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Renal Exam > Renal Pathology (DN) > Flashcards

Renal Pathology (DN) Flashcards

1
Q

Diabetic Nephropathy is the leading cause of _____ in most Western societies in both DM I and II

A

ESRD

*risk related to duration of disease

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2
Q

Diabetics will increase risk of developing diabetic nephropahty drastically ____ to ____ years after Dx with diabets and ____ to ____ years after onset of proteinuria

A

20-25 yrs

2-3 yrs

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3
Q

Pathology of DN: Hyperfiltration

See increased GFR due to:

A

glucose dependent afferent arteriolar dilation and Ang II mediated cnx of efferent arteriole

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4
Q

As a result of hyperfiltration in early DM we see increase ________ pressure post glom
This cause wht to the Na+

A

increases colloid osmotic P

increase Na reabsorption in PT

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5
Q

Besides increasing GFR, what other effect does Ang II have

A

causes hypertrophic PT growth

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6
Q

How can we control the hyperfiltration aspect of DN?

A

Glycemic control!

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7
Q

Pathogeneis of DN: HYpertrophy
Seen when:
Assoicated with:

A

early onset w/ size of kids increasing several cm

see increased number of mesangial cells and capillary loops–> increases SA

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8
Q

Pathogenesis of DN: Mesangial Cells

Results in:

A

Mesangial expansion with nodular diabetic glomerulosclerosis = Kmmelsteil Wilson lesion

  • mediated by glucose and AGEs
  • -> increased size and more ECM deposition
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9
Q 
Pathogenesis DN: Proteinuria
What happens to the 
1. GBM
2. Podocytes
3. Serum proteins
A
  1. GBM accumulate type IV col and net reduction of (-) heparin sulfate
  2. Podocyte feet increase width and apoptosis trig by AngII and TGF-B, also decreaed migration from Ang II
  3. Serum pros cross BM from disrupted holes
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10
Q

Pathogeneis DN: Fibrosis

What do we see early on and what causes this

A

early on see tubulointerstitial fibrosis from GFs TGF-B and ANG II

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11
Q

In fibrosis seen in DN, tubular cells change phenotype to____

A

fibroblasts

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12
Q

What enhances the fibrosis process in DN

A

glucose concentration and AGEs

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13
Q

During Stage 1 and 2 we see ____ GFR and renal _____

A 
Increased GFR (25-50%)
Renal hypertrophy
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14
Q

What stage do we see mesangial expansion and GBM thickening in?

A

Stage 2 of DN; clinically asymptomatic but see on biopsy

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15
Q

What stage is there devo of HTN, persistent microalbuminuria and urinary albumin excretion of 30-300/day?

A

Stage 3: Early nephropathy

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16
Q

See GFR decline, urninary albumin >300 mg/day

50% pts reash ESRD w/in 7-10 yrs and retinopathy in 95%

A

Stage 4: Overt proteinuria

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17
Q

Renal replacement therapy necessary, seen about 15 ys after onset of Type I DM pts with proteinuria (30%)

A

Stage 5: ESRD

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18
Q

Co-morbidities of DN

A
  • HTN
  • Neuropathy
  • Vascular changes
  • Increased mortality
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19
Q

Diabetic retinopathy
• in almost all patients with______diabetes and nephropathy.
• In 50% to 60% of ______diabetes with nephropathy

A

type 1

type 2

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20
Q

What polyneuropathy issues do we see with DN?

A
  • Polyneuropathy.
  • Sensory polyneuropathy: Diabetic foot
  • Autonomic polyneuropathy
  • Silent angina
  • Gastroparesis
  • erectile impotence
  • detrusor paresis
21
Q

Macrovascular complications _____ x more frequent in DN
• Stroke
• coronary heart disease
• peripheral vascular disease

A

(5X more frequent)

22
Q

Key Txs for DN

A
  • HTN therapy
  • Glucose control
  • Reduction of proteinuria
  • Lipid lowering therapy
  • Life style modification
23
Q

• In DM pts with DN, HTN is
almost always present
• Uncontrolled hypertension is
associated with:

A

• more rapid progression of DN
• increased risk of fatal and
nonfatal CV events.

