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FirstAID > Renal > Flashcards

Renal Flashcards

1
Q

Which kidney is usually taken during liver donor transplantation and why?

A

Left Kidney; because it has a longer renal vein

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2
Q

Where is the macula densa located?

A

Distal convoluted tubule

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3
Q

Where are JG cells located?

A

Afferent arteriole

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4
Q

ureterovesicular junction

A

narrowest part of the ureter; common site for stones to get stuck

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5
Q

nephrocalcinosis

A

calcification of the medullary periods; assoc w/hyperparathyroidism

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6
Q

passage of ureters in relation to the uterine artery and ductus deferens?

A

ureters pass under uterine artery and under ductus deferens (retroperitoneal)

  • ->”water passes under the bridge”
  • water=ureters
  • bridge=uterine arteries and ductus deferens
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7
Q

60-40-20 rule (of total body weight):

A 
60% = total body water
40% = ICF
20% = ECF
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8
Q

How to measure plasma volume?

A

radiolabeled albumin

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9
Q

how to measure extracellular volume?

A

Inulin

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10
Q

Glomerular Filtration barrier is composed of:

  • Fenestrated Capillary Endothelium
  • Fused basement membrane
  • Epithelial layer
  • What is each one’s role?
  • Composition?
  • What is lost in nephrotic syndrome? What’s the result?
  • What is lost in Minimal Change disease?
A
  • Fenestrated Capillary Endothelium:
  • Size barrier
  • Fused basement membrane:
  • negative Charge barrier
  • has heparin sulfate
  • lose charge barrier in neprhotic syndrome; get: albuminuria, hypoproteinemia, generalized edema, hyperlipidemia
  • Epithelial layer:
  • consists of podocyte foot processes
  • lose podocytes in MCD
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11
Q

What substances can be used to measure GFR?

A
  • Inulin or Creatinine Clearance.
  • Inulin is freely filtered, but is neither reabsorbed nor secreted.
  • BUT: Creatinine clearance slightly overestimates GFR, b/c creatinine is moderately secreted by renal tubules
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12
Q

What substance can be used to meausre the ERPF (Effective Renal Plasma Flow)?

A

-PAH clearance; b/c all PAH entering kidney is secreted

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13
Q

ERPF vs true RPF?

A

ERPF underestimates true RPF by about 10%

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14
Q

RBF =?

A

RBF = RPF/(1-Hct)

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15
Q

Normal Filtration Fraction =?

A

20%

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16
Q

Effect of prostaglandings on kidney:

Effect of NSAIDs on kidney?

A

Prostaglandins dilate afferent arteriole –> so, get:

  • increased RPF
  • increased GFR
  • constant FF
  • NSAIDs–>inhibit PGs –> get constriction of Afferent Arteriole:
  • decreased RPF
  • decreased GFR
  • constant FF
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17
Q

Effect of Angiotensin II on kidneys?

A

Acts on Efferent Arteriole; constricts EA:

  • decreased RPF
  • increased GFR
  • increased FF
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18
Q

Effect of ACE-inhibitors on kidneys?

A

ACE-inhibitors–> inhibit Ang II –> dilate Efferent Arteriole:

  • increased RPF
  • decreased GFR
  • decreased FF

*so, may have increased Creatinine levels in blood (b/c decreased GFR, and Creatinine clearance is a measure of GRF, so decreased Creatinine clearance –> more Creatinine in blood)

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19
Q

What is Creatinine in urine a measurement of?

A

Glomerular Filtration Rate

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20
Q

Where in kidney is glucose normally reabsorbed?

A

Proximal tubule by Na+/glucose cotransport

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21
Q

At what plasma glucose levels does glucosuria begin (threshold)?
At what glucose levels is Tm (all transporters fully saturated)?

A
  • see glucosuria at plasma glucose levels of 160-200

- all transporters are fully saturated (Tm) at plasma glucose levels = 350 mg/dL

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22
Q

Hartnups disease:

A

deficiency of neutral amino acid (tryptophan) transporter in proximal tubule; so, can’t reabsorb tryptophan
-results in pellagra (niacin/B3 deficiency; b/c B3 is derived from Tryptophan)

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23
Q

Where in nephron is glucose, AAs, and most of bicarbonate, Na, Cl, and water reabsorbed?

