module 8 Flashcards

1
Q

presence or formation of stones in an organ or in a duct of a body

A

Lithiasis

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2
Q

formation of kidney stones in the kidney

A

nephrolithiasis

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3
Q

presence of stones in the urinary tract which can include kidneys,urethers or bladder(urethera)

A

urolithiasis

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4
Q

uremia forms?

A

urine stones

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5
Q

it is condition characterized by the swelling or dilation of both of the kidneys due to the accumulation of urine as there will be a blockage of urine.

A

hydronephrosis

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6
Q

Small, hard Stones (1-3mm);
- Stones have sharp edges
- Radio-Opaque

A

calcium stones( 80% )

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7
Q

Large Stones (Molds to Renal
Pelvis/Calyces) ʹ Hence Staghorn
Chronic Irritation of Epithelium surrounding
Stone > Squamous Metaplasia

A

Triple Phosphate/Struvite/ “Staghorn” Stones
15%

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8
Q

may cause flank discomfort, recurrent
infection or persistent hematuria
- may remain asymptomatic for years and
not require treatment

A

calyx

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9
Q
  • tend to cause UPJ obstruction renal pelvis
    and one or more calyces
A

pelvis

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10
Q
  • often associated with infection
  • infection will not resolve until stone
    cleared
  • may obstruct renal drainage
A

staghorn calculi

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11
Q
  • 5 mm diameter will pass spontaneously in
    75% of patients the three narrowest
    passage points for upper tract stones
    include: UPJ, pelvic brim, UVJ
A

ureter

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12
Q

Factors promoting stone formation

A
  • stasis (hydronephrosis, congenital
    abnormality)
  • medullary sponge kidney * infection
    (struvite stones)
  • hypercalciuria
  • increased oxalate
  • increased uric acid
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13
Q

Loss of inhibitory factors

A
  • magnesium (forms soluble complex with
    oxalate)
  • citrate (forms soluble complex with
    calcium)
  • pyrophosphate
  • glycoprotein
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14
Q
  • Account for 80 - 85% of all stones
  • Ca2+ oxalate most common, followed by
    Ca2+ phosphate description
  • grey or brown due to hemosiderin from
    bleeding
  • radiopaque
A

calcium stones

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15
Q
  • Female patients affected twice as often as
    male patients
  • Etiology and pathogenesis
    o account for 10% of all stones
    o contribute to formation of staghorn
    calculi
    o consist of triple phosphate (calcium,
    magnesium, ammonium)
    o due to infection with urea splitting
    organisms NH2CONH2 + H2O ––>
    2NH3 + CO2
    o NH4 alkalinizes urine, thus
    decreasing solubility
A

struvite stones

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16
Q
  • Account for 10% of all stones
  • Description and diagnosis
    o orange colored gravel, needle
    shaped crystals
    o radiolucent on x-ray
    o filling defect on IVP
    o Radiopaque on CT scan
    o Visualized with ultrasound
A

Uric Acid Stones

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17
Q
  • Autosomal recessive defect in small bowel
    mucosal absorption and renal tubular
    absorption of dibasic amino acids
  • Seen in children and young adults
  • Aggressive stone disease
  • Description
    o hexagonal on urinalysis
    o yellow, hard
    o radiopaque (ground glass)
    o staghorn or multiple
    o decreased reabsorption of “COLA”
    o cystine (insoluble in urine);
    ornithine, lysine, arginine (soluble in
    urine)
A

Cystine Stones

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18
Q
  • Infection of the renal parenchyma with local
    and systemic manifestations of infection
  • may be classified as uncomplicated or
    complicated
A

Acute Pyelonephritis

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19
Q

in the absence of
conditions predisposing to anatomic
or functional impairment of urine
flow

A

Uncomplicated Acute Pyelonephritis

20
Q

occurring in the setting
of renal or ureteric stones,
strictures, prostatic obstruction
(hypertrophy or malignancy),
vesicoureteric reflux, neurogenic
bladder, catheters, DM, sickle-cell
hemoglobinopathies, polycystic
kidney disease, immunosuppression,
and post-renal transplant

A

Complicated Acute Pyelonephritis

21
Q
  • A form of chronic tubulointerstitial nephritis
    of bacterial origin
  • Cortical scarring, tubulointerstitial damage,
    and calyceal deformities seen
  • May be active (persistent infection) or
    inactive (persistent focal sterile scars post-
    infection)
  • Histologically indistinguishable from many
    other forms of TIN (severe vesicoureteral
    reflux, hypertensive disease, analgesic
    nephropathy)
  • Active chronic pyelonephritis may respond
    to antibiotics
  • Need to rule out TB
A

Chronic Pyelonephritis

22
Q

Is patient more than mildly symptomatic or
complicated pyelonephritis in the setting of
stone obstruction a urologic emergency?

