Pathology: Renal Disorders (Usmle Step 1)

Front 1

Angiotensin II: Effects ?
(Kidneys)
(Peripheral arterioles)

Back 1

1. Vasoconstricts efferent arterioles
2. Vascoconstriction of peripheral arterioles

Front 2

EPO: site of production in kidneys?

Back 2

Renal cortex: Interstitial cells of peritubular capillary beds

Front 3

Site of hydroxylation of vit-D: site in kidney?

Back 3

Site: Proximal renal tubule cells

enzyme: 1-alpha-hydroxylase

Front 4

Vitamin D:
1. Effect on bone
2. Effect on intestines?

Back 4

Effect on bone:
Promotes mineralization of bones

Effect on intestines:
Promotes Ca/ Phosphorus absorption in intestines

MOA of mineralization of bone?

Hint 4

Stimulates alkaline phosphatase release--->
Hydrolyzes inhibitors of mineralization (Pyrophosphate)

(Inhibition of inhibitors)

Front 5

Alkaline phosphate containing cells in bone?

Back 5

Osteoblasts

Front 6

Vitamin D: effect on stem cell differentiation in bone?

Back 6

Induces stem cell differentiation into osteoblasts in bone

Front 7

Upper urinary tract causes of hematuria?

Back 7

1. Renal stone
2. RCC
3. Glomerulonephritis

Which of the above is associated with dysmorphic RBCs?

Hint 7

Glomerulonephritis

Front 8

Effect of PGE2 on kidneys?

Back 8

Vasodilation of afferent arteriole

Front 9

Lower urinary tract TUMORS associated with hematuria?

Back 9

1. Infection
2. Transitional cell Ca
3. BPH

Front 10

MCC of hematuria in absence of of infection?

Back 10

Transitional cell Ca

Front 11

MCC of lower urinary tract hematuria?

Back 11

Infections

Front 12

MCC of microscopic hematuria?

Back 12

BPH (adult males)

Front 13

Drugs associated with hematuria?

Back 13

1. Anticoagulants
2. Cyclophosphamide

Front 14

Cyclophosphamide:
Complication?
Rx?

Back 14

Complication: hemorrhaigc cystitis

Rx: MESNA

Front 15

Proteinuria: general proteinuria is ____(cut off for protein level excretion in urine over 24 hrs)

Back 15

>150mg/24hrs
>30mg/dl(dipstick)

Front 16

Qualitative test for protein- specific for albumin?

Back 16

Dipstick test

Front 17

Qualitative test : Non specific?

Back 17

SSA

Front 18

Quantitative test for proteinuria?

Back 18

24 hr urine protein

Front 19

Types of proteinuria: Name em?

Back 19

1. Functional
2. Overflow
3. Glomerular
4. Tubular

Front 20

Normal serum BUN levels?

Back 20

7-18mg/dl

Front 21

Part of the nephron where BUN is reabsorbed?

Back 21

Proximal tubule

Front 22

Serum of BUN depends upon which 4 factors?

Back 22

1. GFR
2. Protein content in the diet
3. Functional status of urea cycle

Front 23

When and where does extrarenal loss of BUN occur?

Back 23

When serum levels are very high

Site: Skin

Front 24

MCC of increased BUN?

Back 24

Congestive heart failure

Front 25

Causes of increased BUN?

Back 25

1. CHF
2. Hemorrhage

3. Acute glomerulonephritis
4. Acute/CRF
5. Post renal disease

6. Third degree burns
7. Post-op states
8. Increased diet proteins

(REMEMBER:
Conditions that either:
1. Increase production
2. Decrease GFR
cause increased BUN)

Front 26

Why does increased GFR cause decreased BUN or vice versa)

Back 26

Increased GFR means less time for proximal tubule to reabsorb BUN and vice versa

Front 27

Causes of decreased BUN?

Back 27

1. Normal pregnancy
2. SIADH

3. Liver failure

4. Malnutrition

Front 28

Glomerular BM damage produces what sort of proteinuria?
(Selective/non selective)

Back 28

NON selective proteinuria

Front 29

Glomerular BM loss of charge produces what sort of proteinuria?
(Selective/non selective)

Back 29

Selective

Mechanism?

Hint 29

Loss of albumin only and not globulin.

(negative charge of BM repels negatively charged albumin)

Front 30

Renal Disease associated with selective proteinuria?

Back 30

Lipoid nephrosis aka Minimal change disease

Front 31

What is 'Overflow' proteinuria?

Back 31

Amount filtered> amount reabsorbed

Front 32

Disease associated with overflow proteinuria?

Back 32

1. Multiple myeloma
2. Hemoglobinuria
3. Myoglobinuria

Front 33

Disease conditions associated with increased CK+proteinuria?

Back 33

Myoglobinuria:
1. Crush injury
2. Mcardle's disease

Front 34

Proteinuria not associated with renal disease?

Back 34

Called "functional proteinuria"

CHF
Exercise
Fever
Orthostatic proteinuria

What is "orthostatic proteinuria"?

Hint 34

Proteinuria on standing

Front 35

Proteinuria in:
Nephrotic syndrome?
Nephritic syndrome?

(prot levels)

Back 35

1. Nephrotic syndrome > 3g/24hrs

2. Nephritic syndrome>150mg/24hrs

Front 36

What is "tubular proteinuria"

Back 36

Defect in proximal tubular reabsorption of ___(HMW/LMW) proteins

Hint 36

LMW proteins

(Defect in proximal tubular reabsorption of LMW proteins)

Front 37

Conditions associated with "tubular proteinuria"?

Back 37

Heavy metal poisoning
Fanconi syndrome
(inability to absorb:
AA,
uric acid,
phosphate,
bicarbonate)

Hartnup disease
(inability to absorb tryptophan)
in GI and kidneys

Front 38

Normal levels of creatinine in serum?

Back 38

0.6-1.2mg/dl

Front 39

Unique feature of creatinine in terms of its renal processing?

Back 39

Filetered but neither reabsorbed nor filtered.

Name another substance that has a similar but a better property?

Hint 39

Inulin

Front 40

"Azotemia"?

Back 40

Increased BUN and creatinine

Front 41

Creatinine values ____(increase/decrease) with age

Back 41

Increase

Front 42

Creatinine values____(increase/decrease) with muscle wasting

Back 42

Decrease

Front 43

Normal BUN: creatinine ratio?

Back 43

15

Front 44

Types of azotemia?

Back 44

1. Prerenal
2. Renal
3. Postrenal

Front 45

Prerenal azotemia: associated condition causing it?

Back 45

Conditions causing decreased cardiac output

Front 46

BUN:creatinine ratio in prerenal azotemia:
a. 15
b. <15
c. >15

Back 46

>15


why?

Hint 46

BUN and creatinine effectively both increased in blood due to decreased filtration

But since BUN is reabsorbed unlike creatinine-->
BUN values > creatinine
therefore--> BUN: creat>15

Front 47

Renal azotemia BUN:creat ratio:
a. 15
b. <15
c. >15

Back 47

<15


why?

Hint 47

BUN and creat both decreased d/t decreased GFR
BUN finds a way to be lost thru extrarenal routes
BUN and creat both NOT reabsorbed in tubules because of destruction from intrarenal disease

Front 48

Post renal azotemia BUN:creat ratio?
a. 15
b. <15
c. >15

Back 48

Initially>15
Persistent <15

Why?

Hint 48

Back pressure decreases GFR
--> decreased BUN and Creat

Decreased GFR increases reabsorption of BUN
(Creat never reabsorbed)

Persistent<15
Since persistence of obstruction damages renal tubules

Front 49

Name associated conditions for the following urine colors:
1. Yellow
2. Red/pink
3. Smoky
4. Black

Back 49

Yelow:
Concentrated urine
Bilirubinuria
Vitamins

Red/pink:
Hematuria
Hemoglobinuria
Myoglobinuria
Porphyria
Drugs: Rifampin, Phenopyridine

Smoky: Acid pH urine with hemturia
(hemoglobin--->hematin)
g. glomerulonephritis

Black urine: Alkaptonuria
(Homogentic acid turns black on exposure to light)

Front 50

Cloudy alkaline urine: associated condition?