A

Early proximal tubule

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24
Q

Where in kidney is there “isotonic absorption”?

A

Early proximal tubule

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25
Q

Which part of nephron generates and secretes ammonia?

A

Early proximal tubule

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26
Q

Which part of the nephron is the most hypertonic/concentrated urine?

A

Thin descending limb of loop of Henle
–>impermeable to sodium; passively reabsorbs water b/c sodium can’t get in, so the medulla is hypertonic –> water leaves nephron into medulla, making urine more concentrated.

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27
Q

Which part of nephron is impermeable to water?

A

Thick ascending limb of loop of Henle

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28
Q

Which part of nephron is the “diluting segment”, where urine has the lowest osmolality?

A

Early distal convoluted tubule

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29
Q

Where are Na, K, and Cl actively reabsorbed and Mg and Ca indirectly reabsorbed?

A

Thick ascending limb of loop of Henle (this is the part that is also impermeable to H20; so, have reabsorption of electrons + water cannot leave (nor enter) –> so this portion of the loop makes the urine less concentrated as it ascends; eventually, it has the lowest osmolality at the early distal convoluted tubule)

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30
Q

Where in nephron does PTH act?

A

Early proximal tubule: PTH inhibits Na/P cotransport –> get increased phosphate excretion

Early distal convulted tubule: increased Ca/Na exchange –> get increased Ca reabsorption

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31
Q

Where in nephron does Angiotensin II act?

A

Early proximal tubule –> AT II stimulates Na/H exchange –> increased Na and water reabsorption

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32
Q

ADH vs Aldosterone:

A

ADH primarily regulates osmolarity; but, also responds to low blood volume, when necessary (b/c low volume takes precedence over osmolarity)

Aldosterone primarily regulates blood volume

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33
Q

Juxtaglomerular Apparatus:

A
  • JG cells in AA
  • Macula densa = Na sensor –> in distal convoluted tuule

*JGA defends GFR via the RAAS system: JG cells secrete renin in response to low renal BP, low Na delivery to distal tubule, and increased sympathetic tone (beta-1 receptors)

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34
Q

Which cells secrete renin?

A

JG cells (in Afferent Arteriole)

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35
Q

How may NSAIDs cause acute renal failure?

A

NSAIDs inhibit the renal production of prostaglandins, which normally keep the afferent arterioles vasodilated and maintain GFR
-NSAIDS–>constrict AA–>decrease both RPF and GFR

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36
Q

4 endocrine functions of the kidneys:

A

1) Erythropoietin production

2) 1,25-(OH)2-vitamin D production –> in proximal tubule; convert vit D to active form
* Note: vitamin D–> increases Ca and P absorption in intestines
* note: PTH acs directly on the kidney to reabsorb P, but not reabsorb P
* note: PTH also stimulates formation of active Vitamin D, which increases absorption of both Ca and P in intestines!

3) Renin –> beta-1 effect
4) Prostaglandins –> vasodilates AA to increase GFR

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37
Q

Hormones that act on the kidney:

A

1) ANP
2) PTH
3) AT II
4) Aldosterone
5) ADH

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38
Q

ANP = Atrial Natriuretic Peptide

A
  • secreted in response to increased atrial pressure (ie high preload or high blood volume)
  • causes: increased GFR and increased Na filtration, but not increased Na reabsorption
  • NET effect: Na+ loss and volume loss
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39
Q

PTH:

A

-secreted in response to low plasma Ca, high plasma P, or low plasma vitamin D
-causes: increased Ca reabsorption in DCT, decreased P reabsorption in PCT, and increased vit D production
Also causes: increased Ca and P absorption from gut (b/c of effects of Vitamin D)

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40
Q

AT II = Angiotensin II

A

-Causes EA constriction –> decreased RPF, increased GFR and increased FF; also get compensatory Na reabsorption in proximal and distal nephron (b/c goal is to increase BP!)

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41
Q

Aldosterone:

A
  • secreted in response to low blood volume (via Ang II) and elevated plasma K
  • causes: increased Na reabsorption, increased K secretion, and increased H secretion
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42
Q

ADH/Vasopressin

A
  • secreted in response to elevated plasma osmolarity and decreased blood volume
  • causes increased # of water channels and increased water reabsorption
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43
Q

6 situations that shift K+ out of cells –> causing HYPERkalemia:

A
  • decreased insulin (like in DKA)
  • beta-blockers
  • acidosis/severe exercise
  • hyper-osmolarity
  • digitalis
  • cell lysis
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44
Q

4 situations that shift K+ into cells –> causing HYPOkalemia:

A
  • insulin
  • beta-agonists (ie albuterol)
  • alkalosis
  • hypo-osmolarity
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45
Q

Too rapid correction of Hyponatremia?

A

get Central Pontine Myelinosis (irreversible; acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness)

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46
Q

U waves on ECG, flattened T waves, arrhythmias and paralysis?

A

low serum K+

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47
Q

Peaked T waves, wide QRS, arrhythmias:

A

high serum K+

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48
Q

effects of low serum Ca?

A
  • Tetany

- Neuromuscular irritability

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49
Q

effects of high serum Ca?

A

“stones, bones, groans, moans”

  • delirium
  • renal stone
  • abdominal pain
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50
Q

effects of low serum Phosphate?

A

bone loss and osteomalacia

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51
Q

effectsof high serum Phosphate?

A

renal stones, metastatic calcifications

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52
Q

Compensatory response to respiratory acidosis or alkalosis?

A
  • -> kidneys!
  • if respi acidosis –> kidneys increase renal HCO3 reabsorption
  • if respi alkalosis –> kidneys decrease renal HCO3 reabsorption

–> these compensatory mechanisms take time, are delayed! (unlike compensation of metabolic acidosis/alkalosis, which can be done quickly by breathing more/less!)

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53
Q

Causes of metabolic acidosis with a high anion gap?

A

MUDPILES!

  • Methanol (formic acid)
  • Uremia
  • DKA
  • Paraldehyde or Phenformin
  • Iron tablets or INH (Isoniazid)
  • Lactic acidosis, hypoxia
  • Ethylene glycol (oxalic acid)
  • Salicylates (ie aspirin)
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54
Q

Causes of normal anion gap metabolic acidosis?

A
  • Diarrhea
  • Glue sniffing
  • Renal tubular acidosis (RTA)
  • Hyperchloremia
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55
Q

Causes of Respiratory alkalosis:

A
  • Hyperventilation (early high-altitude exposure)

- Initially after aspirin ingestion (then becomes anion-gap metabolic acidosis)

56
Q

Causes of metabolic alkalosis with compensation (Hypoventilation):

A
  • Diuretics
  • Vomiting
  • Antacids
  • Hyperaldosteronsim (increases H+ secretion)

***These are all cases where get rid of acid!

57
Q

Causes of Respiratory Acidosis:

A
  • any time can’t get rid of CO2!
  • airway obstruction
  • acute lung disease
  • chronic lung disease
  • opiods, narcotics, sedatives
  • weakened respiratory muscles
58
Q

How to calculate anion gap:

A

Anion gap = Na - (Cl + HCO3) = Na - Cl - HCO3

59
Q

3 types of RTA (Renal Tubular Acidosis)

A
  • Type 1 = “distal”: defect in CT’s ability to excrete H+ (so increased urinary pH)
  • associated with hypokalemia and risk for calcium kidney stones
  • Type 2 = “proximal”: defect in PT HCO3 reabsorption
  • associated with hypokalemia and hypophosphatemic rickets
  • Type 3 = “hyperkalemic”: Hypoaldosteronism or lack of Ct response to aldosterone
  • associated with hyperkalemia and can’t excrete ammonium in PT
  • decreased urinary pH d/t decreased buffering capacity
60
Q

RBC casts

A

Glomerulonephritis

-Also: ischemia, malignant HTN

61
Q

WBC casts

A
  • Acute pyelonephritis
  • Tubulointerstitial inflammation
  • Also: transplant rejetion
62
Q

“muddy brown”/Granular casts

A

Acute tubular necrosis

63
Q

Waxy casts

A

advanced/chronic renal disease

64
Q

Hyaline casts

A

nonspecific

65
Q

What does the presence of casts in urine indicate?

