Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRRAB II > Renal Pathology Lecture I > Flashcards

Renal Pathology Lecture I Flashcards

1
Q

What forms the backbone of the GBM?

A

Type IV collagen monomers. —3 alpha chains combine to for triple helix to make a monomer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a large reason why the overall charge of GBM negative?

A

Heparin sulfate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the function of the filtration slit diaphragm?

A

Exclusion of large proteins and albumin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 general categories of renal disease

A
  1. Glomerular (often immune mediated)
  2. Tubulointerstitial (toxic/ischemic and inflammatory)
  3. Vascular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Azotemia

A

Increased BUN and creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pre-renal causes of azotemia

A

Hypoperfusion (hemorrhage, shock, dehydration, CHF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Post-renal causes of azotemia

A

Obstruction of urine flow (stone or tumor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Uremia

A

Azotemia and clinical symtoms (gastroenteritis, anemia, peripheral neuropathy, pruritis, pericarditis etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Nephritic syndrome

A

Hematuria, mild to moderate proteinuria, HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Nephrotic syndrome

A

> 3.5g/day of proteinuria, edema, hypoalbuminemia, hyperlipidemia, lipiduria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acute renal failure clinical presentation

A
  • -Rapid onset azotemia
  • -Oliguria or anuria
  • -Due to glomerular, tubulointerstitial, or vascular disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Chronic renal failure clinical presentation

A

–GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical presentation of renal tubular defects

A

Polyuria
Nocturia
Electrolyte imbalances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

4 stages of renal disease

A
  1. Diminished renal reserve
  2. Renal insufficiency
  3. Renal failure
  4. End-stage renal disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diminished renal reserve

A

GFR around 50% of normal. Normal range BUN/Cr

Asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Renal insufficiency

A

GFR 20-50% of normal
Azotemia
Anemia
HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Renal failure

A

GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

End stage renal disease

A

GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clearance equation and definition

A

–Approximation of GFR

C=UV/P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Best analyte to measure clearance

A

Inulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cockcroft-gault formula

A

CrCL=((140-age)x weight (kg))/(72 x serum creatinine x0.85 (if female)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MDRD formula

A

GFR=175 x serum creatinine^-1.154 x age^-.203 x 0.742 (if female) and 1.212 (if black)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is chronic kidney disease defined by?

A

Persistent reduction in GFR to less than 60. Less than 30 recommend seeing nephrology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When are clearance measurements still used?

A
  • -Unusual body size
  • -Rapidly changing kidney function
  • -GFR 60+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

BUN

A
  • Rough est. of glomerular function
  • Normal 10-20 mg/dl
  • Combined w/serum creatinine, helps determine causes of azotemia
  • Sensitive to decreased renal perfusion
26
Q

Pre-renal factors increasing BUN

A
  • -Increased synthesis of urea

- -Decreased renal perfusion/low flow states

27
Q

Renal factors increasing BUN

A

Glomerular disease, ATN, interstitial disease

28
Q

Post-renal factors increasing BUN

A

Urinary tract obstruction (BPH, prostatic carcinoma, tumor, retroperitoneal mass, urinary calculi

29
Q

Factors decreasing BUN

A
  • -Decreased synthesis
  • -Hemodilution
  • -Generally not diagnostically useful
30
Q

Creatinine

A
  • -Normal 0.7-1.5
  • -Most found in muscle.
  • -Slightly better est. of glomerular function than BUN
31
Q

Pre-renal increases in creatinine

A
  • -Increased synthesis (muscle hypertrophy, muscle necrosis, anabolic steroid use, high meat diet, intense exercise)
  • -Decreased renal perfusion (CHF, hypotension, shock, etc.)
32
Q

Post-renal increase in creatinine

A

UTI

33
Q

Normal BUN: creatinine ratio

A

10-15: 1

34
Q

When do you see elevated BUN:creatinine ration

A

Pre-renal conditions. Disproportionate increase in proximal urea reabsorption.