Cloudy acidic urine: associated condition?

Back 50

Cloudy alkaline urine: Normal finding with increased phosphates

Cloudy acidic urine: Normal finding with increased uric acid

Front 51

Specific gravity value that indicates urine concentration?

Back 51

Sp.gravity>1.023

What does it exclude?

Hint 51

Excludes renal disease

Front 52

Specific gravity value that indicates hypotonic urine?

Back 52

Sp.gravity>1.012

Front 53

Vegans have ___(acidic/alkaline) urine

Meat eaters have ____(acidic/alkaline) urine?

Back 53

Vegans have alkaline urine
(citrate--->HCO3)

Meat eaters have acidic urine
(organic acids in meat)

Front 54

Alkaline pH + NH3 smelling urine indicates?

Back 54

Urease producing organisms in urine
(Proteus)

Front 55

With increasing age beyond ____ yrs the annual increase in CCr is ____ml/minute

Back 55

Increasing age beyond 50yrs the annual CCr increase is 1ml/min

Front 56

How is CCr calculated?

Back 56

Ucr/Bcr x Uv

Ucr= urine creat
Bcr= blood creat
Uv=Urine volume

Front 57

Glucose dipsticks detects glusoe in urine at value greater than ___?

Back 57

30mg/dl

Front 58

Condition with :
1. glucosuria and increased serum glucose?
2. glucosuria with normal serum glucose?

Back 58

1. Diabetes

2.
Pregnancy (normal finding)
Benign glucosuria

Front 59

1st sign of diabetic nephropathy?

Back 59

Diabetic nephropathy

Front 60

Ketone not detected by standard dipstick test?

Back 60

B-hydroxy butyric acid

Front 61

Ketonuria: causes?

Back 61

1. DKA
2. Pregnancy
3. Starvation
4. PREGNANCY (normal finding)
5. Isopropyl alcohol

Front 62

Conditions with:

A:
1. Increased urine bilirubin
2. Decreased UBG

B:
1. Absent bilirubin
2. Increased UBG

C:
1. Increased bilirubin
2. Increased UBG

Back 62

A: Obstructive jaundice
B: Hemolysis
C: Hepatitis

Front 63

Conditions that causes nitrites to be present in blood?

Back 63

Nitrate reducing pathogens:
Ecoli

Requires ___hrs to reduce nitrates to nitrites

Hint 63

4hrs

Front 64

Why does the nitrite dipstick test have poor sensitivity?

Back 64

Because patients have increased urinary frequency as a result urine exposure to pathogen may be <4hrs--> no reduction of nitrates to nitrites

Front 65

Esterase dipstick test is used to detect?

Back 65

Leukocyte esterase activity in infections (neutrophils)

Front 66

What is sterile pyuria?

Back 66

+ve neutrophils
-ve gram culture
(no organisms)

Front 67

Conditions associated with sterile pyuria?

Back 67

1. C.trachomatis urethritis
2. Tb
3. Drug nephritis

Front 68

Definition of hematuria?
(Besides "blood in urine")

Back 68

2-3 RBCs/HPF

Front 69

What do dysmorphic RBCs indicate?

Back 69

Hematuria of glomerular origin

Front 70

Definition of pyuria?

Back 70

>10 WBCs /HPF

Front 71

Oval fat cells are seen in _____(renal condition)

Back 71

Nephrotic syndrome

What are the "oval fat cells" ?

Hint 71

Renal tubular bodies

Front 72

Casts in urine indicate disease of ____origin (part of nephron)

Back 72

tubular

Front 73

What are urine casts?

Back 73

Protein matrix with entrapped cells, debris or protein

Front 74

What do urine casts indicate?

Back 74

Renal origin of disease

Front 75

What are hyaline casts?
What do they indicate?

Back 75

Ghost casts (acellular) made up of proteins

No significance
Unless___?

Hint 75

significant in presence of proteinuria

Front 76

RBC cast indicates____(nephritic/nephrotic)type of glomerulonephritis?

Back 76

Nephritic

Front 77

Typical casts seen in nephrotic syndrome?

Back 77

Fatty casts

Front 78

Renal tubular cell casts seen in ____

Back 78

Renal tubular necrosis

Front 79

What are "waxy" or "broad" casts in urine?

Back 79

1. Refractile
2. Acellular casts

Indicates_____

Hint 79

CRF

Front 80

Crystals found in urine: Name em?

Back 80

1. Calcium oxalate
2. Uric acid
3. Triple phosphate
4. Cystine

Front 81

Conditions associated with :
1. Ca-oxalate CRYSTALS in urine
2. Uric acid CRYSTALS in urine
3. Triple phosphate CRYSTALS in urine
4. Cystine CRYSTALS in urine?

Back 81

1. Ca-oxalate:
a. Pure vegan diet
b. Ethylene glycol poisoning
c. Ca-oxalate stone

2. Uric acid crystals:
a. Gout
b. Chemotherapy (extensive cell destruction)

3. Triple phosphate:
Sign of UTI-___producing pathogens

4. Cystine:
Cystinuria(___shaped crystals)

Hint 81

Urease producing pathogen
Cystine crystals are "hexagonal"

Front 82

Part of the kidney susceptible to infarction?

Back 82

Medulla(10% of blood supply to kidney)
Cortex receives 90%

Front 83

Why are the kidneys susceptible to infarction rather than ischemia?

Back 83

Since they are supplied by end arteries that have no collaterals.

Front 84

Part of the nephron that is the site of production of renin?

Back 84

Afferent arterioles "Juxtaglomerular cells"

Front 85

Tone of the afferent arterioles is controlled by ______

Back 85

PGE2

effect?

Hint 85

Vasodilation

Front 86

Tone of the efferent arterioles is controlled by ______

Back 86

ATII

Front 87

NSAIDs predispose to ______(renal condition)

Back 87

Infarction


Why?

Hint 87

Since NSAIDs inhibit production of PGE2 that maintains dilated state of afferent arterioles

Front 88

Glomerular BM consists of type ___collagen

Back 88

Type IV

Front 89

Glomerular capillaries contain ___type of epithelia that are important for filtration process

Back 89

Fenestrated

Front 90

Negative charge of the glomerular BM is attributed to ______(polysaccharide)

Back 90

Heparan sulfate

Front 91

Loss of negative charge in GBM results in ____type of proteinuria

Back 91

Selective


Protein lost in selective proteinuria?

Hint 91

-vely charged albumin

Front 92

Proteins that are permeable across the GBM are ____

Back 92

LMW and cationic proteins
(mainly amino acids)

Front 93

Causes of GBM thickening?

Back 93

1. Deposition of immune complexes:
Membranous glomerulonephritis

2. Synthesis of type IV collagen:
Diabetes mellitus

Front 94

Cells responsible for production of GBM?

Back 94

Visceral epithelial cells
(the ones with foot processes sitting on endothelial cells)

Front 95

Function of podocytes?

Back 95

Foot processes act as a filtration barrier to proteins

Front 96

Characteristic finding in nephrotic syndrome in the foot processes of the podocytes?

Back 96

Effacement/fusion

Front 97

Chief determinant of protein filtration of proteins?

Back 97

1. Charge
2. Size

Front 98

Mesangial cells: functions?

Back 98

Support the glomerular capillaries

Front 99

Renal disease associated with immune complex deposits in mesangial cell layer

Back 99

IgA glomerulopathy

Front 100

Glomerular cell responsible for the "crescents" observed in crescentic glomerulonephritis

Back 100

Parietal epithelial cells

Front 101

MC congenital renal disorder?

Back 101

Horseshoe kidney

Front 102

Horseshoe kidney: anatomically associated with which vessel?

Back 102

Inferior mesenteric artery

How?

