Robbins Ch. 20 the Kidney Review Questions

7/27/2019 Robbins Ch. 20 the Kidney Review Questions

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1. BRS Pathology - Table 17-1

Glomerular Diseases

(memorize this table)

2. Tubular and interstitial

disorders are frequently

caused by what?

toxins or infectious agents

3. Glomerular diseases are

frequently caused by what?

immunologically mediated

4. 1. What is azotemia?

2. What is it related to?

1. elevated of BUN and creatinine

2. decreased glomerular filtration rate

5. Nephritic syndrome? HEMATURIA, mild proteinuria, oliguria, azotemia, and hypertension

- is due to glomerular disease and is dominated by the acute onset of usually grossly visible hematuria (r

blood cells in urine), mild to moderate proteinuria, and hypertension; it is the classic presentation of

acute poststreptococcal glomerulonephritis.

*Hallmark = glomerular inflammation and bleeding

-limited proteinuria


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9. Basement membrane

thickening in EM, how does

the thickening happen?

immune complex deposition, synthesis of protein components

Basement Membrane Thickening:

- By light microscopy, this change appears as thickening of the capillary walls, best seen in section

stained with periodic acid-Schiff (PAS).

- By electron microscopy such thickening takes one of two forms:

1) Deposition of amorphous electron-dense material, most often immune complexes, on the

endothelial or epithelial s ide of the basement membrane or within the GBM itself. Fibrin, amyloid,

cryoglobulins, and abnormal fibrillary proteins may also deposit in the GBM.2) Thickening of the basement membrane due to increased synthesis of its protein components, as

occurs in diabetic glomerulosclerosis.

10. Hyalinosis, what do you seen

microscopically?

pink (eosinophilic)

- Hyalinosis, as applied to the glomerulus, denotes the accumulation of material that is

homogeneous and eosinophilic by light microscopy

11.What is hyalinosis a common

feature of?

focal segmental glomerulosclerosis

12.What is sclerosis

characterized by?

accumulations of extracellular collagenous matrix, either confined to mesangial areas as is often th

case in diabetic glomerulosclerosis, or involving the capillary loops, or both.

13.As kidney disease progresses,

what are the 2 major histologic

characteristics seen?

- focal segmental glomerulosclerosis

- tubulointersitital fibrosis

14.What are the 3 types of

Rapidly Progressive

(Crescentic)

Glomerulonephritis?

Type 1, 2, and 3:

1) Anti-GBM antibody

2) Immune complex

3) Pauci-immune - lack of immune anti-GBM or immune complexes by immunofluorescence and

electron microscopy.

- Most patients with this type of RPGN have circulating antineutrophil cytoplasmic antibodies

(ANCAs) that produce cytoplasmic (c) or perinuclear (p) staining patterns, and play a role in some

vasculitides.

15. 1. What would you see via lightmicroscopy (LM) for RPGN?

2. What would you see via

electric microscopy (EM) for

RPGN?

3. What would you see,

nephritic or nephrotic

syndrome?

1. nothing much2. loss of foot processes (podocytes)

- Electron microscopy discloses deposits in those cases due to immune complex deposition (type II

- Regardless of type, electron microscopy may show distinct ruptures in the GBM, the severe injury

that allows leukocytes, proteins, and inflammatory mediators to reach the urinary space, where the

trigger the crescent formation

3. nephrotic syndrome

16. 1. What do you seen in focal

segmental glomerulosclerosis?

2. Nephritic or nephrotic?

1. effaced foot processes & sclerosis of focal segments (portions of structures are involved)

2. Nephrotic

17. Histologically what do you

seen inmembranoproliferative

glomerulonephritis?

- alterations in glomerular basement membrane

- proliferation of glomerular cells- leukocyte infil tration

18. In Berger disease, what kind

of deposits would you see?

IgA

19.What is the most common type

of glomerulonephritis

worldwide?

Berger disease (IgA Nephropathy)

20. In Alport syndrome, what type

of abnormal collagen do you

have?

