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STEP 7: Renal Urinary Tract PATHOMA FA CORBETT > UTI STONES OTHER PATHOMA/FA > Flashcards

UTI STONES OTHER PATHOMA/FA Flashcards

1
Q

What are the clinical signs of CYSTITIS?

A

DYSURIA (painful urination), FREQUENCY, URGENCY, SUPRAPUBIC PAIN

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2
Q

What is the gold standard confirmatory test of CYSTITIS?

A

CULTURE - >100,000 CFU

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3
Q

What type of infection is most common for a UTI? Which sex is a UTI more frequent in? What are the risk factors?

A

ASCENDING infection - Greater incidence in FEMALES

Risk factors: Sexual intercourse, Urinary stasis, and Catheters

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4
Q

What are the 3 types of UTIs?

A
  1. CYSTITIS - Infection of bladder
  2. PYELONEPHRITIS - Infection of kidney
  3. CHRONIC PYELONEPHRITIS - Interstitial fibrosis + Tubular atrophy
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5
Q

What are the laboratory findings of CYSTITIS? Include urinalysis, urine dipstick, and culture.

A
  1. URINALYSIS - cloudy urine >10WBC/hpf
  2. DIPSTICK - LEUKOCYTE ESTERASE + NITRITES (presence of bacteria - converts urinary nitrAtes into nitrItes)
  3. CULTURE - >100,000 CFU
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6
Q

What are the 5 possible bacterial agents of CYSTITIS? Which is the most common?

A 
E. COLI* Most common 
S. saprophyticus 
Klebsiella
Proteus mirabilis
Enterococcus faecalis
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7
Q

Pt with suspected UTI has dysuria, polyuria, and suprapubic pain. On urinalysis, it is noted that the urine is alkaline and smells like ammonia. What is the most likely infection and most likely etiological agent?

A

CYSTITIS by Proteus mirabilis

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8
Q

Pt has DYSURIA, POLYURIA, INCREASED URGENCY, and suprapubic pain. Pt was suspected to have cystitis. On urinalysis, pt’s WBC >10/hpf and urine dipstick showed +LE and nitrites. But pt’s urine culture was negative. What does the pt most likely have? What are the 2 possible etiological agents?

A

Pt has URETHRITIS - Demonstrates STERILE PYURIA (+LE, >10WBC/hpf but -Urine culture)
Most likely etiological agents: Chlamydia OR Neisseria

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9
Q

What is the most common clinical Sx of CYSTITIS?

A

DYSURIA

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10
Q

What is the main difference in clinical sign between PYELONEPHRITIS and CYSTITIS?

A

CYSTITIS - No systemic signs (no fever, chills, night sweats)
PYELONEPHRITIS - Yes, systemic signs (fever, chills, nightsweats)

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11
Q

What are the clinical Sx of PYELONEPHRITIS?

A

Systemic signs (fever, chills, night sweats) + FLANK PAIN (Inflammation-induced sensitization of nerves in renal capsule) + Sx of CYSTITIS (since most pyelonephritis cases are ascending)

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12
Q

What is seen in the urine in pts with PYELONEPHRITIS?

A

WBC Casts - Increased WBC ascend from URETERS -> TUBULES -> KIDNEY and get casted/sent to urine

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13
Q

What are the 3 possible etiological agents of PYELONEPHRITIS? Which is the most common?

A
  1. E.coli ** most common
  2. KLEBSIELLA
  3. ENTEROCOCCUS FAECALIS
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14
Q

Which LIKELY pathogens can cause BOTH PYELONEPHRITIS and CYSTITIS? (3)

A

E. COLI ** + KLEBSIELLA + ENTEROCOCCUS

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14
Q

What areas of the kidney are affected by CHRONIC PYELONEPHRITIS resulting from multiple occurrences of acute pyelonephritis?

A

INTERSTITIAL FIBROSIS + CORTICAL SCARRING in the UPPER/LOWER POLES of the kidney + TUBULAR ATROPHY + BLUNTED CALYCES

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15
Q

What is the most common cause of CHRONIC PYELONEPHRITIS in children?

A

VESICOURETERAL REFLEX - Congenital malformation of the ureters not forming a particular angle with the bladder -> Backflow of urine from bladder to ureter and to kidney

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16
Q

What is the general cause of CHRONIC PYELONEPHRITIS in adults?

A

OBSTRUCTION (BPH or CERVICAL CARCINOMA)

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17
Q

What is seen on biopsy of a CHRONIC PYELONEPHRITIC KIDNEY? What is seen on H&E staining that resembles another organ?

A

BIOPSY - Cortical scarring on upper and lower poles + Blunted calyces
H&E - Thyroidization of the kidney (Resembling colloids of a follicle are eosinopilic proteinacious material in atrophic tubules)

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18
Q

What type of cellular element is seen in CHRONIC PYELONEPHRITIS?

A

WIDER WAXY CASTS = Diseased dilated duct (chronic renal failure/end-stage renal disease)

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19
Q

Ddx of CYST FORMATION within SHRUNKEN KIDNEYS: (2)

A
  1. MEDULLARY CYSTIC KIDNEY DISEASE

2. END-STAGE RENAL FAILURE PT who receives DIALYSIS (shrunken kidneys, increased risk of cyst formation with dialysis)

20
Q

What are the 3 clinical signs of NEPHROLITHIASIS as pt tries to pass the kidney stone down the ureter?

A
  1. HEMATURIA
  2. COLICKY PAIN
  3. UNILATERAL FLANK TENDERNESS
21
Q

When is surgical intervention of NEPHROLITHIASIS required?