Hint 102

Kidney is trapped behind the root of inferior mesenteric artery

Front 103

Majority of the horseshoe kidneys are found fused at the ____pole

Back 103

Lower

Front 104

Horseshoe kidneys: important clinical association (chromosomal anomaly)?

Back 104

Turner's syndrome

Front 105

Horse shoe kidney: compilations?

Back 105

1. Infection
2. Stone formation

Front 106

Cystic diseases of the kidneys: name em

Back 106

1. Renal dysplasia
2. Juvenile polycystic kidney disease
3. Adult polycystic kidney disease

Front 107

Following condition is associated with?

Back 107

Potter facies associated with oligohydramnios-
Unilateral renal agenesis

Front 108

MC cystic disease in children?

Back 108

Renal dysplasia


Inheritance pattern?

Hint 108

None

Front 109

Renal dysplasia: Gross features?

Back 109

Enlarged cystic irregular mass

Presentation is _____(unilateral/bilateral)?

Hint 109

Either

Front 110

Renal dysplasia: Complication?

Back 110

CRF

Front 111

Juvenile polycystic kidney disease: Inheritance pattern?

Back 111

AR


Presentation is bilateral/unilateral?

Hint 111

Bilateral

Front 112

Juvenile polycystic kidney disease: important clinical associations?

Back 112

1. Liver cysts
2. Congenital hepatic fibrosis
--->
3. Portal hypertension

Front 113

Juvenile polycystic kidney disease:
Maternal findings?
Fetal findings at birth?

Back 113

Maternal oligohydramnios

1. Potter facies
2. Low set ears
3. Parrot beak nose
4. Lung hypoplasia

Front 114

Adult polycystic kidney disease: Inheritance pattern?

Back 114

AD


Defect in chromosome ____

Hint 114

Chromosome 16

Front 115

Adult polycystic kidney disease: Common age of occurance?

Back 115

Occurs by the age of 20-25yrs

Front 116

Adult polycystic kidney disease:
Important clinical associations?

Back 116

1. Liver cysts
2. Pancreatic cysts
3. Splenic cysts

4. Hypertension
5. Berry aneurysms-->
6. Strokes/lacunar infarcts
7. Mitral prolapse

8. Sigmoid diverticulitis

9. Renal cell carcinoma

MC of all of the above associations?

Hint 116

Hypertension

Front 117

Adult polycystic kidney disease:
Rx?

Back 117

Renal transplant

Front 118

Gross appearance of Polycystic kidney disease?

Back 118

Multiple cysts spread across the kidneys
Complete destruction of renal architecture
Cysts anywhere in cortex or medulla anywhere along the kidney tubule

Front 119

Medullary sponge kidney: Inheritance pattern?

Back 119

No inheritance pattern

Front 120

Adult polycystic kidney disease: Location of cysts?

Back 120

Located anywhere in the cortex or medulla

Completely destroyed architecture
Anywhere along the tubules

Bilateral

Front 121

MCC of death in Adult polycystic kidney disease?

Back 121

CRF

Front 122

Medullary sponge kidney most often discovered with _____

Back 122

IVP

Front 123

Medullary sponge kidney: Gross appearance?

Back 123

Striations in papillary ducts of medulla
("Swiss cheese appearance")

Front 124

Acquired polycystic kidney disease: MCC?

Back 124

Dialysis


Approximately ___% of people develop

Hint 124

50%

Front 125

In Acquired Polycystic Kidney disease: Complications?

Back 125

Obstruction due to:
1. Interstitial fibrosis
2. Oxalate crystals

Renal cell carcinoma

All polycystic kidney diseases have RCC as a potential complication

Front 126

Characteristic finding in anti-GBM disease?
(Pattern of immunofluorescence)

Back 126

Linear patterned immunofluorescence

Front 127

Proliferative glomerulonephritis more than ____nuclei in a glomeruli

Back 127

More than 100

Front 128

Glomerulopathy that has a thickened glomerulus basement membrane but no proliferative changes

Back 128

Membranous glomerulopathy

Front 129

Glomerulopathy that has a thicknened GB and hypercellular glomeruli

Back 129

Membranoproliferative glomerulonephritis

Front 130

Focal segmental glomerulosclerosis?

Back 130

Fibrosis involving a single segment of the involved glomerulus

Front 131

Crescentic glomerulonephritis?

Back 131

Proliferation of ___ epithelial cells around the glomerulus

Hint 131

Parietal epithelial cells

Front 132

Goodpasture's syndrome shows ____type of pattern on immunofluorescence
(linear/granular)

Back 132

Linear


Why?

Hint 132

Due to uniform distribution of antigens along the BM

(Antibodies line up thus on immunofluorescence)

Front 133

Granular pattern of immunofluorescence indicates ?

Back 133

Immune complex deposition

(Type III hypersensitivity)

Front 134

Electron microscopy is useful to detect?

Back 134

1. Fusion of podocytes
2. Damage to visceral epithelial cells
3. Detect sites of immune complex deposits

What are the sites of immune complex deposits?

Hint 134

1. Subendothelial
2. Subepithelial
3. Intra-membranous
4. Mesangial

Front 135

Mechanisms of glomerular injury?

Back 135

1. Immune complex deposits
2. Antibodies against GBM antigens
3. T-cell producing cytokines

Which of the above types is associated with loss of negative charge of GBM?

Hint 135

T-cell mediated destruction through cytokine production

Front 136

Most of the glomerulonephritides are type _____hypersensitivity

Back 136

Type III

Principal cell that mediates this damage?

Hint 136

Neutrophils

(IC---> activates immune complex--->C5a---> Chemotactic for neutrophils

Front 137

ABs directed against GBM: associated disease?

Back 137

Goodpasture's syndrome

Front 138

Cytokines produced through T-cells:
effects on glomerulus?

Back 138

1. Loss of -ve charge on GBM
2. Fusion of podocyte foot processes

Front 139

Most important clinical/microscopic finding in Nephritic syndrome?

Back 139

RBC casts in urine

Front 140

Is tubular function affected in nephritic syndrome?

Back 140

NO

Front 141

Clinical findings in nephritic syndrome?

Back 141

1. Hypertension
2. Periorbital puffiness

3. Hematuria

4. Proteinuria>150mg/day(<3g/day)
5. BUN: Cr ratio abnormal

Front 142

BUN: Cr ratio in nephritic syndrome?

Back 142

>15
Decreased GFR but intact tubular function

Front 143

Glomerulopathies associated with nephritic syndrome: Name em

Back 143

1. IgA nephropathy(Buerger's disease)
2. Diffuse proliferative glomerulonephritis
3. Post-strept glomerulonephritis
4. (rapidly progressive)Crescentic glomeruonephritis

Which one the above is most frequent/
MCC of Nephritic syndrome?

Hint 143

IgA glomerulonephritis

Front 144

Nephritis associated with bouts of hematuria following upper respiratory tract infection?

Back 144

IgA glomerulopathy

Front 145

Is CRF a complication associated with IgA glomerulopathy?

Back 145

YES

Front 146

Type of immunofluorescence associarted with IgA glomerulopathy?

Back 146

Granular

Front 147

IgA glomerulopathy: pathology?

Back 147

1. Increased mucosal synthesis of IgA
2. Decreased clearance of IgA

Front 148

IgA glomerulopathy is ____(proliferative/non-proliferative) and _____(focal/diffuse)

Back 148

Proliferative and focal

Front 149

IgA glomerulopathy results in deposition of IgA in ____(part of nephron)

Back 149

Mesangium

Front 150

Glomerulonephritides that activate:
1. Classic pathway
2. Alternate pathway

Back 150

1. Classic pathway: Diffuse proliferative glomerulonephritis

2. Alternate pathway:
i. IgA glomeruloptahy
ii. Post-streptococcal glomerulopathy

Front 151

MCC of post-infectious glomerulonephritis: associated pathogen?

Back 151

Group A strept

Usually follows infection of?