Type IV collagen


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21.Alport syndrome: - thin basement membrane lesion

- the most common cause of benign familial hematuria

- is manifest by hematuria with progression to chronic renal failure, accompanied by nerve deafness and

various eye disorders, including lens dislocation, posterior cataracts, and corneal dystrophy

22. Can you diagnosis

Berger disease with

light microscopy?

no, the disease can be suspected by LM, but the Dx is made only by immunocytochemical techniques

23.Acute kidney injury oracute tubular necrosis

is caused by what?

- ischemia- toxic injury

- urinary obstruction

- acute tubulointerstitial nephritis

24. Table 20-5 - pg 918

(highlighted)

25.What is a neoplasm

that can cause

tubuleinterstitial

nephritis?

multiple myeloma

26. Most common cause of

clinical

pyelonephritis?

ascending infection

27. 1) Vesicoureteral

reflux:

2) What do you seen

because of that?

1) urine goes back from bladder to ureters

- Although obstruction is an important predisposing factor in ascending infection, it is incompetence of the

vesicoureteral valve that allows bacteria to ascend the ureter into the renal pelvis. An incompetent

vesicoureteral orifice allows the reflux of bladder urine into the ureters (vesicoureteral reflux)

2) increased infection

- The effect of vesicoureteral reflux is s imilar to that of an obstruction in that there is residual urine in the

urinary tract after voiding, which favors bacterial growth.

28.What is acute

pyelonephritis?

acute suppurative inflammation of kidneys caused mostly by bacteria

- Acute pyelonephritis is caused by bacterial infection and is the renal lesion associated with urinary tract

infection.

29.

Most common bacteriathat causes

pyelonephritis is

what?

E. coli (O157:H7)


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30. Figure 20-32 -

"know what is

going on there"

Typical coarse scars of chronic pyelonephritis associated with vesicoureteral reflux. The scars are usually polar an

are associated with underlying blunted calyces.

- Chronic pyelonephritis is a disorder in which chronic tubulointerstitial inflammation and renal scarring are

associated with pathologic involvement of the calyces and pelvis

31. Benign

nephrosclerosis

is a term used todescribe what?

renal pathology associated with renal sclerosis of renal arterioles and small arteries

32. Know what kind

of a histologic

picture you would

see with benign

nephrosclerosis /

Figure 20-38 -

"know why that

happens"

Close-up of the gross appearance of the cortical surface in benign nephrosclerosis illustrating the fine, leathery

granularity of the surface.

- The kidneys are either normal or moderately reduced in size, with average weights between 110 and 130 gm. Th

cortical surfaces have a fine, even granularity that resembles grain leather (Fig. 20-38). The loss of mass is due

mainly to cortical scarring and shrinking

- On histologic examination there is narrowing of the lumens of arterioles and small arteries, caused by thickenin

and hyalinization of the walls (hyaline arteriolosclerosis) (Fig. 20-39). Corresponding to the fine surface

granulations are microscopic subcapsular scars with sclerotic glomeruli and tubular dropout, alternating with

better preserved parenchyma. In addition, the interlobular and arcuate arteries show a characteristic lesion tha

consists of medial hypertrophy, reduplication of the elastic lamina, and increased myofibroblastic tissue in theintima, which combine to narrow the lumen. This change, called fibroelastic hyperplasia, often accompanies

hyaline arteriolosclerosis and increases in severity with age and in the presence of hypertension

- Consequent to the vascular narrowing, there is patchy ischemic atrophy, which consists of (1) foci of tubular

atrophy and interstitial fibrosis and (2) a variety of glomerular alterations. The latter include collapse of the GBM

deposition of collagen within the Bowman space, periglomerular fibrosis, and total sclerosis of glomeruli. When

the ischemic changes are pronounced and affect large areas of parenchyma, they can produce regional scars and

histologic alterations that may resemble those seen in renal ablation injury


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33. Malignant

hypertension (+

gross

morphology):

Malignant nephrosclerosis is the form of renal disease associated with the malignant or accelerated phase of

hypertension;

- Morphology. On gross inspection the kidney size depends on the duration and severity of the hypertensive

disease. Small, pinpoint petechial hemorrhages may appear on the cortical surface from rupture of arterioles or

glomerular capillaries, giving the kidney a peculiar "flea- bitten" appearance.

