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Pathology Term 5 > Week 1 - RENAL > Flashcards

Week 1 - RENAL Flashcards

Normal Pathophysiology, Glomerulonephritis, Acute Renal Failure, Chronic Renal Failure

1
Q

Which kidney is higher?

A

Left

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2
Q

True or False?

Lobulations are prominent in the adult kidney

A

False

-more prominent in fetal kidney

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3
Q

Where are the glomeruli, distal tubules and loop of henle located?

A

glomeruli –> cortex

distal tubules/loop of henle –> medulla - renal pyramid

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4
Q

What is the most distal part of the nephron? and where is it located?

A

renal papillae

-tip of the renal pyramids

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5
Q

What are the 3 layers of the glomerulus?

A
  1. inner endothelial layer
  2. basement membrane
  3. podocytes (foot processes)
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6
Q

Outline the filtration membrane

A

endothelium
-big holes –> stops only cells (everything else filtered out)

basement membrane
-stops all large proteins (globulins)

foot processes
-stops smallest proteins (albumin)

**therefore only water and solutes come out of filtration membrane

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7
Q

What is the pathogenesis of oliguria in nephritic syndrome?

A

-marked inflammation cuses obstruction/compression to glomerular capillaries –> little urine produced (but there is hematuria, proteinuria as well)

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8
Q

Compare nephritic and nephrotic syndorme?

A

Nephritic

  • inflammation –> oliguria
  • damage to all 3 layers of filtration membrane (endothelium, basement membrane and foot processes)
  • cells, blood, proteins in urine
  • proteinuria (non-selective) + hematuria
  • oedema due to salt + water retention –> HTN
  • decreased GFR

Nephrotic

  • no inflammation –> polyuria
  • damage confined to foot processes (therefore no hematuria/proteinuria)
  • only albuminuria (selective proteinuria)–> oedema
  • lipiduria
  • hyperlipidemia
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9
Q

What is uremia?

A

disease characterised by:

  • fatigue, N/V, encephalopathy –> renal failure
  • increased BUN, creatinine, urea
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10
Q

What is azotemia?

A

increased blood urea nitrogen

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11
Q

What is the pathogenesis of headache in renal failure?

A
  • fluid retention
  • acidosis
  • uremia
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12
Q

What is the pathogenesis of SOB/pallor in renal failure?

A

anemia –> decreased EPO

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13
Q

What is the pathogenesis of N/V in renal failure?

A

renal osteodystrophy

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14
Q

What are some causes of painless/asymptomatic hematuria?

A

DM, IgA nephropathy, TB, cancer, SLE, vasculitis (polyarteritis), HSP, bacterial endocarditis, exercise hematuria

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15
Q

What is proteinuria with casts vs. proteinuria without casts?

A 
with casts (glomerulonephritis)
without casts (UTI)
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16
Q

What is oliguria and anuria and what are the causes?

A
  • oliguria <500mL/day
  • anuria <50mL/day

*dehydration, nephritic syndrome, renal failure, obstruction

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17
Q

What are some causes of polyuria and what is it?

A

> 3L/day

-increased fluid intake, DM, nephrotic syndrome, D. insipidus, osmotic

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18
Q

Where does ADH mainly act on?

A

collecting duct

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19
Q

What is the glomerular filtrate?

A

180L/day

  • mostly reabsorbed (only 1-2L urine/day)
  • 1.2L blood filtrated/min
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20
Q

What are the immunological causes of glomerulonephritis?

A
  • glomerular Ag (anti GBM) –> autoimmune; crescentic
  • non-glomerular Ag (complement activation due to Ab against Ag in glomerulus) –> insitu*, SLE, strep A
  • circulating immune complex deposition (Ag/Ab) –> SLE, infections
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21
Q

What are the morphological types of glomerulonephritis?

A
  • diffuse –> all glomeruli
  • focal –> some glomeruli
  • global –> whole glomerulus
  • segmental –> part of glomerulus
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22
Q

What is the commonest cause of glomerular damage?