Hint 151

Skin or pharynx

Front 152

Type of immunofluorescence in post-strept glomerulonephritis?
(granular or linear)

Back 152

Granular

Front 153

Post-strept glomerulonephritis: _____ deposits(subepithelial/subendothelial )

Back 153

Subepithelial

Front 154

Post strept glomerulonephritis is _____(proliferative/non-proliferative) and ____(diffuse/focal)

Back 154

Proliferative and diffuse

Front 155

Post-strept glomerulonephritis: markers of disease? (antibodies etc)

Back 155

1. Anti DNAse B titres
Streptozyme test+ve

ASO titres ___(-ve/+ve)

Streptozyme test detects?

Hint 155

NEGATIVE
(ASO is degraded by oil in skin)

Detects:
1. Anti-DNAse
2. Anti-hyaluronidase
3. Anti-NAD

Front 156

Does post-strept glomerulonephritis progress to CRF?

Back 156

No

Front 157

Post-strept is usually ____(resolving/non-resolving)

Back 157

Self-resolving

Front 158

IgA nephropathy: does it progress to CRF?

Back 158

YES


Rx?

Hint 158

Steroids
A/hypertensives

Front 159

Diffuse proliferative glomerulonephritis: Major cause?

Back 159

SLE

Front 160

Diffuse proliferative glomerulonephritis has ____(subepithelial/subendothelial) deposits?

Back 160

Subendothelial

Associated microscopic finding?

Hint 160

Wire-looping of capillaries

Front 161

Microscopic pattern observed in Diffuse proliferative glomerulonephritis?

Back 161

"Wirelooping of capillaries"

Hyalin thrombi in capillaries

(Neutrophilic infiltration)

Front 162

Diffuse proliferative glomerulonephritis causes activation of ____(alternate/classic) pathway?

Back 162

Classic


What activates the classic pathway in DPG?

Hint 162

DNA-a/DNA IC

Front 163

Serum ANA test has a ____pattern that corresponds to presence of anti-dsDNA ABs

Back 163

Rim pattern

Front 164

Does diffuse proliferative glomerulonephritis progress to CRF?

Back 164

YES

Front 165

Does RPGN progress to CRF?

Back 165

NO, it progresses to ARF

Wegner's granulomatosis

Front 166

RPGN: important clinical associations?

Back 166

1. Wegner's granulomatosis
2. Goodpaasture's syndrome
3. Microscopic PAN (p-ANCA)
4. Wegner's granulomatosis(c-ANCA)

Front 167

RPGN: HLA association

Back 167

HLA-BR2

Front 168

RPGN: type of immunofluorescence?

Back 168

Linear

Front 169

Glomerulonephritis associated with:
1. MC nephropathy
2. Subepithelial deposits
3. Subendothelial deposits
4. Hematuria with URTI
5. Progress to CRF
6. Associated with ARF
7. "Wire-looping" capillaries
8. Granular IF appearance
9. Linear IF appearance
10. Rim patterned serum test
11. HLA-BR2 association
12. SLE association
13. Self resolving
14. Wegner's granulomatosis
15. Mesangial deposits
16. +ve streptozyme test
17. Plasma exchange for Rx
18. Alternate complement path
19. Classical complement path
20. Requires renal transplant
21. "episodic bouts of hematuria"
22. Diffuse proliferative pattern
23. Focal proliferative pattern
24. Hyaline thrombi in capillary lumen
25. Mimicks Henoch Schnlein Purpura
26. Severe hypertension
27. Parietal cell proliferation
28. Does not require steroids for rx
29. Requires steroids+cyclophosphamide
30. pANCA+ve
31. cANCA+ve
32. Hyaline thrombi
33. No electron dense deposits
34. Good-Pasture syndrome
35. AB against collagen

Back 169

1. MC nephropathy: IgA nephropathy
2. Subepithelial deposits: Post-strept
3. Subendothelial deposits:
Diffuse proliferative(SLE)
4. Hematuria with URTI: IgA nephropathy
5. Progress to CRF: IgA nephropathy +
Diffuse proliferative
6. Associated with ARF: RPGN
7. "Wire-looping" capillaries: Diffuse proliferative
8. Granular IF appearance: Diffuse proliferative
IgA nephropathy
9. Linear IF appearance: RPGN
10. Rim patterned serum test: Diffuse proliferative
11. HLA-BR2 association: RPGN
12. SLE association: Diffuse proliferative
13. Self resolving: Post-strept
14. Wegner's granulomatosis: RPGN
15. Mesangial deposits: IgA nephropathy
16. +ve streptozyme test: Post-strept
17. Plasma exchange for Rx: RPGN
18. Alternate complement path: IgA nephropathy + Post-strept
19. Classical complement path: Diffuse proliferative
20. Requires renal transplant: RPGN
21. "episodic bouts of hematuria": IgA nephropathy
22. Diffuse proliferative pattern: Post-strept + Diffuse proliferative
23. Focal proliferative pattern: IgA nephropathy
24. Hyaline thrombi in capillary lumen: Diffuse proliferative
25. Mimicks Henoch Schnlein Purpura: IgA nephropathy
26. Severe hypertension: Post-strept
27. Parietal cell proliferation: RPGN
28. Does not require steroids for rx: Post-strept
29. Requires steroids+cyclophosphamide: Diffuse proliferative + RPGN
30. pANCA+ve: RPGN
31. cANCA+ve: RPGN
32. Hyaline thrombi: Diffuse proliferative
33. No electron dense deposits: RPGN
34. Good-Pasture syndrome: RPGN
35. AB against collagen: RPGN

Front 170

Injury in nephrotic syndrome to glomeruli is mediated by ____as compared to nephritic syndrome where injury is mediated by ____

Back 170

Nephrotic: Cytokines(T-cells)
Nephritic: Neutrophils

Front 171

Nephrotic syndrome: Effects of damage mediated by cytokines?

Back 171

1. Loss of -ve charge on GBM
2. Fusion of podocytes
(aka effecement of foot processes)

Front 172

Clinical findings in nephrotic syndrome?

Back 172

1. Hypercoagulable state
2. Hypercholesterolemia
3. Hypoalbuminemia
4. Hypogammaglobulinemia
5. Hypertension(in some)
6. Fatty casts (maltese cross)

Front 173

Nephrotic syndrome: Name the diseases

Back 173

1. Minimal change dz
2. Focal segmental glomerulosclerosis
3. Diffuse membranous glomerulopathy
4. Type I MPGN
5. Type II MPGN

(whenever there's a MEMBRANE in the disease name its nephrotic)

Front 174

MCC of nephrotic syndrome in children?

Back 174

Minimal change disease

Front 175

Secondary cause of minimal change disease?

Back 175

Hodgkin's lymphoma

Front 176

Minimal change disease:microscopic findings?

Back 176

1. Normal structured glomerulus
2. +ve fat stains in glomerulus and tubules
3. EM: Fusion of podocytes, no deposits

Front 177

Minimal change disease: Immunofluorescence?

Back 177

Negative

Front 178

Minimal change disease: Normotensive/hypertensive?

Back 178

Normotensive

Front 179

Focal segmental glomerulosclerosis: causes?

Back 179

Primary or
Secondary:
HIV
IV drug abuse(heroin)

Front 180

Focal segmental glomerulosclerosis: Microscopic findings?

Back 180

1. EM: Focal damage of visceral epithelial cells
2.

Front 181

Minimal change disease: Pathogenesis?

Back 181

Loss of -ve charge on GBM--> ____type of proteinuria

Hint 181

Selective(Loss of albumin in urine)

Front 182

Focal segmental glomerulosclerosis: type of proteinuria (selective/non-selective)

Back 182

Non-selective

Front 183

Focal segmental glomerulosclerosis: Does it progress to CRF?

Back 183

YES

Rx?

Hint 183

Cortiosteroids

Front 184

MCC of nephrotic sydrome in adults?