A
  • ->casts indicate that hematuria/pyuria is of renal origin
  • so, with bladder cancer, kidney stones –> have hematuria, but no casts
  • with acute cystitis –> have pyuria (WBCs), but no casts
66
Q

Nephritis vs Nephrotic syndromes:

A
  • Nephritic–> Inflammatory; hematuria and RBC casts in urine
  • ->have azotemia (increased BUN and increased Creatinine), oliguria, HTN (d/t salt retention), and mild proteinuria ( Proteinuria (>3.5g/day), frothy urine, hyperlipidemia, fatty casts, edema
  • ->associatd with thromboemolism and increased risk of infection (b/c loss of immunglobulins)

***lose charge barrier (fused basement membrane) of glomerular filtration barrier in nephrotic syndrome

67
Q

Lumpy bumby appearance of glomeruli on LM?

A

Acute PSGN

68
Q

child with peripheral and periorbital edema, dark urine, elevated anti-ASO, elevated anti-DNAse B, decreased C3 and total complement levels

A

Acute PSGN

69
Q

supepithelial humps on EM

A

Acute PSGN

70
Q

Wegener’s vs Goodpasture

A

both cause Crescentic/RPGN

  • ->Goodpastures only affects lung and kidneys (hematuria + hemoptysis)
  • ->Wegener’s: c-ANCA; and can also affect upper airways, so may present with sinusitis, nasal perforation, as well as hematuria, hemoptysis
71
Q

subendothelial and maybe intramembranous IgG-based immune complexes, often with C3 deposition seen on EM

A

Diffuse Proliferative GN

72
Q

wire looping of capillaries on LM

A

Diffues Proliferative GN

–>see in SLE or MPGN (Membranoproliferative GN)

73
Q

most common cause of death in SLE?

A
  • Diffuse Proliferative GN (associated with anti-dsDNA marker)
  • -> can present as nephrotic and nephritic syndrome concurrently
74
Q

Nephritis + IgA immune complexes in mesangium + URI or acute gastroenteritis

A

Berger’s disease = IgA nephropathy

–>related to Henoch-Schonlein disease (vasculitis, also have IgA immune complexes)

75
Q

Nephritis with mutation in type IV collagen –> split Basement membrane, X-linked

A

Alport syndrome = “can’t see, can’t pee, can’t hear”

–>have nerve disorders, ocular disorders, deafness

76
Q

most common glomerular disease in HIV pts?

A

Focal Segmental Glomerulosclerosis

77
Q

Most common cause of adult nephrotic syndrome?

A

Membranous GN

78
Q

Spike and dome appearance on EM with subepithelial deposits

A

Membranous GN

79
Q

Foot process effacement on EM

A

Minimal Change Disease

80
Q

Treatment for Minimal Change Disease?

A

Corticosteroids

81
Q

Selectively lose albumin, but not globulins:

A

Minimal Change Disease

82
Q

What conditions are associated with nephrotic syndrome caused by Amyloidosis (have amyloid deposits in mesangium)?

A

Associated w/chronic conditions:

  • multiple myeloma
  • TB
  • Rheumatoid arthritis
83
Q

Tram-track appearance on LM with GBM splitting

A

Type I Membranoproliferative GN

84
Q

Glomerulonephritis associated with HBV, HCV

A

Type I Membranoproliferative GN

85
Q

“dense deposits” on EM

A

Type II Membranoproliferative GN

86
Q

Pathology behind Diabetic Glomerulonephropathy:

A

Non-enzymatic glycosylation of GBM –> increased permeability and thickening
Also: nonenzymatic glycosylation of efferent arterioles –> increased GFR –> mesangial expansion

***see GBM thickening on LM! and mesangial expansion..

87
Q

Kimmelstein-Wilson lesion:

A

-Diabetic glomerulonephropathy

88
Q

Most common type of kidney stones?

A

Calcium (Calcium oxalate, Calcium phosphate, or both)

89
Q

Calcium kidney stones:

  • ph they precipitate at?
  • x-ray appearance?
  • what conditions may cause them?
A
  • most common type of kidney stones; may be calcium oxalate or calcium phosphate or both
  • precipitate at neutral or decreased pH
  • radiopaque on x-ray
  • conditions that cause hypercalcemia (like cancer, elevated PTH) can lead to hypercalciuria and stones
  • may get oxalate crystals from ethylene glycol (antifreeze) or vitamin C abuse
90
Q

Vitamin C abuse may lead to what type of kidney stones?

