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MHD V: Renal > 11.3: Clinical III > Flashcards

11.3: Clinical III Flashcards

1
Q

Two types of clinical hematuria (visualization)?

A

Gross: visible to the eye
Microscopic: cannot visualize w/o microscope

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2
Q

What are some imposters of hematuria?

A
  1. Free hemoglobinuria: in hemolysis
  2. Myoglobinuria: rhabdomyolysis
  3. Menstrual contamination
  4. Anticoags: not normally only MASSIVE warfarin OD
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3
Q

Can anticoagulants cause hematuria?

A
  • Not normally in themselves
  • They can unmask sources of bleeding we otherwise did not know of
  • Massive warfarin OD can cause however
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4
Q

How do we find the cause of hematuria?

A
  • The majority of the time we do not find source
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5
Q

Limitations of dipstick test for hematuria?

A
  • Low specificity: free hdb and myoglobin will set off

- When positive, most proceed to microscopic

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6
Q

Gross hematuria is associated with higher risk of what?

A
  • Urologic cancers
  • Higher risk than microscopic
  • **Should also receive full workup in adults
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7
Q

Sequelae of hematuria?

A
  1. Acute urinary retention: from clots in tract

2. Anemia if severe: very rare

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8
Q

What is microscopic hematuria?

A
  • > 2 RBCs per high power field of microscope

- If there is presence of microscopic, and ptn. has risk factors for urologic cancer, they should be worked up

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9
Q

Two types of hematuria (source)?

A
  1. Glomerular: dysmorphic RBCs on microscopy
  2. Non glomerular
    a. Upper tract
    b. Lower tract: bladder, urethra, etc.
    * **DD is different between the two types
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10
Q

What are dysmorphic RBCs on microscopy consistent w/?

A

Glomerular hematuria

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11
Q

DD for microscopic glomerular hematuria?

A
  1. IgA nephropathy
  2. Thin basement membrane disease
  3. Hereditary nephritis: Alport’s syndrome
  4. MFGS
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12
Q

Another name for hereditary nephritis?

A
  • Alport’s syndrome

- Also associated with hearing defficits

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13
Q

Another name for Thin basement membrane disease?

A

Benign familial hematuria

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14
Q

What happens in DD for microscopic nonglomerular hematuria as you get older? What puts you at higher risk

A
  • **Above 50, cancers are higher likelihood
  • 5% of microscopic hematuria have urologic cancer
  • Smoking: carcinogens are being held in bladder while we wait to pee
  • Exposure to other dermal or respiratory toxins
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15
Q

What is exercise hematuria?

A

Caused by bladder bouncing up and down while jogging

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16
Q

What is Factitious hematuria?

A

Mental health ptn. puts own blood in urine to alarm health care team

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17
Q

How to test for upper tract urologic cancers?

A

CT urogram: Cat scan w/ or w/o contrast

  • IV contrast allows view of kidney function
  • *Use ultrasound if ptn. is at risk for contrast induced nephropathy
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18
Q

How to test for lower tract urologic cancers?

A

Cystoscopy

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19
Q

Describe situations for which repeat urinalysis prior to more involved workup for hematuria is indicated?

A
  • Ptn is asymptomatic with low risk for urologic cancer and has recently:
    1. Menstruated
    2. Had sex
    3. Vigorously exercised
    4. Trauma
  • **If ptn. has UTI, you can treat UTI then repeat urinalysis
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20
Q

What is pyuria?

A

Presence of pus in urine, typically from bacterial infection

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21
Q

What suggests glomerular hematuria in urinalysis?

A
  • Dysmorphic RBCs / RBC casts
  • Proteinuria
  • Elevated BUN / Cr
  • **Refer to nephrology for glomerular source
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22
Q

What suggests nonglomerular hematuria in urinalysis?

A
  • Normal renal indices
  • Lack of proteinuria
  • Isomorphic RBCs
  • **Work up non glomerular tract via imaging upper and lower
23
Q

When is CT urogram not preferred scanning method for upper tract hematuria?

A
  1. Kidney disease

2. Pregnancy

24
Q

What is urokinase?

A
  • Enzyme in urinary tract that serves to break up clots
  • Tends to prevent clots at source of bleeding unfort and not down stream leading to blockage
  • As such cather is needed to irrigate and dilute urokinase so clot can form
25
Q

Main treatment for persistent gross hematuria?

A
  • Foley catheter with bladder irrigation
26
Q

What is nephrolithiasis?

A

Kidney stones

27
Q

Why are kidney stones higher in the south US?

A
  • People in sun more getting more Vitamin D
  • Leads to higher Ca absorption
  • Mixes with P in urine leading to stones
  • **Also higher in summer, more warmth and more concentrated urine leading to more stones
28
Q

What does oxalate cause?

A

Nephrolithiasis: kidney stone formation

29
Q

Presentation of nephrolithiasis?

A
  1. Moderate colic
  2. Some extent of hematuria
  3. Pain
30
Q

Where is pain from stone in upper ureter?

A
  1. Flank pain

2. Upper anterior abdominal pain

31
Q

Where is pain from stone in lower ureter?

A
  1. Groin pain

2. Pain in ipsilateral testical and labia

32
Q

Composition of majority of stones in US?

A
  • Calcium oxalate or Ca phosphate
33
Q

Steps of stone formation?

A
  1. Urinary crystal (free ion) saturation in equilibrium w/ salt
  2. Supersaturation occurs from increased ion excretion or more concentrated urine leading to start of formation
  3. Nucleation = key phase: mix becomes more heterogeneous aggregation and growth ensue
34
Q

What promotes Ca stone formation?

A
  1. Low PH
  2. High Ca in urine
  3. Low urinary volume
  4. Uric acid: high protein diet
  5. Injury
  6. Low citrate
  7. High Na / Mg
35
Q

What inhibit stone formation?

A
  1. High urine flow rates

2. Citrate

36
Q

What can cause hypercalciuria?

A
  1. Hyperparathyroidism
  2. Vitamin D excess
  3. Sarcoidosis
  4. Loop diuretcs
37
Q

What happens to oxalate in GI tract?

A
  • Combines with Ca to precipitate and poop out
  • Unbound is absorbed and proceeds to kidney
  • When bound to Ca in kidney forms stones
38
Q

What happens when more oxalate is absorbed?

A
  • Higher likelihood of stone formation, occurs in:
    1. Low dietary Ca
    2. IBD: Crohn’s
39
Q

Four most common types of stones?

A
  1. Ca stones
  2. Uric acid
  3. Struvite
  4. Cystine stones
40
Q

What promotes uric acid stones?

A
  1. Metabolic acidosis w/ low urine PH
  2. Hyperuricosuria: high purine / protein diet
  3. Metabolic syndrome: Insulin resistance leading to defect in renal ammonia
41
Q

What leads to struvite stones?

A
  1. Chronic URTI with urease producing bacteria
  2. Leads to ammonia and alkaline urine promoting struvite
  3. More common in women: shorter ureters
42
Q

What are the urease producing bacteria?

A
  1. Proteus
  2. Haemophilus
  3. Klebsiella
  4. Ureaplasma urealyticum
43
Q

What is a nidus?

A
  • Protected area for stone formation
44
Q

Problem with struvite stones?

A
  • They are very large: need to be removed by laser or surgery
45
Q

Medical illnesses related to nephrolithiasis?

A
  1. IBD
  2. Thyroid / PTH disease
  3. Sarcoidosis
  4. RTA
46
Q

Clinical response to pth. with nephrolithiasis?

A
  • CT scan WITHOUT contrast

- Full metabolic workup which is 24 hour urine collection twice

47
Q

How do do you calculate likelihood of stone passage?

A
  • 10 - stone dimension = % change of passing?

- 1mm stone = 99% chance of passing

48
Q

Which stones have highest likelihood of passing?

A

Smaller stones in distal ureter

49
Q

When is interventional treatment necessary for stones?

A
  • > 6mm
  • Have Not passed after 4 weeks of treatment
  • Intractable pain
  • Associated UTI
50
Q

Medical therapy for stone management?

A
  1. Analgesics: NSAIDs just as effective as opioids
  2. 2 - 3 L oral intake daily
  3. Alpha blockers causing ureters to relax
51
Q

How do we prevent Ca future stones?

A
  1. Low Na / animal protein diet
  2. Normal dietary Ca
  3. Thiazide diuretics: decrease Ca excretion
52
Q

What happens if restrict Ca?

A
  • Oxalate absorption in GI increase rather than pooping out
53
Q

How do we prevent uric acid stones?

A
  1. Low purine / animal protein diet
  2. Medications: Na/bicarb, K / citrate
    - Alkalinizes urine
  3. Allopurinol: decreases uric acid levels
54
Q

How do we treat struvite stones?

A
  1. Antibiotics for the infection that is causing

2. Complete removal of stones

MHD V: Renal (28 decks)

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