

A
  • Lethargy, fatigue from accumulation of waste products
  • day-night sleep reversal
  • anorexia, nausea, vomiting (FOW - full of waste!)
  • Pruritis
  • Restless legs syndrome
  • Uremic pericarditis
30
Q

What are the management goals for chronic kidney disease?

A

Preserve renal function and delay progression to end-stage renal diseaes

Present or minimize adverse effects

Institute renal replacement therapy when necessary

31
Q

How would you slow down the progression of chronic kidney disease (CKD)?

A

Control the HTN with ACE-I or ARB

Reduce proteinuria

Control blood sugar

Smoking cessation

Dialysis when GFR <10 ml/min

Disease-specific therapy aws indicated

32
Q

What is the most common cause of chronic kidney disease and end-stage renal disease in the US?

A

Diabetes

33
Q

What does chronic kidney disease result in?

A
  • HTN
  • Metabolic acidosis
  • Increased risk of hyperkalemia
  • Secondary hyperparathyroidism due to phosphorous retention and impaired calcitrol production
  • Anemia due to Epi deficiency
34
Q

How is end-stage renal disease (ESRD) treated?

A

With dialysis or kidney transplantation.

Renal (19 decks)

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