A

true

23
Q

Another name for Incomplete Glomerular-Membrane Damage

A

NEPHROTIC SYNDROMES

24
Q

Another name for complete Glomerular-Membrane Damage

A

Nephritic Syndromes

25
Q
  • Normal GFR
  • +++Polyuria
  • ++++ Proteinuria (>3000mg/day: Nephrotic)
    o > Granular (Protein) Casts.
    o > Edema (Especially Periorbital)
    o > Hypercoagulability (Loss of
    Antithrombin-III in Urine)
    o > Immunocompromise state (Loss of
    Ig in Urine)
    o Hyperlipidemia (Attempted Hepatic
    Compensation for dec. Plasma
    Osmolarity)
  • Serum Creatinine Mildly Elevated
    o (Dehydrated due to Polyuria; But
    Edematous due to Proteinuria)
A

NEPHROTIC SYNDROMES

26
Q

THE Childhood cause of Nephrotic
Syndrome (1-8yrs)

A

MCD (Minimal Change Disease) / Foot Process
Disease

27
Q

> 50% of Adult Nephrotic Syndrome

A

MGN (Membranous Glomerulonephrosis)

28
Q
  • <35% of Adult Nephrotic Syndrome
  • Vey similar to MCD but in adults
A

FSGS (Focal Segmental Glomerulosclerosis)

29
Q
  • Dec GFR
  • Oliguria
    o > Renal Hypertension
    (Hypoperfusion of JG Cells due to
    dec GFR)
A

NEPHRITIC SYNDROMES

30
Q

THE Childhood cause of Nephritic
Syndrome (3-15yrs)

A

PSGN (Post-Strep Glomerulonephritis)

31
Q

THE Adult (15-30yrs)
Cause of Nephritic Syndrome

A

IgA Nephropathy (Berger’s Disease)

32
Q

NOT a Separate Disease; ANY
Glomerulonephritis can > RPGN

A

RPGN (Rapidly Progressive Glomerulonephritis)

33
Q

Acute Renal Failure

A

Rapid loss of kidney function͟

34
Q

Before the Blood Reaches the Kidney

A

Pre-Renal Renal Failure

35
Q

The kidney itself is
damaged
- Acute glomerular nephritis
- Tubular diseases e.g., acute tubular necrosis
- Interstitial diseases e.g., auto immune
disorders such as SLE
- Vascular diseases e.g., polyarteritis nodosa

A

Intra-Renal Renal Failure

36
Q

Due to outflow obstruction from the
kidneys

A

Post-Renal Renal Failure

37
Q

4 Stages of Chronic Renal Failure

A

Stage 1 = > 90 ml/min GFR (Normal) plus
other signs of renal disease
Stage 2 = 90-60 ml/min GFR
Stage 3 = 60-30 ml/min GFR
Stage 4 = 30-15 ml/min GFR
Stage 5 = <15 ml/min GFR

38
Q

General Effects/Problems Encountered in
Renal Failure:

A

o Acid Base Balance
o Electrolyte Balance
o Fluid Balance
o Dec Erythropoiesis
o Renin Angiotensin System > Renal
Hypertension
o Calcium Metabolism
o Uremia
o Dec Urine Output
o Dec Toxin Excretion

39
Q

Dec U:C

A

Intra Renal
(Infection/toxin/Ischemia/Hypoxia/)
PATHOLOGIC KIDNEY

40
Q

Inc U:Cr

A

EITHER Pre Renal
OR
Post Renal

41
Q

inc P: CR = Inc Protein in Urine

A

Proteinuria therefore Daily Creatinine Excretion is Constant

42
Q

30-300mg Urine Protein:Creatinine Ratio

A

Microalbuminuria

43
Q

> 300mg Urine Protein:Creatinine Ratio

A

Macroalbuminuria/Proteinuria͘͟

44
Q

> 3000mg Protein:Creatinine Ratio

A

Nephrotic Syndrome

45
Q

continuum of progressive
nephron loss and declining renal function

A

Chronic Renal Failure

46
Q

a gradual decrease in the functioning of the kidneys

A

dwindles