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1
Q

Renal tubular defects - types

A
  1. Fanconi syndrome
  2. Bartter syndrome
  3. Gitelman syndrome
  4. Liddle syndrome
  5. Syndrome of apparent minelocorticoid excess
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2
Q

Fanconi syndrome - pathophysiology / results in

A

Generalized reabsorptive defect in early proximal convoluted tubule –> increased amino acids, glucose, HCO3- and PO4- – Metabolic acidosis (proximal renal tubular acidosis)

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3
Q

causes of Fanconi syndrome

A
  1. hereditary defects (Wilson disease, tyrosinemia, glycogen storage disease, cystinosis)
  2. iscemia
  3. multiple myeloma
  4. nephrotoxins/drugs (expired tetracyclines, ifosfamide, cisplatin, tenofovir, lead poisoning)
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4
Q

Bartter syndrome - pathophysiology (and result in)

A

Reabsorptive defect in thick ascending loop oh Henle
–> affects Na+/K+/2CL- cotransporter –>
1. hypokalemia
2. metabolic alkalosis
3. hypercalciuria
LIKE LOOP DIURETICS

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5
Q

Gitelman syndrome - pathophysiology (results in)

A 
Reabsosptive defect in Distal convoluted tubule 
LIKE THIAZIDE
1. hypokalemia
2. hypomagnesia
3. metabolic alkalosis
4. hypocalciuria
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6
Q

Gitelman syndrome vs Barrter syndrome according to severity

A

Barrter is more severe

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7
Q

Liddle syndrome - pathophysiology

A

Gain of function mutation –> increased Na+ reabsorption in collecting tubules (high activity of epithelial channel)

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8
Q

situation that mimics Liddle syndrome

A

hyperaldosternism (but aldosterone is nearly undetectable)

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9
Q

Liddle syndrome –> ….. (result in)

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low aldosterone
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10
Q

Liddle syndrome - mode of inheritance / treatment

A

AD

amiloride

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11
Q

Syndrome of Apparent Mineralocorticoid excess - pathophysiology

A

hereditary deficiency of 11β-hydroxysteroid dehydrogenase which normally converts cortisol (can activate mineralocorticoid receptors) to cortizone (inactivate on mineralocorticoid receptors) in cell containing mineralocorticoid receptors –> increased mineralocorticoid activity

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12
Q

Syndrome of Apparent Mineralocorticoid excess - manifestations

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low serum aldosterone levels
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13
Q

P02, PCO2, HCO3-, ph - normal ranges

A

PO2: 75-105 mm Hg
PCO2: 33-44 mm Hg
HCO3-: 22-28 mEq/L
pH: 7.35-7.45

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14
Q

Winters formula?? is a formula used to evaluate

A

respiratory compensation in a metabolic acidosis

PCO2=1.5 (HCO3-) + 8 +/- 2

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15
Q

Winters formula - explanation

A

If measured PCO2 is bigger than predicted PCO2 –> concominant respiratory acidosis
If measured PCO2 is smaller than predicted –> concomitant respiratory alkalosis

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16
Q

Metabolic alkalosis - DDx

A
  1. loop diuretics
  2. vomiting
  3. antiacids
  4. hyperaldosteronism
  5. thiazide use
  6. Hypokalemia
  7. several renal tubular defects
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17
Q

Respiratory alkalosis - DDx

A

Hyperventilation:

  1. Hysteria
  2. Hypoxemia (eg. high altitude)
  3. Pulmoary embolism
  4. Tumor
  5. salicylates (early)
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18
Q

Respiratory acidosis - DDx

A

Hypoventilation:

  1. Airway obstruction
  2. Acute lung disease
  3. Chronic lung disease
  4. Opioids/sedatives
  5. weakening of respiratory muscles
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19
Q

Metabolic acidosis - next step

A

Check anion gap = Na+ - (CL+HCO3-):
more than 12 –> anion gap metabolic acidosis
8-12 –> normal anion gap metabolic acidosis

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20
Q

anion gap metabolic acidosis - DDx

A
  1. Methanol (formic acid)
  2. Uremia
  3. Diabetic ketoacidosis
  4. Propylene glycol
  5. Iron tablets
  6. ISONIAZIDE
  7. Lactic acidosis
  8. Ethylene glycol (–> oxalic acid)
  9. Salicilates (late)
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21
Q

normal anion gap metabolic acidosis - DDx

A
  1. Hyperalimentation (artificial supply of nutrients, typically intravenously)
  2. Addison disease
  3. Renal tubular acidosis
  4. Diarrhea
  5. Acetazolamide
  6. Spironolactone
  7. saline infusion
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22
Q