35
Q

What type of BUN:creatine ratio will you see in renal disease?

A

Normal ratio

36
Q

Fraction of excreted sodium (FeNa)

A

(Urine Na x plasma Cr x 100)/ (urine Cr x plasma Na)

37
Q

What does it mean if FeNa

A

Favors pre-renal disease

38
Q

What does it mean if FeNa >2.0

A

Favors renal disease (ATN)

39
Q

Proteinuria normal value

A

50 mg

40
Q

Tests for proteinuria

A
  • -Dipstick test (only sensitive to albumin, pH dependent, can get false + w/gross hematuria or dilute urine)
  • -Acid precipitation (detects albumin and globulins, false + w/some meds and gross hematuria)
41
Q

Causes of proteinuria w/o renal disease

A
  1. Postural (orthostatic)
  2. Transient
  3. Functional (heavy exercise, cold exposure, fever)
  4. CHF
  5. Massive obesity
  6. Constrictive pericarditis
  7. Renal vein thrombosis
42
Q

Proteinuria w/renal disease

A
  1. Glomerular pattern (albumin, small globulins, can reach nephrotic range)
  2. Tubular pattern (beta2 microglobulin, will never reach nephrotic range)
43
Q

% of people w/UT malformations

A

10%

44
Q

What 2 things account for 20% of chronic kidney disease in children?

A

Renal dysplasia and hypoplasia

45
Q

What accounts for 10% of chronic kidney disease in adults?

A

Polycystic kidney disease

46
Q

Kidney agenenis

A
  • -Bilateral incompatible with life.
  • -Unilateral w/normal function
  • -Lack of proper ureteric bud development
47
Q

Kidney hypoplasia

A
  • -Failure to develop to normal size
  • -Bilateral or unilateral
  • -No scarring
  • -Decreased # of renal lobes (6 or less)
  • -Most cases are acquired (slow scarring)
48
Q

Ectopic kidneys

A

–Typically found just above pelvic brim or in pelvis

49
Q

Horseshoe kidney

A
  • -Fusion of upper (10%) or lower poles (90%) to form single horseshoe shaped kidney.
  • Not very uncommon
50
Q

Cystic renal dysplasia

A
  • -Unilateral or bilateral
  • -Gross: Enlarged, multi-cystic, irregular
  • -Micro: undifferentiated mesenchyme, cartilage, immature collecting ductules, variably sized cysts lined by flattened epithelium
  • -sporadic disorder
  • -Most also have lower tract anomalies
51
Q

Autosomal dominant (adult) polycystic kidney disease

A
  • -Hereditary
  • -Autosomal dominant
  • -Bilateral disease
  • -Multiple expanding cysts destroy renal parenchyma
  • -Only involving portion of kidney initially
52
Q

Adult PCKD genetics

A

PKD1 gene on chromosome 16p13.3 in most cases

53
Q

Adult PCKD gross kidney findings

A
  • -Bilaterally enlarged kidneys, may be huge

- -Look like a bag of cysts

54
Q

Adult PCKD micro findings

A
  • -Cysts with variable lining

- -Normal parenchyma present between cysts

55
Q

Clinical findings in adult PCKD

A

Asymptomatic

or pain and hematuria

56
Q

Extra-renal anomalies in adult PCKD

A

Liver cysts (40% of pts)
Intracranial berry aneurysms
Mitral valve prolapse

57
Q

Autosomal recessive (childhood) PCKD categories

A

–Perinatal
–Neonatal
–Infantile
–Juvenile
Only last 2 survive infancy

58
Q

Gross findings in AR PCKD

A

Enlarged, smooth kidneys externally, cut sections show small cysts in the cortex and medulla

59
Q

Micro findings in AR PCKD

A

Dilation of all collecting tubules (uniform cuboidal lining of cysts)

60
Q

General info about AR PCKD

A
  • -Bilateral
  • -Liver cysts and bile duct proliferation in almost all patients
  • -May see congenital hepatic fibrosis in 2 forms that survive infancy

CRRAB II (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions