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UA exam 2 > renal disease > Flashcards

renal disease Flashcards

1
Q

Origin of majority of glomerular disorders

A

Immune in origin

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2
Q

Damage to glomerulus may consist of:

A

cellular proliferation
leukocytic infiltration
thickening of the glomerular basement membrane

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3
Q

Scarring of glomerulus

A

sclorosis

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4
Q

Non-immune causes of glomerular damage

A

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

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5
Q

Glomerulonephritis

A

Sterile, inflam process
blood, proteins, casts in urine

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6
Q

Acute post-strep glomerulonephritis

A

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

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7
Q

Acute post strep glomerulonephritis findings

A

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

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8
Q

Rapidly Progressive Glomerulonephritis (Crescentic)

A

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

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9
Q

RPGN Findings

A

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

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10
Q

Goodpasture’s Syndrome

A

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

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11
Q

Goodpasture syndrome antibody

A

Attaches to basement membrane
initiates complement
produces capillary destruction

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12
Q

Goodpasture’s findings

A

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

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13
Q

Vasculitis

A

systemic vascular system
Wegener’s Granulomatosis
Henocj-Schonlein purpura

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14
Q

Vasculitis Findings

A

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

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15
Q

Henoch-Schonlein purpura

A

Children following upper respiratory infection
Red patches on skin

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16
Q

Henoch-Schonlein purpura findings

A

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

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17
Q

Membranoproliferative GN
Membranous GN

A

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

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18
Q

Membranous glomerulonephritis

A

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

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19
Q

Membranoproliferative GN

A

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

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20
Q

Membranoproliferative GN findings

A

decreased serum complement
RBCs
Proteinuria

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21
Q

Berger’s disease

A

Most common glomerular nephritis
serum increase in IgA
Mucosal infection

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22
Q

Berger’s disease findings

A

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

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23
Q

Chronic GN

A

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

24
Q

Nephrotic syndrome

A

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

25
Q

Nephrotic syndrome findings

A

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

26
Q

minimal change disease

A

lipid nephrosis
some proteins pass through glomerulus

27
Q

minimal change disease findings

A

edema
fat droplets
market proteinuria
hematuria
Unknown etiology

28
Q

Focal segmental glomerulosclerosis (FSGS)

A

only certain glomeruli
elevated protein/RBCs
IgM and C3

29
Q

FSGS Associations

A

Unknown
Genetic
heroin abuse/drug toxicity
HIV
Diabetes
Infection

30
Q

Alport syndrome

A

inherited disorder
Basement membrane thins

31
Q

Diabetic nephropathy

A

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

32
Q

Diabetic nephropathy damage

A

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

33
Q

Tubular disorders

A

damage to tubules (antifreeze)
Metabolic/hereditary disorder

34
Q

Acute Tubular Necrosis (ATN)

A

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

35
Q

ATN findings

A

Lots of casts of various sorts
RTE cells

36
Q

Fanconi’s syndrome

A

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

37
Q

Nephrogenic Diabetes insipidus

A

Don’t respond to ADH
Low specific gravity
urinate frequency

38
Q

Renal Glycosuria

A

Reabsorption of glucose affected
normal serum glucose, increased urine glucose

39
Q

Interstitial disease

A

affect the interstitium
infection and inflamm
most common: UTI

40
Q

Cystitis

A

Most common UTI
Infection of bladder

41
Q

Cystitis findings

A

WBCs
Bacteria
RBCs
Proteinuria

42
Q

Acute pyelonephritis

A

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

43
Q

Acute pyelonephritis findings

A

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

44
Q

Chronic pyelonephritis

A

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

45
Q

Chronic pyelonephritis findings

A

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

46
Q

Acute Interstitial Nephritis (AIN)

A

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

47
Q

AIN WBCs/stains

A

Eosinophils (Allergic reaction)
Hansel stain

48
Q

AIN findings

A

Absence of bacteria
Eosinophils

49
Q

Renal Failures

A

Acute and chronic
Final stage: end stage renal failure

50
Q

Renal failure findings

A

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

51
Q

Acute renal failure

A

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

52
Q

Acute renal failure

A

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

53
Q

Renal Lithiasis

A

stones in ureters, kidney,bladder

54
Q

Lithotripsy

A

High energy shock waves to break stones

55
Q

Conditions for kidney stone formation

A

pH
Chem concentration
Urinary stasis
certain crystals

56
Q

Renal lithiasis examination

A

examine chemically/xray crystalography
75% calcium oxalate or phosphates

57
Q

Renal lithiasis management

A

maintain urine pH
Hydration
Diet restrictions

UA exam 2 (7 decks)

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