Renal tubular acidosis - types

A
  1. Distal tubular acidosis (type 1)
  2. Proximal renal tubular acidosis (type 2)
  3. Combined proximal and distal renal tubular acidosis (type 3)
  4. Hyperkalemic renal tubular acidosis (type 4)
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23
Q

Metabolic acidosis - predicted compensatory response

A

1 meq/L decrease in HCO3- –> 1.3 mmHg decrease in PCO2

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24
Q

Metabolic alkalosis - predicted compensatory response

A

1 meq/L increase in HCO3- –> 0.7 mmHg increase in PCO2

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25
Q

Respiratory acidosis - predicted compensatory response

A

acute: 1 mmHg increase in PCO2 –> 0.1 meg/L increase in HCO3-
chronic: 1 mmHg increase in PCO2 –> 0.4 meq/L increase in HCO3-

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26
Q

Respiratory alkalosis - predicted compensatory response

A

acute: 1 mmHg decrease in PCO2 –> 0.2 meq/L decrease in HCO3-
chronic: 1mmHg decrease in PCO2 –> 0.4 meg/L decrease in HCO3-

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27
Q

Renal cell carcinoma - risk factors

A
  1. Smoking
  2. obesity
  3. gene deletion of chromosome 3 (sporadic or inheritance as von Hippel-Lindau
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28
Q

von Hippel-Lindau disease - manifestations

A
  1. hemangioblastomas in retina, brain stem, cerebellum, spine
  2. angiomatosis (cavernous hemangiomas in skin, mucosa, orgnas)
  3. bilateral renal cell carcinoma
  4. pheochromocytomas
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29
Q

Renal cell carcinoma - paraneoplastic syndromes

A
  1. EPO
  2. ACTH
  3. PTHrP
  4. RENIN
30
Q

Renal cell carcinoma - prognosis? (why)

A

poor:

  1. Resistant to chemotherapy and radiation therapy
  2. Silent cancer –> comonly presents as a metastatic neoplasm
31
Q

Renal oncocytoma - clinical manifestations

A
  1. painless hematuria
  2. flank pain
  3. abdominal mass
32
Q

Renal oncocytoma - treatment

A

often rsected to exclude malignancy

33
Q

Squamous cell carcinoma of the bladder - clinical manifestation

A

painless hematuria

34
Q

Squamous cell carcinoma of the bladder - risk factors

A
  1. Schistosoma haematobium infection (Middle East)
  2. Chrinic cystitis
  3. smoking
  4. chronic nephrolithiasis
35
Q

Transition cell carcinoma - manifestations

A

painless hematuria

36
Q

Calcium oxalate stones are precipitated by (beside low ph)

A
  1. ethylene glycol (antifreeze) ingestion
  2. vitamin C abuse
  3. malabsorption (Crohn disease)
  4. hypocitraturia –> low ph
37
Q

kidney calcium stone treatment

A

calcium oxalate –> thiazides, citrate, low-sodium diet

calcium phosphate –> thiazides

38
Q

Ammonium magnesium phosphate stone (sturvite) are caused by

A

infection with urease + bugs (eg. Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella) that hydrolize urea to ammonia –> urina alkalization

39
Q

Ammonium magnesium phosphate stones (sturvite) - treatment

A
  1. eradication of underling infection

2. surgical removal of stone

40
Q

Uric acid stones - risk factors

A
  1. low urine volume
  2. arid climates
  3. acidic ph
  4. strong association with hyperuricemia
41
Q

Cystine stones - treatment

A
  1. low sodium diet
  2. alkalinization of urine
  3. chelating agents if refractory
42
Q

kidney stones - types/precipitating factors/x-ray/CT

A
  1. calcium oxalate –> low ph, radiopaque in both
  2. caclicum phosphate –> high ph, radiopaque in both
  3. Ammonium magnesium phosphate, high ph, radiopaque in both
  4. Uric acid –> low ph, radiolucent in x-ray, minimally vissible in CT
  5. Cystine –> low ph, radiolucent in xray, sometimes vissuble in CT
43
Q

kidney stones - types and urine crystals

A
  1. Calcium oxalate –> shaped like envelope or dumbbell
  2. Caclicum phosphate –> wedge-shaped prism
  3. Ammonium magnesium phosphate –> coffin lid
  4. Uric acid –> Rhomboid or rosettes
  5. Cystine –> hexagonal
44
Q

Urinary incontinence - types

A
  1. Stress incontinence
  2. Urgency incontinence
  3. Mixed incontinence
  4. Overflow incontinence
45
Q

urinary Stress incontinence - mechanism

A

Outlet incompetence (urethral hypermodility or intrinsic sphincteric deficiency –> leak with high intra-abdominal pressure (eg. sneezing, lifting)

