renal disease

Question 1

Origin of majority of glomerular disorders

Answer 1

Immune in origin

Question 2

Damage to glomerulus may consist of:

Answer 2

cellular proliferation
leukocytic infiltration
thickening of the glomerular basement membrane

Question 3

Scarring of glomerulus

Answer 3

sclorosis

Question 4

Non-immune causes of glomerular damage

Answer 4

Chemicals and toxins
disruption of the wall of negativity
deposition of amyloid material
basement membrane thickening

Question 5

Glomerulonephritis

Answer 5

Sterile, inflam process
blood, proteins, casts in urine

Question 6

Acute post-strep glomerulonephritis

Answer 6

damage to glomerular membrane
symptoms: oliguria, hematuria
following a group A strep infection (M proteins in the cell wall)

Question 7

Acute post strep glomerulonephritis findings

Answer 7

Immune complexes deposited at glomerular membranes
Elevated: BUN and ASO titer

Question 8

Rapidly Progressive Glomerulonephritis (Crescentic)

Answer 8

More serious acute Glomerular disease
Example is SLE
Symptoms started by deposition of immune complexes
Crescentic formations containing macrophages, fibroblasts, polymerized fibrin

Question 9

RPGN Findings

Answer 9

Markedly elevated protein
GFR decreases as disease progresses
Eventually loss of function (glomerulosclerosis)

Question 10

Goodpasture’s Syndrome

Answer 10

Follows viral respiratory infections
Cytotoxic autoantibodies
Anti-glomerular basement membrane antibody
detectable in serum

Question 11

Goodpasture syndrome antibody

Answer 11

Attaches to basement membrane
initiates complement
produces capillary destruction

Question 12

Goodpasture’s findings

Answer 12

proteinuria, RBCs/RBCs casts
progress to end stage renal failure

Question 13

Vasculitis

Answer 13

systemic vascular system
Wegener’s Granulomatosis
Henocj-Schonlein purpura

Question 14

Vasculitis Findings

Answer 14

Similar to acute glomerulonephritis
Kidney dmg due to: immune complex, autoantibodies, immune mediated inflamm
Antineutrophilic cytoplasmic antibody (ANCA)

Question 15

Henoch-Schonlein purpura

Answer 15

Children following upper respiratory infection
Red patches on skin

Question 16

Henoch-Schonlein purpura findings

Answer 16

increased protein
RBC/RBC casts
Raised platelets. distinguishes from TTP and ITP

Question 17

Membranoproliferative GN
Membranous GN

Answer 17

M-GN -> IgG complexes
Mprolif GN -> children

Question 18

Membranous glomerulonephritis

Answer 18

Thickening of basement membrane
IgG complexs
Proteinuria, RBCs, tend towards thrombosis

Question 19

Membranoproliferative GN

Answer 19

Type 1: Thickening of Bowman’s capsule wall
Type 2: dense deposits in Glomerular basement membrane
Children
poor prognosis

Question 20

Membranoproliferative GN findings

Answer 20

decreased serum complement
RBCs
Proteinuria

Question 21

Berger’s disease

Answer 21

Most common glomerular nephritis
serum increase in IgA
Mucosal infection

Question 22

Berger’s disease findings

Answer 22

Macroscopic hematuria
follows infection or strenuous exercise
20-40% of people suffer chronic GN

Question 23

Chronic GN

Answer 23

Accumulation of damage from acute GN
symptoms: fatigue, anemia, hypertension
edema, oliguria
Findings: Hematuria, Proteinuria, Glycosuria, decrease eGFR, increase BUN and creatinine

Question 24

Nephrotic syndrome

Answer 24

Massive proteinuria
low serum albumin
high serum lipids
pronounced edema (due to low albumin)

Question 25

Nephrotic syndrome findings

Answer 25

proteinuria RBC fat droplets oval fat bodies RTE epi cells fatty/waxy casts

Question 26

minimal change disease

Answer 26

lipid nephrosis some proteins pass through glomerulus

Question 27

minimal change disease findings

Answer 27

edema fat droplets market proteinuria hematuria Unknown etiology

Question 28

Focal segmental glomerulosclerosis (FSGS)