Back 184

Diffuse membranous glomerulopathy

Front 185

Secondary cause of: Diffuse membranous gomerulonephritis?

Back 185

1. Drugs-
i. Caprtopril
ii. Gold therapy

2. Infections:
i. HBV
ii. Plasmodium malariae
iii. Syphilis

3. SLE
4. Carcinoma, Hodgkin's lymphoma

Front 186

Diffuse membranous glomerulonephritis: Microscopic appearance?

Back 186

1. Diffuse thickening of membranes
2. "Spike and dome" appearance on silver staining
3. Subepithelial deposits with granular IF
What is the "spike and dome appearance"?

Hint 186

Spike= GBM
Subepithelial deposits= Dome

Front 187

Diffuse membranous glomerulonephritis:
Deposits are ____(subepithelial/subendothelial)

Back 187

Subepithelial


IF pattern is ____(Linear/granular)

Hint 187

Granular

Front 188

Diffuse membranous glomerulonephritis: Rx?

Back 188

Corticosteroids

Front 189

Nephrotic syndrome that is preceded by respiratory tract infection?

Back 189

Minimal change disease

Front 190

SLE associated nephritic syndrome?
SLE associated nephrotic syndrome?

Back 190

Nephritic: Diffuse proliferative
Nephrotic: Diffuse membranous

MOA of both?

Hint 190

1. Diffuse proliferative activates classical pathway
2. Diffuse proliferative mediated by T-cell cytokines

Front 191

MC type of MPGN?
(Type I or Type II)

Back 191

Type I

Front 192

Type MPGN has ____presentation (nephrotic or nephritic)?

Back 192

Can be either: 60% of times its nephrotic

Front 193

Type I MPGN: important clinical associations?

Back 193

1. HBV
2. HCV
3. Cryoglobulinemia

Front 194

Type I MPGN: Sub-____(endothelial/epithelial) deposits?

Back 194

Subendothelial deposits
IF +ve

Front 195

Type I MPGN: Microscopic features?

Back 195

1. Subendothelial deposits
2. +ve IF
3. Tram tracking d/t splitting of GBM by mesangial ingrowth

Front 196

Type I MPGN may/may not progress to CRF?

Back 196

Majority progress to CRF

Front 197

Type II MPGN: Pathology?

Back 197

Sustained activity of C3

(D/t autoAB against C3 nephritic factor convertase--->inhibits it--->prevents degradation of C3)

Front 198

Type II MPGN: Microscopic findings?

Back 198

1. Intramembranous deposits
"dense deposit disease"
2. EM: Tram tracks

Front 199

Type II MPGN: does it progress to CRF?

Back 199

YES

Front 200

Nephrotic syndrome associated with/ is/ etc:
1. Selective proteinuria
2. Non-selective proteinuria
3. Hematuria
4. "dense-deposit disease"
5. Microscopic hematuria
6. Captopril
7. Cryoglobulinemia
8. "Spike and dome" pattern
9. Usually "normotensive"
10. Hodgkin's lymphoma
11. Subepithelial deposits
12. Subendothelial deposits
13. "Tram tracks"
14. Plasmodium malariae
15. Syphilis
16. HIV
17. +ve fat stain in glomerulus and tubules
18. Progression to CRF
19. No CRF progression
20. No deposits/-ve IF
21. SLE
22. Classical and alternate path activation
23. Hypertension
24. No/minimal response to steroids
25. May have neprotic or nephritic presentation
23. "early" hypertension
24. Normal microscopic structure
25. Respiratory infection
26. Focal Visceral epithelial damage
27. Immunization
28. Silver stained used
29. Gold therapy
30. Carcinoma
31. "Intramembranous" deposits
32. GBM ingrowth of Mesangium
33. Diffuse membrane thickening
34. HBV
35. Decreased C3 levels
36. IV heroin abuse
37. -ve IF

Back 200

1. Selective proteinuria: Minimal change disease
2. Non-selective proteinuria: Focal segmental glomerulosclerosis
3. Hematuria: MPGN I and II
4. "dense-deposit disease": MPGN type II
5. Microscopic hematuria: Focal segmental GS
6. Captopril: Diffuse membranous glomerulopathy
7. Cryoglobulinemia: MPGN type I
8. "Spike and dome" pattern: Diffuse membranous GP
9. Usually "normotensive": Minimal change
10. Hodgkin's lymphoma: Minimal change, Diffuse membranous GP
11. Subepithelial deposits: Diffuse membranous GP
12. Subendothelial deposits: MPGN type I
13. "Tram tracks": MPGN Type I and II
14. Plasmodium malariae: Diffuse membranous GP
15. Syphilis: Diffuse membranous GP
16. HIV: Focal segmental GS
17. +ve fat stain in glomerulus and tubules: Minimal change
18. Progression to CRF: Type I and II MPGN, Focal segmenatal and Diffuse membranous
19. No CRF progression: Minimal change
20. No deposits/-ve IF: Minimal change, Focal segmental GS
21. SLE: Diffuse membranous GP
22. Classical and alternate path activation: MPGN Type I
23. Hypertension: FSGS, MPGP, MPGNs
24. No/minimal response to steroids: FSGS, MPGNs
25. May have neprotic or nephritic presentation: MPGNs
23. "early" hypertension: FSGS
24. Normal microscopic structure: Minimal change
25. Respiratory infection: Minimal change
26. Focal Visceral epithelial damage: FSGS
27. Immunization: Minimal change
28. Silver stained used: Diffuse membranous
29. Gold therapy: Diffuse membranous
30. Carcinoma: Diffuse membranous
31. "Intramembranous" deposits
32. GBM ingrowth of Mesangium: MPGNs
33. Diffuse membrane thickening: Diffuse membranous
34. HBV: Type I MPGN, Diffuse membranous
35. Decreased C3 levels: MPGN type II
36. IV heroin abuse: FSGS
37. -ve IF: FSGS, minimal change

Front 201

Diabetes associated glomerulopathy?

Back 201

Nodular glomerulosclerosis

(Kimmelstiel-Wilson disease)

Front 202

MCC of renal failure in the United States?

Back 202

Nodular glomerulosclerosis

Front 203

Which has a higher incidence of renal failure in the US:
1. Type I DM or
2. Type II DM?

Back 203

Type I DM

Front 204

Which disease has a high correlation with diabetic glomerulopathy?

Back 204

Diabetic glomerulopathy

Front 205

Pathogenesis of Diabetic glomerulopathy?

Back 205

1. Non-enzymatic glycosylation of the GBM---> Glucose attaching to AA---> Increases vessel and tubular permeability

2. Arterolosclerosis of efferent arterioles
(efferent before afferent)

3. Osmotic damage to glomerular endothelial cells

4. Hyperfiltration damage to mesangium

5. Increased deposition of GBM(type IV collagen)

Front 206

Diabetic glomerulopathy: Increased deposition of type IV collagen in GBM in which 3 structures of nephron tubules?

Back 206

1. Mesangium
2. Tubular BM
3. Glomerular BM

Front 207

Diabetic glomerulopathy: microscopic findings?

Back 207

1. Nodular masses in mesangial matrix
2. Arteriolosclerosis (efferent>afferent)
3. Fusion of podocytes on EM
4. Non specific immunofluorescence

Front 208

Is there IF in diabetic glomerulopathy?

Back 208

YES

Front 209

Initial laboratory manifestation of diabetic glomerulopathy?

Back 209

Microalbuminuria

When does it happen after developing diabetes?

Hint 209

After 10 years of poor glycemic control

Front 210

Microalbuminuria is detected by dipstick at ranges as less as___?

Back 210

1.5 mg/dl

Front 211

What is the significance of detecting microalbuminuria in terms of rx?

Back 211

Microalbuminuria indicates initiation of rx with ACE inhibitors

(Decreases AT-II mediated vasoconstriction of efferent areterioles)- Mechanism INDEPENDENT of BP lowering mechanism of these drugs

Front 212

Renal diseases associated with DM?