46
Q

urinary Stress incontinence - increased risk with

A

obesity
vaginal delivery
prostate surgery

47
Q

urinary Urgency incontinence - mechanism

A

Overactive bladder (detrusor instability) –> leak with urge to void immediately

48
Q

urinary Urgency incontinence - treatment

A
  1. pelvic floor muscle strengthening (Kegel) exercise
  2. bladder training (timed voiding, distraction and relaxation techniques)
  3. antimuscarinics
49
Q

Overflow incontinence - mechanism

A

incomplete emptying (detrusor underactivity - weak to emoty the bladder or outlet obstruction) –> leak with overfilling –> increased postvoid residual (urinary retention) on cathetirization or ultrasound

50
Q

Overflow incontinence - treatment

A 
catherterization
relieve obstruction (α-blockers for BPH)
51
Q

3 MCC of UTI (in order)

A
  1. E. Coli
  2. S. saprophyticus
  3. Klebsiella pneumoniae
52
Q

UTI - diagnostic markers

A
    • leukocyte esterase –> WBC activity
    • Nitrate test –> reduction of urinary nitrates by bacterial species (indicates gram (-) organism, esp E. coli)
    • Urease test –> urease-producing bags (eg. Proteus, klebsiella)
53
Q

acute renal failure (Acute kidney injury) - TYPES

A
  1. Prerenal azotemia
  2. Intrinsic renal failure
  3. postrenal azotemia
54
Q

Prerenal azotemia - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr

A
  • urine osmolairty –> more than 500
  • urine Na+ less than 20
  • FENa less than 1%
  • Serum BUN/Cr >20
55
Q

Intrinsic renal failure - due to

A
  • acute tubular necrosis or ischemia/toxins

- less commonly due to acute glomerulonephritis (RPGN, hemolytic uremic syndrome) or acute interstitial nephritis

56
Q

intrinsic failure - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr

A
  • urine osmolairty –> less than 350
  • urine Na+ more than 40
  • FENa more than 2%
  • Serum BUN/Cr less than 15
57
Q

postrenal azotemia - urine osmolairty (mOsm/Kg), urine Na+ meq/L, FENa, Serum BUN/Cr

A
  • urine osmolairty –> less than 350
  • urine Na+ more than 40
  • FENa more than 1% (mild) or 2% (severe)
  • Serum BUN/Cr varies
58
Q

Acute interstitial renal nephritis (tubulointesritital nephritis) - clinical presentation/findings

A 
IT CAN BE ASYMPTOMATIC
1. Fever
2. rash
3. hematuria (casts)
4. costovertebral angle tenderness 
5. pyuria (classically eosinophils) 
6. azotemia
7. oliguria
(days to weeks after the factor) 
RESULTS IN ACUTE RENAL FAILURE
59
Q

causes of Acute interstitial renal nephritis (tubulointesritital nephritis)

A
  1. drugs that act as haptens, inducing hypersensitivity (eg. diuretics, penicillin derivatives, PPIs, sulfonamides, rifampin, NSAID)
  2. Systemic infections (eg. mycoplasma)
  3. Autoimmune diseases (eg. Sjogren syndrome, SLE, sarcoidosis)
60
Q

Acute interstitial renal nephritis (tubulointesritital nephritis) may progress to

A

renal papillary necrosis

61
Q

renal papillary necrosis - symptoms/findings

A
  1. gross hematuria
  2. proteinuria
  3. flank pain
62
Q

causes of renal papillary necrosis

A
  1. Sickle cell disease or trait
  2. acute pyelonephritis
  3. NSAID (or phenacetin)
  4. DM
  5. Acute interstitial renal nephritis
    May be triggered by recent infection or immune stimulus
63
Q

MCC of acute kidney injury in hospitalized patients

A

Acute tubular necrosis

64
Q

Acute tubular necrosis - prognosis

A

can be fatal, esp during initial oligurinc phase

65
Q

Acute tubular necrosis - FENa

A

more than 2%

66
Q

Acute tubular necrosis - key finding

A

granular (muddy brown) casts

67
Q

Acute tubular necrosis - stages

A
  1. inciting event
  2. Maintenance phase - oliguric
  3. Recovery phase - polyuric
68
Q

Acute tubular necrosis - maintenance phase - risk for

A
  1. hyperkalemia
  2. metabolic acidosis
  3. uremia
69
Q

Acute tubular necrosis - Recovery phase - findings

A

BUN and creatinine fall

70
Q

Acute tubular necrosis - recovery phase - risk for

A

hypokalemia

71
Q

Acute tubular necrosis can be caused by …. (groups)

A
  1. ischemic factors

2. nephrotoxic factors

72
Q

Acute tubular necrosis - nephrotoxic factors - mechanism

A

2ry to injury resulting from toxic substance (eg. aminglycosides, radiocontrasts agents, lead, cisplatin), crush injury (myoglobinuria), hemoglobinuria

Renal (15 decks)

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