34. Malignant

Hypertension.

What would you

see histologically?

Two histologic alterations characterize blood vessels in malignant hypertension (Fig. 20-40):

- Fibrinoid necrosis of arterioles. This appears as an eosinophilic granular change in the blood vessel wall, whic

stains positively for fibrin by histochemical or immunofluorescence techniques. This change represents an acut

event; it may be accompanied by limited inflammatory infiltrate within the wall, but prominent inflammation is n

seen. Sometimes the glomeruli become necrotic and infiltrated with neutrophils, and the glomerular capillaries

may thrombose.

- In the interlobular arteries and arterioles, there is intimal thickening caused by a proliferation of elongated,

concentrically arranged smooth muscle cells, together with fine concentric layering of collagen and accumulatio

of pale-staining material that probably represents accumulations of proteoglycans and plasma proteins. This

alteration has been referred to as onion-skinning because of its concentric appearance. The lesion, also called

hyperplastic arteriolitis, correlates well with renal fai lure in malignant hypertension. There may be superimpose

intraluminal thrombosis. The arteriolar and arterial lesions result in considerable narrowing of all vascular

lumens, ischemic atrophy and, at times, infarction distal to the abnormal vessels.

35. Shigga-like toxin

E. coli strain?

O157:H7

36. Hereditary

disorder

characterized bymultiple

expanding cysts of

kidneys, destroys

parenchyma, and

caused renal

failure?

polycystic kidney disease

37. Be able to tell

difference

between

childhood and

adult polycystic

kidney disease,grossly

(Figure 20-47 A-

D)Figure 20-47: A and B) Autosomal-dominant adult polycystic kidney disease (ADPKD) viewed from the externa

surface and bisected. The kidney is markedly enlarged and contains numerous dilated cysts. D) Liver cysts in adu

PKD


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38. Figure 20-47c:

ARPKD

Fig. 20-47 C) Autosomal-recessive childhood PKD, showing smaller cysts and dilated channels at right angles t

the cortical surface.

39. Hydropnephrosis

of the kidney -

what does it look

like grossly?

(Figure 20-50)

- Hydronephrosis of the kidney, with marked dilation of the pelvis and calyces and thinning of the renal

parenchyma.

- Hydronephrosis is the term used to describe dilation of the renal pelvis and calyces associated with progressive

atrophy of the kidney due to obstruction to the outflow of urine.- The kidney may be slightly to massively enlarged, depending on the degree and the duration of the obstruction

The earlier features are those of s imple dilation of the pelvis and calyces, but in addition there is often significan

interstitial inflammation, even in the absence of infection. In chronic cases the picture is one of cortical tubular

atrophy with marked diffuse interstitial fibrosis. Progressive blunting of the apices of the pyramids occurs, and

these eventually become cupped. In far-advanced cases the kidney may become transformed into a thin-walled

cystic structure having a diameter of up to 15 to 20 cm (Fig. 20-50) with striking parenchymal atrophy, total

obliteration of the pyramids, and thinning of the cortex

40. 1. Benign tumor

consisting of

vessels, smooth

muscle, and fat

2. What do youusually see it in?

1. angiomyolipoma

2. tuberous sclerosis

41. Kidney tumor -

"mahogany

brown"

Oncocytoma

- This is an epithelial tumor composed of large eosinophilic cells having small, round, benign-appearing nuclei

that have large nucleoli. It is thought to arise from the intercalated cells of collecting ducts.

- In gross appearance the tumors are tan or MAHOGANY BROWN, relatively homogeneous, and usually well

encapsulated. However, they may achieve a large size (up to 12 cm in diameter). There are some familial cases in

which these tumors are multicentric rather than solitary.