A

immune-mediated

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23
Q

What are the 2 types of immune complex deposition in glomerulus?

A

Linear –> insitu

Granular (lumpy) –> circulating (irregular) **more common

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24
Q

What are the 3 characteristic features of nephrotic syndrome?

A
  • massive albuminuria
  • hypoalbuminemia
  • hyperlipidemia

*non-inflammatory

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25
What is the commonest secondary cause of nephrotic syndrome?
DM
26
What are the primary glomerular diseases of nephrotic syndrome?
1. minimal change disease (MCD) 2. focal segmental glomerulosclerosis (FSGS) 3. membranous GN (MGN)
27
What is the commonest type of nephrotic syndrome in children?
minimal change GN AKA: nil disease; lipoid nephrosis *80% nephrotic synd. in kids
28
What is the etiology of minimal change GN?
-idiopathic; destruction of podocytes
29
What is the microscopy of minimal change GN?
normal routine microscopy | -loss of foot processes only visible on electron microscopy**
30
What is the prognosis of minimal change GN?
- spontaneous remission in majority | - some may progress to chronic renal failure or focal segmental glomerulosclerosis (FSGS)
31
What is the morphology of FSGS?
- segmental collapse necrosis - IgM deposit - podocyte damage (like MCD) - protein casts
32
What is collapsing glomerulopathy?
When FSGS becomes severe and the whole glomerulus is affected --> HIV; drugs, etc
33
True or False? | FSGS is associated with NHL
False | -HL
34
What are the secondary causes of FSGS?
- HIV - HL - IgA nephropathy
35
What are the primary and secondary causes of membranous GN?
primary: -autoantibody to podocyte Ag secondary: -HBV, SLE, malignancy, gold/mercury poisoning, drugs (anti-inflamm.)
36
What is the pathogenesis of membranous GN?
- Ab against podocyte Ag - directly activating complement (C3, C5b-C9) - only proteinuria - no inflammation*
37
How do lab + clinical findings of membranous GN differ to MCD lab/clinical findings?
MCD --> selective proteinuria (only albumin) membranous GN --> damage is increased - non-selective proteinuria (albumin + globulin); hematuria maybe present; still NO inflammation
38
Why is membranous GN known as 'wire loop'?
-morphologically, glomerular capillaries appear like thick wires due to marked deposition of antibodies
39
What is the morphology of membranous GN?
- wireloop thick BM (some damage) - sub-epithelial humps of IgG + C3, effacement of foot processes - no inflammation --> nephrotic - protein casts
40
What is the commonest type of nephrotic syndrome in adults?
membranous GN
41
What are the characteristic features of nephritic syndrome?
- oliguria - hematuria - azotemia - HTN - non-selective proteinuria
42
What are the primary glomerular diseases in nephritic syndrome?
1. post-strep proliferative GN 2. IgA nephropathy 3. rapidly progressive GN
43
What is the commonest cause of nephritic syndrome in children?
acute post-strep diffuse proliferative GN ('post infectious GN')
44
What is the etiology of post-strep proliferative GN?
- autoimmune - GABH strep (Type 12 - nephritogenic sp) - other bacteria/virus, etc can cause it too
45
What is the pathogenesis of post-strep proliferative GN?
- 1-4wks post-infection - insitu immune complex depostion - C3/IgG coarse subepithelial deposits --> inflammation with neutrophil infiltration/mesangial cell proliferation --> compression of glomerular capillaries --> oliguria + severe damage --> hematuria/non-selective proteinuria
46
What is the lab findings in post strep proliferative GN?
- oliguria - hematuria - RBC casts - non-selective proteinuria - decr. serum complements (C3 - hypocomplementemia)
47
What is the morphology of post-strep proliferative GN?
