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Renal > Q-bank > Flashcards

Q-bank Flashcards

1
Q

What happens to Afferent and Efferent arterioles as systemic BP increases?

A

Afferent constricts and efferent dilates (in response to decreased Renin)

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2
Q

How does kidney treat Creatinine?

A

Freely filtered and secreted in PCT

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3
Q

What is Diabetes Insipidus characterized by?

A

Polyuria, Polydipsia, and hypernatremia

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4
Q

What is the most common cause of Potter sequence?

A

Malformation of Ureteric buds

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5
Q

In which part of the nephron does the osmolarity stay the lowest?

A

Early DCT, even in presence of high ADH levels

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6
Q

Where does PTH act to increase reabsorption of Ca2+?

A

DCT

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7
Q

In Nephrotic Syndrome, one gets hyperlipidemia due to increases in what?

A

Cholesterol, LDL, and TG’s

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8
Q

Where is the Macula Densa located?

A

Right at the junction of the cortical Thick ascending limb and the early DCT

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9
Q

How does a Carbonic Anhydrase inhibitor affect H+ excretion?

A

It decreased H+ (NH+) excretion

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10
Q

What is Acetazolamide?

A

CA inhibitor

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11
Q

Where is Carbonic Anhydrase located?

A

PCT

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12
Q

Where is phosphate reabsorbed? How?

A

PCT (Na+-Phosphate Co-transporter) or Active Transport

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13
Q

Where does the majority of H2O and salt reabsorption occur?

A

PCT ~65% (even in the presence of ADH)

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14
Q

If hyponatremia is corrected to fast, which part of the brain can be demyelinated?

A

Basis Pontis

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15
Q

What is the pH fof Calcium kidney stones?

A

Ca-Phos are Basic and Ca-oxalate are Acidic

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16
Q

What is the pH for Ammonium Mg-Phos kindey stones?

A

Alakaline

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17
Q

What is the pH for Uric Acid kidney stones?

A

Acidic

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18
Q

What is the pH for Cystine kidney stones?

A

Acidic

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19
Q

What causes Ammonium Mg-Phos kidney stones?

A

Urease(+) bacteria, commonly indwelling catheters

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20
Q

What can DIC cause in the kidneys?

A

Diffuse Cortical Necrosis

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21
Q

What do urinary casts indicate?

A

Hematuria/pyuria of RENAL origin

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22
Q

Define Creatinine excretion

A

Creatinine excretion= GFR x Plasma Concentration

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23
Q

Describe Diabetic Glomerulonephropathy

A

Mesangial expansion, GBM thickening, and glomerulosclerossis (Kimmelstiel-Wilson lesions, PAS+)

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24
Q

Why does Creatinine clearance slightly overestimate GFR?

A

Because Creatinine is freely filtered, but also 10-15% secreted into PCT

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25
Q

What kind of cells does Wilms tumor have?

A

Blastemic, epithelial, and stromal cell types

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26
Q

What is Berger Disease?

A

IgA deposits in mesangial cells
Usually follows URI or gastoenteritis
Recurrent episodes of hematuria

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27
Q

What do you see on biopsy of Rapidly Progressive Glomerulonephritis?

A

Crescents (Bowman’s capsule)

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28
Q

What can cause Rapidly Progressive Glomerulonephritis?

A
  1. anti-GBM
  2. ANCA+ vasculitis
  3. Immune complex deposition
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29
Q

Define respiratory acidosis

A

Increased PCO2

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30
Q

Define metabolic acidosis

A

Decreased HCO3- (because being used up)

31
Q

Which part of the eye is composed of Type IV collagen?

A

Lens of the eye

32
Q

What is the most common Nephrotic Syndrome in children?

A

Minimal Change Disease

33
Q

In terms of susceptibility, how does the cortex compare to the medulla?

A

The medulla has lower O2-tension–> Cortex is more susceptible to hypoxia

34
Q

What are the major complications of Kidney stones?

A

Hydronephrosis and pyelonephritis

35
Q

What stimulates ADH release?

A

Increased plasma osmolarity

36
Q

What is the shape of Cystine kidney stones?

A

Hexagonal

37
Q

What test can be used to test Cystine stones?

A

Nitroprusside Test, which will be PURPLE

38
Q

How does ADPKD present?

A

40-50 yo, severe HTN, hematuria, renal insufficiency, anemia (decreased EPO)

39
Q

ADPKD is due to mutations in which genes?

A

PKD1 and PKD2

40
Q

What is the underlying pathology of Minimal Change Disease?