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42. Major types of

renal cell

carcinoma

(adenocarcinoma

of the kidney)

- clear cell carcinoma

- papillary carcinoma

- Chromophobe renal carcinoma

- Collecting duct (Bellini duct) carcinoma

43.Which type of

renal cell

carcinoma is

associated with

von Hippel

Lindau

syndrome?

clear cell carcinoma

- current studies implicate the VHL gene in the development of both familial and sporadic clear cell tumors

44. Morphology of

Acute

Pyelonephritis

(pg 941 Blue box)

The hallmarks of acute pyelonephritis are patchy interstitial suppurative inflammation, intratubular aggregates o

neutrophils, and tubular necrosis. The suppuration may occur as discrete focal abscesses involving one or both

kidneys, which can extend to large wedge-shaped areas of suppuration (Fig. 20-28). The distribution of these

lesions is unpredictable and haphazard, but in pyelonephritis associated with reflux, damage occurs most

commonly in the lower and upper poles.

- Figure 20-28 Acute pyelonephritis. Cortical surface shows grayish white areas of inflammation and abscess

formation.45. Three

complications of

acute

pyelonephritis

are encountered

in special

circumstances.

- Papillary necrosis is seen mainly in diabetics and in those with urinary tract obstruction. Papillary necrosis is

usually bilateral but may be unilateral. One or all of the pyramids of the affected kidney may be involved. On cut

section, the tips or distal two thirds of the pyramids have areas of gray-white to yellow necrosis (Fig. 20-30). On

microscopic examination the necrotic tissue shows characteristic coagulative necrosis, with preservation of

outlines of tubules. The leukocytic response is limited to the junctions between preserved and destroyed tissue.

- Pyonephrosis is seen when there is total or almost complete obstruction, particularly when it is high in the urina

tract. The suppurative exudate is unable to drain and thus fills the renal pelvis, calyces, and ureter with pus.

- Perinephric abscess is an extension of suppurative inflammation through the renal capsule into the perinephric

tissue


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46. Figure 20-38

Figure 20-38 Close-up of the gross appearance of the cortical surface in benign nephrosclerosis illustrating the fine

leathery granularity of the surface.

47.Autosomal-

dominant

(adult)

polycystic

kidney disease(ADPKD)

is a hereditary disorder characterized by multiple expanding cysts of both kidneys that ultimately destroy the renal

parenchyma and cause renal failure

48.ADPKD

Morphology.

- In gross appearance, the kidneys are usually bilaterally enlarged and may achieve enormous sizes; weights as high

as 4 kg for each kidney have been reported. The external surface appears to be composed solely of a mass of cysts, up

3 to 4 cm in diameter, with no intervening parenchyma (Fig. 20-47A and B).

- However, microscopic examination reveals functioning nephrons dispersed between the cysts.

- The cysts may be filled with a clear, serous fluid or, more usually, with turbid, red to brown, sometimes hemorrhagi

fluid. As these cysts enlarge, they may encroach on the calyces and pelvis to produce pressure defects. The cysts arise

from the tubules throughout the nephron and therefore have variable lining epithelia. On occasion, papillary epitheli

formations and polyps project into the lumen. Bowman capsules are occasionally involved in cyst formation, and

glomerular tufts may be seen within the cystic space

- About 40% have one to several cysts in the liver (polycystic liver disease) that are usually asymptomatic.

49.Autosomal-recessive

(childhood)

polycystic

kidney disease

(ARPKD)

is genetically distinct from adult polycystic kidney disease. Perinatal, neonatal, infantile, and juvenile subcategorieshave been defined, depending on the time of presentation and presence of associated hepatic lesions. The first two ar

the most common; serious manifestations are usually present at birth, and the young infant might succumb rapidly to

renal failure


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55. Nephrolithiasis: (figure 20-51)

Nephrolithiasis (renal stones) is manifested by severe spasms of pain (renal colic) and

hematuria, often with recurrent stone formation.

56. Table 20-12: Types of Kidney

Stones

57. Table 20-3: The Glomerular

Syndromes

58. Table 20-7: Causes of Nephrotic

Syndrome

59. Table 20-11: Summary of Renal

Cystic Diseases

Robbins Ch. 20 the Kidney Review Questions

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