Back 212

1. Diabetic glomerulopathy
2. Renal papillary necrosis
3. Acute/chronic pyelonephritis

Front 213

Hereditary glomerulonephritis?

Back 213

1. Alport's syndrome
2. Benign familial hematuria

Front 214

Alport syndrome: Hereditary pattern?

Back 214

Autosomal dominant

Front 215

Alport syndrome: Pathology?

Back 215

AB against GBM (type IV collagen)

Front 216

Alport syndrome: Microscopic findings?

Back 216

Lipid accumulation in visceral epithelial cells---->
aka "FOAM CELLS"

Front 217

Alport syndrome: Clinical findings?

Back 217

Sensorineural hearing loss + ocular abnormalities

Front 218

Benign familial hematuria: pathology?

Back 218

Extremely thing GBM

Front 219

Chronic glomerulonephritis: MCC? other causes?

Back 219

#1 RPGN
#2 FSGS
#3 MPGN type I
#4 Membranous glomerulopathy
#5 Diffuse proliferative
#6 IgA nephropathy

Front 220

Chronic glomerulonephritis: gross features?
Microscopic features?

Back 220

Gross:
1. Shrunken kidney

Microscopic:
1. Tubular atrophy
2. Glomerular sclerosis

Front 221

Acute renal failure: Most common cause?

Back 221

Acute tubular necrosis

Front 222

Acute renal failure: definition?

Back 222

Suppression of renal function developing in 24 hrs

Accompanied by anuria or oliguria(<400ml/day)

Front 223

Types of acute tubular necrosis?

Back 223

1. Ischemic
2. Nephrotoxic

Front 224

Ischemic damage to tubular cells: pathogenesis?

Back 224

1. Hypotension/shock--->Prerenal azotemia--->Ischemia to endothelial cells--->Decrease in vasodilators(NO, PGI2) and increase in vasoconstrictors (endothelins)--->vasoconstriction--->Decreased GFR

2. Ischemia--->Tubular cell damage---> Detachment of tubular cells into the lumen---> As "Pigmented renal tubular cells"----> Obstruction--->
1. Decreases GFR
2. Fluid accumulates in the interstitium
3. Oliguria

Front 225

Ischemic tubular necrosis: Sites of tubular damage?

Back 225

1. Straight part of proximal tubule
2. Medullary segment of thick ascending loop
3. Tubular BM disruption

Front 226

Nephrotoxic tubular necrosis: Causes? including MCC?

Back 226

#1 AG (Gentamicin)
2 Radiocontrast agents
3 Heavy metals- lead, mercury
4 Drugs (Polymyxin, Methicillin, Sulfonamides)

Front 227

Nephrotoxic tubular necrosis: Microscopic findings

Back 227

Proximal tubule cell damage
Pigmented tubular cell casts

Front 228

Condition associated with "pigmented tubular epithelial cells"

Back 228

Acute tubular necrosis
(either ischemic or nephrotoxic)

Front 229

Acute tubular necorosis: Clinical/laboratory findings?

Back 229

1. Oliguria
2. Pigmented renal tubular casts
3. Hyperkalemia
4. Anionic gap acidosis
5. BUN/Cr<15
6. Hypokalemia in diuretic phase


MAINLY
Hyperkalemia + Acidosis + BUN: Cr<15

Front 230

Acute tubular necrosis: Associated electrolyte imbalance

Back 230

1. Hyperkalemia
2. Acidosis
3. Hypokalemia in diuresis phase

Front 231

Acute tubular necrosis:
Rx?

Back 231

1. Rx pre-renal azotemia
2. Low dose dopamine
3. Fenoldopam
4. Dialysis

Front 232

Tubulointerstitial nephritis: Causes?

Back 232

1. Acute pyelonephritis
2. Drugs: methicillin
3. Infections: Legionnaire's disease, Leptospirosis
4. SLE
5. Lead poisoning
6. Urate nephropathy
7. Multiple myeloma

(Remember renal conditions caused by SLE:
1. Diffuse membranous
2. Diffuse proliferative
3. Tubulointerstitial nephritis)

Front 233

Nephrotoxicities associated with lead poisoning?

Back 233

1. Nephrotoxic ATN
2. Tubulointerstitial nephritis

Front 234

Acute pyelonephritis: Commonly affects what patient population?

Back 234

Women


why?

Hint 234

Since urethra in women in short in length

Front 235

MCC of acute pyelonephritis?

Back 235

E-coli

2nd MCC:
Enterococci

Front 236

Acute pyelonephritis: risk factors?

Back 236

1. Indwelling catheter
2. Urinary tract obsrtuction
3. Medullary sponge kidney
4. Diabetes mellitus
5. Pregnancy
6. Sickle cell disease

Front 237

Acute pyelonephritis: Pathogenesis?

Back 237

1. Vesico-ureteric reflux(Intravesical portion of the ureter is inadequately compressed-->reflux)

2. Ascending infections (E-coli)from urethritis/ cystitis

3. Hematogenous spread
(uncommon)

Front 238

When is hematogenous spread(as a cause) of pyelonephritis suspected?

Back 238

When the causative/isolated organism turns out to be staph aureus

Front 239

Acute pyelonephritis: Gross features?

Back 239

1. Grayish white areas of abscess in cortex/medulla
2. Micro-abscess formation in tubular lumens and interstitium

(Mainly ABSCESSES)

Front 240

Acute pyelonephritis: Clinical features?

Back 240

1. Spiking fever
2. Increased frequency of urination
3. Painful urination

(Acute pyelonephritis:
1. Fever
2. Flank pain
3. WBC casts)

Front 241

Acute pyelonephritis: Laboratory features?

Back 241

1. Pyuria
2. Hematuria
3. Bacteriuria(E-coli)

Front 242

Acute pyelonephritis: Complications?

Back 242

1 Chronic pyelonephritis
2. Perinephric abscess
3. Renal papillary necrosis
4. Septicemia/with shock

Front 243

Chronic pyelonephritis: Pathogenesis?

Back 243

Repeated attacks of Acute pyelonephritis
(Vesic-ureteric reflux starting in young girls)

2. Lower UTI --->
Hydronephrosis
(prostate hyperplasia, renal stones)

Front 244

Types of Chronic pyelonephritis?

Back 244

1. Reflux type
2. Obstructive type

Front 245

Gross findings in reflux type of pyelonephritis?

Back 245

1. U-shaped cortical scars over the calyx
2. Blunt calyx (visible through IVP)

Front 246

Gross findings in obstructive type of pyelonephritis?

Back 246

1. Uniform dilation of calyces
2. Thinning of cortical tissues

Front 247

Chronic pyelonephritis: Clinical findings?

Back 247

1. Recurrent attacks of acute pyelonephritis
2. Hypertension
3. Progression to CRF

Front 248

Chronic pyelonephritis is a common cause of _____in chidldren

Back 248

Hypertension

Front 249

Chronic pyelonephritis: Microscopic findings?

Back 249

1. Chronic inflammation (scarring of glomeruli)
2. Tubular atrophy
"thyroidization of tubule":
Eosinophilic material filling the tubules. (resembles thyroid tissue)

Front 250

Acute drug induced tubulo-interstitial nephritis: associated drugs?

Back 250

1. Penicillin
2. **Methicillin**
3. Rifampin
4. Sulfonamides
5. NSAIDs
6. Diuretics

Front 251

Sulfonamides: nephrotoxic effects?

Back 251

1. Nephrotoxic ATN
2. Tubulointerstitial nephritis

Front 252

Pathogenesis: Tubulointerstitial nephritis: (type of hypersensitivity)

Back 252

Combination of Type II and Type IV hypersensitivity

When does it occur?

Hint 252

2-4 weeks after beginning a drug

Front 253

Tubulointerstitial nephritis: Clinical findings?

Back 253

Fever
Oliguria
Rash

WITHDRAWAL OF DRUG CEASES DISEASE

Front 254

Tubulointerstitial nephritis: Laboratory findings?