Answer 28

only certain glomeruli elevated protein/RBCs IgM and C3

Question 29

FSGS Associations

Answer 29

Unknown Genetic heroin abuse/drug toxicity HIV Diabetes Infection

Question 30

Alport syndrome

Answer 30

inherited disorder Basement membrane thins

Question 31

Diabetic nephropathy

Answer 31

Most common cause of end stage renal disease monitored via microalbumin testing

Question 32

Diabetic nephropathy damage

Answer 32

GM thickening proliferation of mesangial cells deposition of cellular material vascular sclerosis

Question 33

Tubular disorders

Answer 33

damage to tubules (antifreeze) Metabolic/hereditary disorder

Question 34

Acute Tubular Necrosis (ATN)

Answer 34

Damage to the RTEs Ischemia: decrease blood flow -> lack of O2 Toxic Substances: Aminoglycosides, antifungals, antifreeze, etc

Question 35

ATN findings

Answer 35

Lots of casts of various sorts RTE cells

Question 36

Fanconi's syndrome

Answer 36

Failure of tubular reabsorption (proximal convoluted tubules) Substances affected: phosphorous, Na, K, Bicarb, H2O Can acquire from heavy metals and MM

Question 37

Nephrogenic Diabetes insipidus

Answer 37

Don't respond to ADH Low specific gravity urinate frequency

Question 38

Renal Glycosuria

Answer 38

Reabsorption of glucose affected normal serum glucose, increased urine glucose

Question 39

Interstitial disease

Answer 39

affect the interstitium infection and inflamm most common: UTI

Question 40

Cystitis

Answer 40

Most common UTI Infection of bladder

Question 41

Cystitis findings

Answer 41

WBCs Bacteria RBCs Proteinuria

Question 42

Acute pyelonephritis

Answer 42

upper UTI Bacteria ascending from lower UTI conditions: calculi, pregnancy, urine reflux

Question 43

Acute pyelonephritis findings

Answer 43

WBC casts (tubular infection). Differentiates between upper and lower UTI

Question 44

Chronic pyelonephritis

Answer 44

Congenital structural defects Can't empty collecting ducts often in children

Question 45

Chronic pyelonephritis findings

Answer 45

WBC casts Granular/waxy/broad casts (tell urinary status)

Question 46

Acute Interstitial Nephritis (AIN)

Answer 46

NO BACTERIA Inflamm of renal interstitium or tubules Allergic reaction to medications

Question 47

AIN WBCs/stains

Answer 47

Eosinophils (Allergic reaction) Hansel stain

Question 48

AIN findings

Answer 48

Absence of bacteria Eosinophils

Question 49

Renal Failures

Answer 49

Acute and chronic Final stage: end stage renal failure

Question 50

Renal failure findings

Answer 50

Marked decreased GFR Rise in BUN Electrolyte imbalance Lack of renal concentrating ability proteinuria, glucosuria waxy/granular/broad casts

Question 51

Acute renal failure

Answer 51

Sudden loss, frequently reversible Pre -> decrease in blood flow Renal -> acute glomerular/tubular disease Post -> stones/tumor obstruction

Question 52

Acute renal failure

Answer 52

RTE/casts -> acuter tube necrosis WBC casts -> interstitial infection/inflamm Abnormal cells -> malignancy

Question 53

Renal Lithiasis

Answer 53

stones in ureters, kidney,bladder

Question 54

Lithotripsy

Answer 54

High energy shock waves to break stones

Question 55

Conditions for kidney stone formation

Answer 55

pH Chem concentration Urinary stasis certain crystals

Question 56

Renal lithiasis examination

Answer 56

examine chemically/xray crystalography 75% calcium oxalate or phosphates

Question 57

Renal lithiasis management

Answer 57

maintain urine pH Hydration Diet restrictions