- diffuse, hypercellular glomeruli with neutrophils - inflammation - collapsed capillaries (narrow/non-patent**) - RBC casts
48
What is a common cause of recurrent hematuria in Young?
``` IgA nephropathy (Berger's disease) -males, Asia-Pacific, Infections* ```
49
What is the etiology of IgA nephropathy?
- abnormal IgA - Abs formed against glycosylated IgA - congenital
50
What is secondary IgA nephropathy?
- associated with celiac/liver disease | - due to lack of removal of IgA from the body
51
What is the morphology of IgA nephropathy?
- IgA containing immune deposits - C3 in mesangium - high serum IgA1
52
What are the clinical features of IgA nephropathy?
- episodic, asymptomatic hematuria --> microscopic hematuria (40%); massive hematuria (40%) - usually following infections
53
What is rapidly progressive GN AKA?
Crescentic GN N.B. not a separate disease --> ANY GN may result in RPGN
54
What is RPGN? and its microscopic features?
``` acute, severe, rapidly progressive renal failure (WEEKS) Micro: -crescent (inflamm exudate) -compressed glomerular capillary -mixed casts within tubules ```
55
Why is it called crescentic GN?
- severe inflammation in glomerulus | - inflamm fluid/exudate secreted from glomerulus into bowman's capsule --> crescent formation of inflammatory exudate
56
What is the pathogenesis of edema in nephritic syndrome?
- oliguria/decreased GFR | - salt and water retention --> HTN
57
What % of crescentic/RPGN leads to chronic GN? and post-streptococcal GN?
crescentic --> 90% - poor prognosis post-strep GN --> 1%
58
What is acute renal failure?
- acute deterioration of renal function - oliguria, anuria, uremia * decreased GFR (<20ml/min) --> BUN + Creatinine increased
59
What is the commonest type of acute renal failure?
Pre-renal (60%) others: intrinsic/renal (30%) + post-renal (10%)
60
What are the pre-renal causes of renal failure?
- hypovolemia, shock, dehydration, cardiac failure | - microangiopathy --> DIC, HUS, TTP, etc- arterial block emboli
61
What are the renal causes of renal failure?
- acute tubular necrosis - acute glomerulonephritis - acute tubulointerstitial nephritis - infiltrations, malignancy, tubular obstructions --> drugs, Hb, myoglobin, myeloma proteins, etc
62
What are the post-renal causes of renal failure?
-urinary tract obstruction --> stones, UTI, tumours, bladder, prostate
63
What is FENa% and its interpretation?
Fractional Excretion of sodium --> % of sodium filtered by the kidney what is excreted in the urine * <1% = pre-renal * >1% = renal * >4% = post-renal
64
What is acute tubular necrosis?
- acute tubular injury (ATI) - necrosis of tubular epithelium --> fall as epithelial casts * *commonest cause of renal ARF**
65
What are the 2 types of acute tubular necrosis?
1. Ischaemic type - obstruction to BVs - patchy (PCT + DCT) - hypovolemia, shock, DIC, HUS, TTP, etc 2. Toxic type - due to toxins - PCT only* - drugs, toxins, mercury, CCL4, radiocontrast, Hb, myoglobin, bilirubin, immunoglobulins - REVERSIBLE* --> dialysis
66
How do the cells of the DCT compare to PCT cells?
DCT cells are typically flatter in appearance
67
What is microscopy of acute tubular necrosis (toxic) and (ischaemic)?
Toxic: - normal glomerulus - necrotic PCT --> NO nuclei - normal DCT (protein cast inside) Ischaemic: - epithelial sloughing (all tubules) - pyknosis of nuclei in both PCT/DCT --> patchy - epithelial casts - pink appearance
68
What is benign nephrosclerosis?
- AKA hypertensive nephropathy/vascular nephrosclerosis - arteriolosclerosis (hyperplastic + hyaline) - pathogenesis (increased hydrostatic pressure - BP) - glomerulosclerosis --> atrophy --> fine granular surface (orange peel) - cortical atrophy** - African race --> apolipoprotein L1 mutation (trypanosoma resistance)