Back 254

BUN: Cr<15
Eosinophilia
Eosinophiluria

Front 255

Analgesic nephropathy: Common patient population affected?

Back 255

Patient in chronic pain

Front 256

Analgesic nephropathy occurs after ____ (time) of aspirin usage

Back 256

>= 3 years

Pathogenesis of aspirin in analgesic nephropathy?

Hint 256

Renal synthesis of PGE2 is inhibited leaving ATII unopposed---> Decreased blood flow

Front 257

Effects of analgesic nephropathy (complications)?

Back 257

1. Renal papillary necrosis
(sloughing of renal papillae)
2. Hypertension
3. Transitional cell carcinoma
4. CRF

Front 258

Does analgesic nephropathy progress to CRF?

Back 258

YES

Front 259

Analgesic nephropathy: X-ray findings?

Back 259

"Ring" sign on IVP

Front 260

Urate nephropathy: pathology?

Back 260

Deposition of urate crystals in ____and ____ (regions of nephrons)

Hint 260

Tubules and interstitium

Front 261

Urate nephropathy: Causes?

Back 261

1. Rx of cancer
2. Lead poisoning
3. Gout

Front 262

Patients with disseminated cancers should receive _____ before being treated for chemotherapy to avoid tumor lysis syndrome(urate nephropathy)

Back 262

Allopurinol

Front 263

Chronic lead poisoning: Pathogenesis?

Back 263

1. Decreased uric acid excretion (urate nephropathy)--->gout
2. Tubulointerstitial nephritis
3. Nephrotoxic ATN


Microscopic findings?

Hint 263

Proximal tubule cells contain acid fast inclusions

Front 264

Multiple myeloma: Effect on kidney?

Back 264

BJ proteinuria--->tubular casts---> obstruct the lumen---> Giant body reaction --->
Affects tubules + interstitium
--->
Renal failure

Front 265

Nephrocalcinosis: Cause?

Back 265

Due to hypercalcemia
(metastatic calcification)

Front 266

Hypercalcemia: effect in kidneys?

Back 266

Metastatic calcification of BM of collecting tubules--->
Polyuria
Renal failure

Front 267

Chronic renal failure: definition?

Back 267

Progressive irreversible azotemia
GFR<10mL/min

Front 268

CRF: causes?

Back 268

1. Diabetes mellitus
2. Hypertension
3. Chronic glomerulonephritis
4. Cystic renal disease

Front 269

CRF: gross appearance?

Back 269

Bilaterally shrunken kidneys

Front 270

CRF: hematologic effect?

Back 270

1. Normocytic anemia with reticulocytes <3%
(due to decreased erythropoetin)
2. Qualitative platelet defects

Front 271

Renal osteodystrophy: types?

Back 271

1. Osteitis fibrosa cystica
2. Osteomalacia
3. Osteoporosis

Front 272

Osteitis fibrosa cystica: pathogenesis?

Back 272

Hypovitaminosis D--> Hypocalcemia--> PTH increase--> Increases bone resorption--->
Cystic lesions in the bone--->
Hemorrhage into the cystic lesions-->
Brown discoloration

Front 273

Osteomalacia: Pathogenesis?

Back 273

Hypovitaminosis D---> Hypocalcemia----> Decreased bone mineralization--->
Fx and bone pain

Front 274

Osteoporosis: Pathogenesis?

Back 274

Loss of organic bone matrix and minerals--->
Reduced bone mass

Chronic metabolic acidosis--->
Excess H+ get buffered

Front 275

Renal osteodystrophy: Cardiovascular findings?

Back 275

1. Hypertension
2. Hemorrhagic fibrinous pericarditis
3. CHF
4. Accelerate atherosclerosis

Front 276

CRF: Electrolyte abnormalities?

Back 276

1. Acidosis
2. Hyperkalemia
3. Hyponatremia
4. Hypocalcemia

Front 277

Hypocalcemia: effects?

Back 277

Hyperphosphatemia
(Due to decreased excretion of PO4)--->
Drives calcium into bone and soft tissue

"Metastatic calcification"

Front 278

Biomarker of kidney function?

Back 278

Cystatin C

Front 279

Rx for CRF?

Back 279

Non pharmacological
1. Sodium restriction
2. Low protein diet
3. Kidney transplant

General:
1. ACE inhibitors
2. Dialysis
3. EPO stimulators
4. Calcium supplementation
5. Phosphate binders

Name one phosphate binder

Hint 279

Sevelamer

Front 280

Microscopic findings in essential hypertension?

Back 280

1. Hyaline arteriolosclerosis
2. Tubular atrophy
3. Interstitial fibrosis
4. Glomerular sclerosis

Front 281

Hypertension: Gross findings?

Back 281

Small kidneys with granular cortical surface

Front 282

Benign nephrosclerosis: Gross renal findings?

Back 282

Small kidneys with granular cortical surface

Front 283

Malignant hypertension: Risk factors?

Back 283

1. Pre-existing BNS
2. HUS
3. TUP
4. Systemic sclerosis

Front 284

Malignant hypertension:
Microscopic findings?

Back 284

1. "Onion skin appearance" of arteriolar walls
(Smooth muscle hyperplasia and BM duplication)

2. Fibrionoid necrosis
3. Necrotizing arteriolitis
4. Glomerulitis

(Pinpoint hemorrhage on cortical surface)

Front 285

Malignant hypertension:
Clinical findings?

Back 285

1. Rapid increase in BP>210/120
2. Hypertensive encephalopathy
3. Oliguric ARF

Front 286

Hypertensive encephalopathy: findings?

Back 286

1. Cerebral edema
2. Papilledema
3. Retinopathy
4. Intracerebral bleed

Papilledema?
Retinopathy?

Hint 286

Pappiledema: Loss of margins of optic disk
Retinopathy: flame hemorrhage

Front 287

Malignant hypertension: Laboratory findings?

Back 287

1. Azotemia
2. Hematuria with RBC casts
3. Proteinuria

BUN/Cr ratio<15

Front 288

Malignant hypertension: Rx?

Back 288

IV Na-nitroprusside

Front 289

Causes of renal infarction?

Back 289

1. Embolization(left side heart)
2. Atheroembolic renal disease
3. Vasculitis (Polyarteritis nodosa)

MCC of renal infarction?

Hint 289

Embolization

Front 290

Renal infarction:
1. Type of infarct: ___(pale/hemorrhagic)
2. Common site: _____(Cortex/medulla)

Back 290

1. Pale infarct
2. Cortex

Front 291

Renal infarct: Gross findings?

Back 291

Pale infarct in cortex
Irregular/ wedge shaped

Old infarcts: "V-shaped" scar tissue

Front 292

Renal infarcts: clinical findings?

Back 292

Sudden onset flank pain and hematuria

Front 293

Sickle cell disease: renal disease?

Back 293

Infarcts


How are the clinical features different from renal infarction of other causes?

Hint 293

**Painless** hematuria

Front 294

Renal effects of sickle cell disease?

Back 294

1. Renal infarcts
2. Renal papillary necrosis
3. Pyelonephritis
(renal papillary necosis may lead to pyelonephritis)

Front 295

Diffuse cortical necrosis: is a complication of ______

Back 295

Pre-eclampsia/abruptio placentae

Front 296

Diffuse cortical necrosis: Pathogenesis?

Back 296

Pre-eclampsia/abruptio placentae--> DIC---> ____(Cortical/Medullary)necrosis

Hint 296

Cortical necrosis

Front 297

Diffuse cortical necrosis: Microscopic findings?
Gross findings?

Back 297

Microscopic findings: Fibrin clots in arterioles and glomerular capillaries

Front 298

Diffuse cortical necrosis: Gross findings?