A

Calcium oxalate crystals

91
Q

Ethylene glycol (anti-freeze) may lead to what kind of kidney stones?

A

Calcium-oxalate kidney stones

92
Q

Staghorn calculi

A

Get these with ammonium-magnesium-phosphate kidney stones (caused by infection with urease-positive bugs…)

93
Q

Ammonium-Magnesium-Phosphate kidney stones:

  • ph precipitate at?
  • X-ray appearance?
  • Caused by?
A
  • precipitates at elevated pH
  • radio-opaque or radiolucent on xray
  • caused by infection with urease positive bugs (ie proteus, klebsiella) that form ammonium cation that binds to Mg and P and forms stones
94
Q

Uric acid kidney stones:

  • precipitates at what pH?
  • x-ray appearance?
  • associated with?
A
  • low pH
  • radio-lucent
  • assoc with hyperuricemia (ie gout); also diseases with high cell turnover, like leukemia
95
Q

Cystine kidney stones:

  • precipitate at what pH?
  • x-ray appearance?
  • causes?
  • treatment?
A
  • low pH
  • radioopaque
  • usually secondary to cystinuria
  • treat by alkalinizing urine
96
Q

What causes hydronephrosis?

A

Results for complete or partial obstruction of urinary tract

97
Q

polygonal clear cells on histology

A

Renal cell carcinoma

–>cells are filled with lipids and carbohydrates

98
Q

2 main sites of metastasis of renal cell carcinoma?

A

lung and bone

99
Q

Most common renal malignancy of childhood?

A

Wilm’s tumor = Nephroblastoma

–>2-4 yo

100
Q

huge, palpable flank mass and/or hematuria in child 2-4 yo?

A

Wilm’s tumor = Nephroblastoma

101
Q

WAGR complex:

A
  • Wilm’s tumor
  • Aniridia (no iris)
  • Genitourinary malformation
  • mental-motor Retardation
  • d/t deletion on chromosome 11
  • often obese too
102
Q

Squamous cell cancer of the bladder associated with?

A

Schistosomiasis

103
Q

Painless hematuria, no casts:

A

Bladder cancer –> Transitional cell carcinoma

104
Q

most common tumor of urinary tract system?

A

Transitional cell cancer (can occur in renal calyces, pelvis, ureters, bladder…)

105
Q

Problems associated with Transitional Cell Carcinoma?

A

Pee SAC:

  • Phenacetin (analgesic; acetaminophen=phenacetin derivative)
  • Smoking
  • Aniline dyes
  • Cyclophosphamide (alkylating agent, used to treat cancers/immunosuppressant)
106
Q

Histology of Acute vs Chronic Pyelonephritis?

A
  • Acute –> neutrophil infiltration ito renal interstitium

- Chronic –> lymphocytic invasion with fibrosis

107
Q

Thyroidization of kidney (eosinophilic casts in tubules)

A

Chronic pyelonephritis

108
Q

fever + rash + hematuria + flank tenderness 1-2 weeks after taking certain drugs

A

Drug-induced / Acute Interstitial Nephritis

109
Q

What causes Acute Interstitial Nephritis?

A
  • DRUGS!:
  • NSAIDs
  • diuretics
  • penicillins
  • sulfonamides
  • rifampin
  • get interstitial renal inflammation, pyuria, azotemia, 1-2 weeks after taking meds
  • also: fever, rash, hematuria, flank pain
110
Q

Most common cause of acute renal failure in hospital?

A

Acute tubular necrosis

–>can be reversible, but fatal if left untreated

111
Q

3 stages of Acute Tubelar Necrosis:

A

1) Inciting event(ie renal ischemia from shock, sepsis, or crush injury like myoglobinuria)
2) Maintenance phase –> oliguric; 1-3 weeks; risk of hyperkalemia; have muddy brown casts
3) Recovery –> polyuric, risk of hypokalemia; get decreased levels of BUN and serum creatinine

112
Q

Definition of Acute Renal Failure = Acute Kidney Injury:

A

–>abrupt decline in renal function with elevated Creatinine and elevated BUN (so, Azotemia) over several days

113
Q

Pre-Renal Azotemia: Acute Renal Failure

A
  • -> not enough blood to kidney: so decreased RBF (ie hypotension) –> decreased GFR
  • Na, H20, and urea are retained by the kidney (not excreted in urine) to conserve volume
  • So: get elevated BUN/Creatinine ratio
114
Q