A

If clinical Sx last longer than hours (the time that kidney tries to push the stone through the ureters), then surgical intervention is required

22
Q

What is the most common cause of STAGHORN CALICULI in renal calyces of CHILDREN?

A

STAGHORN CALICULI = CYSTINE STONE or AMP STONE

Children (C) = Cystine Stone (C)

23
Q

What is the most common cause of STAGHORN CALICULI in renal calyces of ADULTS?

A

STAGHORN CALICULI = CYS STONE + AMP STONE

Adults (A) = AMP Stone (A)

24
Q

Which type of kidney stone/nephrolithiasis is MOST COMMON?

A

CALCIUM OXALATE (Ca3PO42)

25
Q

What is the most common cause of CALCIUM PHOSPHATE Stone formation?

A

IDIOPATHIC HYPERCALCIURIA

26
Q

Which diseases need to be excluded when CALCIUM PHOSPHATE/OXALATE stones are suspected?

A

HYPERCALCEMIA, PTHrP paraneoplastic syndromes

27
Q

Which bowel disease increases the risk of developing CALCIUM PHOSPHATE/OXALATE stones?

A

CROHN’S DISEASE - Small bowel damage INCREASES oxalate reabsorption -> Binds Ca2+ -> Forms stone

28
Q

What is the treatment of CALCIUM PHOSPHATE NEPHROLITHIASIS?

A

HCTZ - Ca2+ sparing diuretic -> NO Ca2+ to form a stone

29
Q

What is the SECOND most common nephrolithiasis?

A

AMMONIUM MAGNESIUM PHOSPHATE (AMP)

30
Q

What is the most common cause of developing AMMONIUM MAGNESIUM PHOSPHATE stones? What is the acidity/basicity of the urine that facilitates the formation of these stones?

A

Most common cause = UREASE + ORGANISMS (Klebsiella and Proteus)
ALKALINIZATION OF URINE leads to formation of stones

31
Q

What is the treatment of AMP stones? What does this increase the risk of in the future?

A

AMP STONES need to be surgically removed - Staghorn calciculi in renal calyces are too big. Act as source of bacteria to multiply to form UTI

32
Q

What is the treatment plan of AMP kidney stone formation? What is the basis for each component?

A
  1. Surgical removal of stone - Bec stone is too big

2. Eradication of inciting pathogen - Prevent recurrence

33
Q

How are URIC ACID nephrolithias different from other types of stones, with regards to imaging?

A

URIC ACID - RADIOLUCENT and not visible on X-ray

Other stones - RADIOPAQUE on X-ray

34
Q

What are the risk factors of developing URIC ACID CRYSTALS?

A

Hot, arid climates
Low urine volume
Low acidic pH

35
Q

What is the most common type of stone seen in Gout pts?

A

URIC ACID CRYSTALS

36
Q

What two conditions increase the risk of developing URIC ACID STONES?

A
  1. LUEKEMIA + 2. MYELOPROLIFERATIVE DISORDERS - Great turnover of cells -> INCREASED URIC ACID
37
Q

What is the treatment plan of GOUT PTS with URIC ACID STONES?

A
  1. Hydration (maintain urinary outflow)
  2. Alkalinization of urine (since acidification of urine promotes stone formation and precipitation
  3. ALLOPURINOL - Medication that decreases uric acid production
38
Q

What is the most rare cause of nephrolithiasis that is predominantly seen in CHILDREN?

A

CYSTINE STONES

39
Q

WHAT disease is associated with CYSTINE STONE FORMATION?

A

CYSTINURIA - Decreased Cys reabsorption -> INCREASED LUMINAL Cys

40
Q

What is the treatment plan of CYSTINE STONE for CYSTINE STONES?

A

Hydration + Urine alkalinization

41
Q

EOSINOPHILURIA vs NEUTROPHILURIA (+Increased number of bands in peripheral WBC count)

A

EOSINOPHILURIA - Drug-induced AIN

NEUTROPHILURIA - Pyelonephritis

42
Q

PAROXYSMAL HTN + TACHYCARDIA + CUTANEOUS PALLOR + ELEVATED PLASMA METANEPHRINES

A

PHEOCHROMOCYTOMA

43
Q

90% PHEO ‘BOAS’

A

BENIGN, ONE SIDED, ADRENAL ONLY, SPORADIC

44
Q

FIBROMUSCULAR DYSPLASIA (STRING BEADING ON ANGIOGRAM)

A

WOMEN
Abnormal dvlm of arterial wall THROUGHOUT - NOT only at bifurcations (like atherosclerosis)
Most commonly affects RENAL ARTERY (75%), next common in cerebral circln

45
Q

AD PKD vs AR PKD: Where do the cysts arise from? What is the mutation in?

A

AD PKD: Cyst formation in TUBULAR CELLS, Mut PKD1 (85% - POLYCYSTIN) and PKD2 (15%) - Larger protein cell-cell interactions (85%) and 15% Ca2+ channel, hepatic cysts but no fibrosis
AR PKD: Cyst formation in COLLECTING DUCTS, Mut PKHD1 (FIBROCYSTIN Protein localized to cilia that are highly expressed in the LIVER), CONGENITAL HEPATIC FIBROSIS***

46
Q

CVA tenderness + FEVER + INFECTIOUS SIGNS = ___?

A

PYELONEPHRITIS

47
Q

What is the MOST COMMON CAUSE of microscopic hemature with NEGATIVE UROLOGIC workup?

A

BENIGN familial hematuria - THIN BM NEPHROPATHY (Alpha-4 chain of type IV collagen)

ALPORT - (alpha-5 chain of TYPE 4 collagen)

STEP 7: Renal Urinary Tract PATHOMA FA CORBETT (7 decks)

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