A

Abnormal release of Lymphokines by T-cells

41
Q

For Acute Poststreptococcal Glomerulonephritis, what is seen on biopsy?

A

EM: subepithelial “humps and lumps”

42
Q

What are the symptoms of Acute Poststreptococcal Glomerulonephritis?

A

Periorbital edema, Coca-cola-colored urine, HTN, oliguria

43
Q

In Sickling Crisis, where are you most likely to get sickling in nephron vasculature?

A

In the Vasa Recta (lowest O2-tension, high osmolarity)

44
Q

What can Sickling Crisis lead to in the kidneys?

A

Papillary Necrosis (due to sickling in vasa recta)

45
Q

How can hyoerglycemia lead to ADH-resistance?

A

Decreases ability to maintain medullary osmolar gradient

46
Q

What can increase Renin secretion?

A

Increase sympathetic activity and Decrease in Na-/Cl- in Macula Densa

47
Q

What is the equation for Creatinine Excretion?

A

Plasma Creatinine Conc. x GFR

48
Q

What kind of medication can you use to treat neurogenic bladder?

A

Muscarinic AchR Antagonist (Tolterodine)

49
Q

What is a neurogenic bladder?

A

A bladder that does not empty properly due to a neurologic condition. Urinary incontinence

50
Q

How do you distinguish Pre-renal failure from Renal or post-renal? (BUN:Cr ratio)

A

Pre-renal: Increased BUN:Cr ratio

Renal/Post-renal: Decreased BUN:Cr ratio

51
Q

How do you distinguish Pre-renal failure from Renal or post-renal? (FENa)

A

Pre-renal: FENa, 2%

52
Q

How do NSAIDs cause kidney damage?

A

They inhibit Prostaglandins, which are renal protective b/c they dialte afferent arteriole

53
Q

How do Loop Diuretics affect AngII and Renin levels?

A

Increase Renin and AngII

54
Q

What do Loop Diuretics inhibit?

A

Na+/Cl-/K+ co-transporter

55
Q

Which Loop Diuretic for pts w/ sulfa allergies?

A

Ethancrynic acid

56
Q

What kind of electrolyte abnormalities can Loop Diuretics cause?

A

Hypokalemia, Hypochloremic Alkalosis, Hypocalcemia, Hypomagnesemia

57
Q

Which Abx canNOT be taken w/ antacids?

A

Fluroquinolones

58
Q

How do ACE-Inhibitors work?

A

Prevent constriction of Efferent Arteriole–> Decrease GFR

59
Q

What do Macula Densa cells monitor?

A

Na/Cl delivery in DCT

Decrease Na/Cl–> constrict Aff. Arteriole–> Decrease GFR

60
Q

What do the JG cells monitor?

A

Blood Pressure

Decrease BP in Aff. Arteriole–> Renin–> AngII–> Constrict mostly Eff. Arteriole–> Increase GFR

61
Q

How do ACE-Inhibitors affect Na+ and K+ levels?

A

Decreases Na+ reabsorption and Increases serum K+

62
Q

What do you see on ECG with Hyperkalemia?

A

Peaked T-waves, flattened P-waves, and Widened QRS waves

63
Q

What is the mechanism of Spironolactone?

A

Antagonist at Aldosterone Recepor

64
Q

Which diuretic is best for a pt w/ Hypokalemia and ankle swelling?

A

ADH-receptor antagonist

65
Q

As a side effect, Thiazides can increase reabsorption of what?

A

Calcium

66
Q

Which diuretics increase Free H2O excretion w/o affecting Na+ and K+ excretion?

A

ADH

67
Q

What are the effects of Aldosterone?

A

Increase Na+ reabsorption
Increase K+ secretion
Increase H+ secretion

68
Q

How do diuretics cause increases in Aldosterone?

A

Lead to volume depletion–> Renin release–> AngII release—> Aldosterone release

69
Q

How do diuretics affect Aldosterone levels?

A

Increase

70
Q

What ECG changes do you see with Hypokalemia?

A

U-waves
Widened/Flattened T-waves
ST depressions

71
Q

How can you prevent formation of uric acid stones from Tumor Lysis Syndrome?

A

Allopurinol and hydration

72
Q

How do you treat STRESS incontinence?

A

Alpha-agonist

73
Q

How do you treat URGENCY incontinence?

A

Muscarinic-AchR antagonist

74
Q

When should K+-sparing diuretics be avoided?

A

In setting of Hyperkalemic state (burns, crush injury etc.)

Renal (1 decks)

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