Intrinsic Renal: Acute Renal Failure

A

usually d/t acute tubular necrosis or ischemia/toxins

  • ->have necrosis or something that obstructs the tubule, so get fluid backflow across the necrotic tubule –> decreases GFR
  • Also: BUN reabsorption impaired –> decreased BUN/Creatinine ratio
115
Q

Postrenal: Acute Renal Failure

A
  • ->d/t outflow obstruction (ie stones, BPH, neoplasia, congenital anomalies)
  • ->only have bilateral obstruction with postrenal…
116
Q

2 most common causes of chronic renal failure?

A
  • Hypertension

- Diabetes

117
Q

Renal Osteodystrophy:

A
  • get this with chronic renal failure
  • failure of vitamin D hydroxylation –> Calcium wasting and Phosphate retention –> secondary hyperparathyroidism
  • causes subperiosteal thinning of bones
118
Q

Autosomal dominant mutation in PKD1 or PKD2 gene?

A

ADPKD

119
Q

What conditions are associated with ADPKD?

A
  • polycystic liver disease
  • berry aneurysms
  • mitral valve prolapse
120
Q

bilaterally enlarged kidneys + oligohydramnios + small/absent bladder in-utero (by US)?

A

–>ARPKD

121
Q

Thin, nonenhancing, cortical, fluid filled cysts in kidney?

A

Benign simple cysts; incidental finding in elderly

***don’t confuse these with medullary cystic disease –> medullary cysts, fibrosis, progressive renal insufficiency, can’t concentrate urine, small kidney –> poor prognosis!

122
Q

Osmotic diuretic

A

Mannitol

–>increased tubular fluid osmolarity, so helps excrete free H2O)

123
Q

Diuretic with Pulmonary edema side effect?

A

Mannitol

124
Q

Diuretic used to treat altitude sickness?

A

Acetazolamide

  • ->Carbonic anhydrase inhibitor –> helps get rid of HCO3
  • ->can also be used for glaucoma
  • ->may cause hyperchloremic metabolic acidosis….
125
Q

Diuretics used to treat Glaucoma?

A
  • Acetazolamide –> for long-term treatment

- Mannitol –> for emergencies

126
Q

Diuretic of choice to treat edematous states (ie CHF, cirrhosis, nephrotic syndrome, pulmonary edema…)?

A

Furosemide (loop diuretic)

127
Q

Side effects of Furosemide?

A

“OH DANG”

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (Acute Interstitial Nephritis)
  • Gout
128
Q

NSAIDs inhibit the effect of which type of diuretic? Why?

A

NSAIDs inhibit Furosemide
–>Furosemide/Loop diuretics stimulate Prostaglandin release; so, if give NSAIDs + loop diuretics together –> get decreased diuretic response

129
Q

Drugs that are both Ototoxic and Nephrotoxic?

A
  • Aminoglycosides
  • Loop diuretics (Furosemide)
  • Cisplatin and Carboplatin (anti-cancer drugs)
  • Vancomycin
130
Q

Ethacrynic acid

A

Loop diuretic, works the same way as Furosemide. But, not a sulfonamide (unlike furosemide)
–>give to pts with sulfa allergy

131
Q

K+ sparing diuretics:

A

“K+ STAES”

  • Spironolactone
  • Triamterene
  • Amiloride
  • Eplerenone
132
Q

Which diuretics lead to increased urinary K+ (decreased blood K+)?

A

–>all, EXCEPT for K+sparing

133
Q

Which diuretics may lead to decrease pH –> acidemia?

A
  • ->Carbonic anhydrase inhibitors

- ->K+ sparing diuretics

134
Q

Which diuretics may lead to increase pH –> alkalemia?

A
  • ->Loop diuretics

- ->Thiazides

135
Q

Why should ACE-inhibitors NOT be given to pts with renal artery stenosis?

A
  • ->pts with renal artery stenosis depend on EA constriction to maintain renal perfusion; but, ACE inhibitors cause EA dilation –> decreased GFR, decreased FF
  • ->so, ACE inhibitors can cause acute renal failure or complicate an existing renal disease in pts with renal artery stenosis

FirstAID (24 decks)

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