Back 298

**Bilateral**
Diffuse
Pale infarcts

Front 299

Diffuse cortical necrosis: Diagnosis (3 clinical findings)

Back 299

Anuria followed by ARF
in a pregnant woman

Front 300

Obstructive disorders:
Name em

Back 300

1. Hydronephrosis
2. Renal stones
3. Angiomyolipoma
4. Renal cell carcinoma

Front 301

Hydronephrosis: causes?

Back 301

1. Renal stone
2. Retroperitoneal fibrosis
3. Cervical ca/BPH

Front 302

Drug associated with retroperitoneal fibrosis?

Back 302

Methylsergide

Front 303

Hydronephrosis: gross findings?

Back 303

1. Dilated ureter and renal pelvis
2. Compression atrophy of renal medulla and cortex

Front 304

Hydronephrosis: rx?

Back 304

Relieve obstruction: Catheter
Nephrostomy tube
Cystoscopy

Front 305

Renal stone/Urolithiasis: More common in ___(males/females)

Back 305

Males

Front 306

Causes of renal stones:
Most common metabolic cause?
Other causes?

Back 306

1. Hypercalciuria in absence of hypercalcemia
(due to increased absorption of calcium from the gut)

2. Decreased urine volume (concentrates the urine)

3. Reduced urine citrate (citrate chelates Ca)
4. Primary HPTH
5. Dairy products
6. Urinary infection

Common bacteria associated with formation of renal stones?

Hint 306

Proteus

Front 307

Types of renal stones?

Back 307

1. Ca-oxalate
2. Ca-phosphate
3. Magnesium-ammonium-phosphate
4. Uric acid
5. Cysteine

Front 308

MC type of stone in adults?
MC type of stone in children?

Back 308

Adults: Ca-oxalate
Children: Ca-phosphate

Front 309

Ca-oxalate stones are commonly observed in _____

Back 309

Vegans

GI condition associated with increased incidence of Ca-oxalate stone?

Hint 309

Crohn's disease

Front 310

Calcium phosphate stones are associated with _____

Back 310

Dairy consumption

Renal condition associated with Ca-phosphate stone incidence?

Hint 310

Renal tubular acidosis

Front 311

Magnesium ammonium phosphate stone: associated condition as a cause?

Back 311

Proteus infection

Front 312

Renal stones: Clinical findings?

Back 312

1. Flank tenderness-sudden onset
2. Nausea and vomiting
3. Colicky pain
4. Restlesness from pain
5. Gross hematuria

Front 313

Renal stones: Laboratory findings?

Back 313

1. Hematuria
2. Crystals in urine
3. Hypercalcemia (HPTH)

Front 314

Renal stones: Dx?

Back 314

1. Plain film: KUB
2. Ultrasound

Test with highest sensitivity and specificity for detecting renal stones?

Hint 314

Unenhanced spiral CT

Front 315

Use of ultrasound in renal stones: how does it help in dx?

Back 315

Mainly detects hydronephrosis

Front 316

Renal stone:
Ca stones : rx?

Back 316

Ca stones
1. Hydrochlorothiazide
2. Cellulose phosphate

Uric acid stones:
1. Allopurinol
2. Increased urinary pH

Struvite(MAP) stones:
Sx removal
AB to remove urease producers
(due to size- sx required)

Front 317

Sx removal of renal stones?

Back 317

1. Extracorporeal shock wave lithotripsy
2. Ureteroscopic stone extraction

Front 318

Angiomyolipoma?

Back 318

Hamartoma of blood vessels, smooth muscles, adipose cells

Front 319

Angiomyolipoma: Clinical associations?

Back 319

Tuberous sclerosis

Front 320

Renal cell carcinoma: More common in _____men/women

Back 320

Men

Front 321

Renal cell carcinoma: risk factors?

Back 321

1. Smoking
2. Von-Hippel Lindau dz
3. ADPKD
4. Obesity
5. Asbestos
6. Lead

Front 322

Von-Hippel Lindau disease: Inheritance pattern?

Back 322

AD

Defect on chromosome____?

Hint 322

Chromosome 3

Front 323

VHL: associated tumors?

Back 323

Hemangioblastomas in___ and ___
RCC

Hint 323

Hemangioblastomas in cerebellum and retina

(Bilateral RCC)

Front 324

Renal cell carcinoma: Pathogenesis?

Back 324

Sporadic-->
TRANSLOCATION with loss of VHL supressor gene

Front 325

Renal cell carcinoma: Gross appearance?

Back 325

1. Hemorrhagic
2. Cystic
3. Bright yellow
4. Size>3cm

Front 326

Renal cell carcinoma: microscopic finding?

Back 326

Clear cell carcinoma-

What are clear cells? (contents)

Hint 326

Contain lipid and glycogen

Front 327

Renal cell carcinoma has a tendency to invade _____

Back 327

IVC----> right side of the heart

Front 328

Renal cell carcinoma: common sites for metastasis?

Back 328

1. Lungs
2. Bone
3. LNs
4. Skin

Front 329

Renal mets to lung shows ____appearance on X-ray

Back 329

"Cannonball" appearance on X-ray/radiograph
(hemorrhagic)

Front 330

Renal cell carcinoma: sign of poor prognosis?

Back 330

Renal cell carcinoma invasion into the renal vein

Front 331

Renal cell carcinoma: Triad?

Back 331

1. Hematuria
2. Abdominal mass
3. Flank pain

Others:
1. HTN
2. FEVER
3. Weight loss
4. Left sided varicocele

Front 332

Renal cell carcinoma: Laboratory findings?

Back 332

1. Elevated ESR
2. Normocytic anemia
3. EPO secretion--->polycythemia
4. PTH related peptide--->
Hypercalcemia

Another tumor conidtion that also secretes PTH related peptide and EPO?

Hint 332

Hepatocellular carcinoma

Front 333

Renal cell carcinoma: Dx?

Back 333

Ultrasound
Abdominal CT
MRI

Front 334

Renal cell carcinoma: Rx?

Back 334

Nephrectomy

Front 335

Renal cell carcinoma: when does mets typically occur?

Back 335

LATE mets
(10-20 yrs after tumor removal)

Front 336

Renal cell carcinoma: What indicates poor prognosis?

Back 336

1. Invasion into the renal vein
2. Penetration through the renal capsule

Front 337

Renal pelvic cancer: Name em

Back 337

1. Transitional cell carcinoma
2. Squamous cell carcinoma

Front 338

Transitional cell carcinoma: risk factors?

Back 338

1. Smoking
2. Phenacetin use
3. Aromatic amines(aniline)
4. Cyclophosphamide

Front 339

Squamous cell carcinoma: risk factors?

Back 339

1. Renal stones
2. Chronic infections

Front 340

MC primary renal tumor in children?

Back 340

Wilm's tumor

Front 341

Wilm's tumor: Which is more common: sporadic or genetic?

Back 341

Sporadic

Front 342

Wilm's tumor: genetic type- Inheritance pattern?

Back 342

AD

Defect on chromosome ___?

Hint 342

Chromosome 11

Front 343

Wilm's tumor: Genetic type- associated anomalies?

Back 343

WAGR syndorme:
1. Wilm's tumor
2. Aniridae
3. Genital anomalies
4. Retardation

Beckwith-Wiedemann syndrome:
1. Wilm's tumor
2. Enlarged body organs
3. Hemihypertrophy of extremities

Front 344

Wilm's tumor: gross appearance?

Back 344

1. Large
2. Necrotic
3. Grey/tan

Front 345

Wilm's tumor is derived from_____

Back 345

Mesonephric mesoderm

Front 346

Wilm's tumor: Microscopic features?

Back 346

1. Abortive glomeruli and tubules
2. Primitive blastemal cells
3. Rhabdomyoblasts

Front 347

Wilm's tumor : typical presentation?

Back 347

Child with unilateral flank mass and hypertension

Front 348

Wilm's tumor: cause of hypertension?

Back 348

Renin secretion

Front 349

MC site for mets in Wilms tumor?

Back 349

Lungs

Front 350

MCC of transitional cell carcinoma?

Back 350

Smoking