69
What is the gross and microscopic appearance of benign nephrosclerosis?
Gross: - leathery granularity (orange peel) --> due to glomerular scarring in cortex - cortical atrophy Micro: - artery sclerosis - glomerular sclerosis - narrowed capillary lumen
70
What is the microscopic appearance of kidney in malignant hypertension?
fibrinoid necrosis of arteriole
71
What is analgesic nephropathy?
- tubulointerstitial nephritis - progressive chronic use of analgesics (phenacetin*) - chronic eosinophilic interstitial inflammation with tubular injury - renal papillary necrosis, sloughing + calcification (grossly) --> CRF - clinical: hematuria, renal colic, mild proteinuria + leukocyturia - rare urothelial Ca. of renal pelvis
72
What is NSAID nephropathy?
- NOT analgesic - COX inhibition --> decreased PGs --> vasoconstriction --> interstitial nephritis - acute or chronic (like analgesic) *MCD or MGN
73
What is chronic renal failure and what are the common causes?
- progressive scarring of the kidney from any cause (infection, GN, etc) --> resulting in CRF eventually terminating in ESRD (dialysis/transplantation) * HTN + DM = commonest clinical causes
74
What are the 2 major types of CRF?
1. end stage of several types of GN/kidney injury (secondary) 2. primary (de novo) presentation --> idiopathic
75
What are the clinical features of CRF?
- uremia --> N/V, GI bleeding, anemia, itching (pruritis) - metabolic --> acidosis (kussmaul), increased K, BUN, creatinine - osteodystrophy --> decreased vit. D = decreased Ca = increased PTH = increased bone lysis - endocrine --> hyperparathyroidism (secondary) - bleeding --> plt. dysfunction due to uremia (toxins) - anemia --> decreased EPO, bleeding, RBC lysis (uremia - toxins) - skin pigmentation - pericarditis - myopathy, neuropathy, coma
76
What is the most important Ix. for chronic kidney disease? and what is the normal value?
GFR/eGFR | -normal = 120mL
77
How is eGFR calculated?
MDRD formula - Modification of Diet in Renal Disease - 4 variables: age, gender, ethinicity, serum creatinine **(140 - age) x Wt/(0.81 x SCr) [x 0.85 if F]
78
Outline CRF staging
CRF staging = mL/min/1.73m^2 1. GFR > 90mL (asymptomatic) 2. GFR 60-89mL (asymptomatic) 3. GFR 30-59mL (mild kidney failure) 4. GFR 15-29mL (moderate) 5. GFR < 15mL (severe --> ESRD)*--> dialysis/transplant
79
What is the microscopy of ESRD?
1. scarred glomeruli (collagen) 2. atrophic tubules (no epithelium) with only casts 3. interstitial inflammation
80
True or False? | Pyelonephritis is usually bilateral
False | -unilateral*
81
What is vesicoureteral reflux?
- retrograde transport of urine from bladder to kidney | - due to defective sphincter (deranged vesicoureteral junction)
82
What is pyelonephritis? and what are the causes?
- suppurative tubulointerstitial inflammation - acute/chronic; usually unilateral - secondary to UTI/UTO, DM, pregnancy - vesicoureteral reflux (deranged vesicoureteral junction)** commonest cause - papillary necrosis = poor prognosis
83
What are the gross and microscopic features of pyelonephritis?
Gross: - abscess/pus --> atrophy scarring (large wide irregular scars) --> ESRD - small, shrunken Micro: - plenty of inflammatory cells (neutrophils) - WBC casts within tubules +tubular atrophy - scarring of interstitium
84
What are the clinical features of pyelonephritis?
- fever - loin pain - pyuria (pus in urine)
85
What are the gross and microscopic features of diabetic nephropathy?
Gross: - shrunken - atrophic - prominent pelvic fat - papillary necrosis Micro: - necrosis of renal papillae - hyaline arterolosclerosis - nodular glomerularsclerosis (KW/diffuse) - tubular atrophy - interstitial inflammation

Pathology Term 5 (6 decks)

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