24
Q

Recommended BP for all diabetics pts

A 
140/90
• antihypertensive therapies 
improve survival in both type 1 
and type 2 diabetics with DN
Control glucose levels! decreases progression from normo-microalbuminuria
25
Q

What are ways to reduce proteinuria and

A
  • Renin-angiotensin-aldosterone system blockade
  • Renoprotective independent of BP
  • May cause up to 30% decline in GFR but renoprotective in the longterm
26
Q

RAAS works through renal hemodynamic changes

and blocking non-hemodyanmic effects of

A

Ang II

27
Q 
• Most patients with DN have:
– Low HDL
– High TGs
– Smaller LDL particle
• In type 2 diabetic patients with DN, treatment with\_\_\_\_\_\_ provides substantial CV benefit
A

statins

–seen in DN with ESRD

28
Q

Current guidelines
– LDL _____mg/dl for diabetic patients in general and
____mg/dl for diabetic patients with CVD

A

<70

29
Q 
Lifestyle modifications
• Smoking cessation
– Decreases progression of \_\_\_\_\_ 
• weight reduction 
– Possibly improves renal outcome via reduction in \_\_\_\_
A

micro to macro albuminuria

proteinuria

30
Q

• Amyloidosis affecting the kidney
– light chains, secreted by a _______
• 20% of cases associated with multiple myeloma
– Usually _________

A

single clone of B cells

lambda light chains (AL)

31
Q

What kidney manifestations do we see with Amyloidosis?

A

enlarged and hypertension is absent even when renal function is impaired.
Proteinuria, mainly albuminuria, occurs in the absence of microscopic hematuria.
Tubular defects from amyloid deposits

32
Q

What tubular defects from amyloid deposits do we see?

A

– Renal tubular acidosis (mostly as a part of Fanconi syndrome)
– polyuria-polydipsia (resulting from urinary concentration defect)

33
Q

What do we see on LM and IM on amyloidosis?

A

LM: see deposits and Congo-red stain: apple green birefringence
IM: staining for light chain

34
Q

What extra-renal manifestations do we see with amyloidosis?

A 
restrictive cardiomyopathy
GI issues
Splenomegaly
macroglossia
Peripheral nerve damage
skin
joint
35
Q

Light Chain Deposition disease is excess ________ in kidney and 50% of cases co-exsist with _____

A

immunoglobuin light chain, usually Kappa

multiple myeloma

36
Q

Pts with Light chain deposition develop

A

proteinuria
hematuria
chronic renal insufficiency

37
Q

Looking at LM we see nodular glomerulosclerosis
IF: is + for Kappa staining
EM: see granular deposits along the GBM

A

Light Chain deposition

38
Q

Alport Syndrome
• Most commonly ______ (80%) but can be autosomal recessive as well
• Mutation of the ____ gene on chromosome Xq22 which encodes the alpha-5
chain of _________

A

X-linked recessive

COL4A5

type IV collagen
*–> defect in the basement membrane

39
Q

– Affected males have persistent microscopic hematuria
– episodic gross hematuria, precipitated by URI
– Present in the first two decades of life.

A

Alport syndrome

40
Q

Most females with _____ have persistant or intermittent microscropic hematuria while only 7% of _____ never manifest hematuria

A

XLAS

obligate heterozygotes

41
Q

•______ is absent early but develops eventually in all males
with XLAS and in both males and females with ARAS.

A

Proteinuria

42
Q

• ESRD develops in all affected males with XLAS (90% by age 40)– rate determined by the underlying _____

A

COL4A5 mutation.

43
Q

What are the extra-renal manifestations in Alport

A

Cochlear defects
Ocular defects–yellowish flecks or granulations in perimacular distrubtion
Leiomyomatosis

44
Q

Pathology of AS
• LM:
• IF:
EM:

A

• LM: Early =normal. Later global and segmental glomerulosclerosis, interstitial fibrosis
• IF: Negative or non-specific IgM, C
EM: variable thickening, thinning, basket weaving, and lamellation of the GBM

45
Q

Tx for Alport

A

RAAS blockade
Renal replacement eventually necessary
Transplant: 2-3% get anti-GMB disease

46
Q

Inheritance pattern of Thin Basement Membrane Disease (Benign familial Hematuria)

A

autosomal dominance

47
Q

• Continuous or intermittent microhematuria, with or without gross hematuria, and
generally no renal insufficiency

A

Thin basement membrane disease (benign familial hematuria)

48
Q

What do we see on EM in Thin Basement Membrane Disease

A

• EM: Thin GBM (usually < 200 nm)

49
Q

Tx for Thin Basement Membrane Disease

A

-reassurance, very small risk for ESRD

– BMP, urinalysis and BP monitored every 1-2 years

Renal Exam (22 decks)

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