Renal Flashcards Preview

FirstAID > Renal > Flashcards

Flashcards in Renal Deck (135):
1

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

Left Kidney; because it has a longer renal vein

2

Where is the macula densa located?

Distal convoluted tubule

3

Where are JG cells located?

Afferent arteriole

4

ureterovesicular junction

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

5

nephrocalcinosis

calcification of the medullary periods; assoc w/hyperparathyroidism

6

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

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

-->"water passes under the bridge"
-water=ureters
-bridge=uterine arteries and ductus deferens

7

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

60% = total body water
40% = ICF
20% = ECF

8

How to measure plasma volume?

radiolabeled albumin

9

how to measure extracellular volume?

Inulin

10

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?

*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

11

What substances can be used to measure GFR?

-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

12

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

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

13

ERPF vs true RPF?

ERPF underestimates true RPF by about 10%

14

RBF =?

RBF = RPF/(1-Hct)

15

Normal Filtration Fraction =?

20%

16

Effect of prostaglandings on kidney:
Effect of NSAIDs on kidney?

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

17

Effect of Angiotensin II on kidneys?

Acts on Efferent Arteriole; constricts EA:
-decreased RPF
-increased GFR
-increased FF

18

Effect of ACE-inhibitors on kidneys?

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)


19

What is Creatinine in urine a measurement of?

Glomerular Filtration Rate

20

Where in kidney is glucose normally reabsorbed?

Proximal tubule by Na+/glucose cotransport

21

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

-see glucosuria at plasma glucose levels of 160-200
-all transporters are fully saturated (Tm) at plasma glucose levels = 350 mg/dL

22

Hartnups disease:

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)

23

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

Early proximal tubule

24

Where in kidney is there "isotonic absorption"?

Early proximal tubule

25

Which part of nephron generates and secretes ammonia?

Early proximal tubule

26

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

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.

27

Which part of nephron is impermeable to water?

Thick ascending limb of loop of Henle

28

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

Early distal convoluted tubule

29

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

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)

30

Where in nephron does PTH act?

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

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

31

Where in nephron does Angiotensin II act?

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

32

ADH vs Aldosterone:

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

33

Juxtaglomerular Apparatus:

-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)

34

Which cells secrete renin?

JG cells (in Afferent Arteriole)

35

How may NSAIDs cause acute renal failure?

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

36

4 endocrine functions of the kidneys:

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

37

Hormones that act on the kidney:

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

38

ANP = Atrial Natriuretic Peptide

-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

39

PTH:

-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)

40

AT II = Angiotensin II

-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!)

41

Aldosterone:

-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

42

ADH/Vasopressin

-secreted in response to elevated plasma osmolarity and decreased blood volume
-causes increased # of water channels and increased water reabsorption

43

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

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

44

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

-insulin
-beta-agonists (ie albuterol)
-alkalosis
-hypo-osmolarity

45

Too rapid correction of Hyponatremia?

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

46

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

low serum K+

47

Peaked T waves, wide QRS, arrhythmias:

high serum K+

48

effects of low serum Ca?

-Tetany
-Neuromuscular irritability

49

effects of high serum Ca?

"stones, bones, groans, moans"
-delirium
-renal stone
-abdominal pain

50

effects of low serum Phosphate?

bone loss and osteomalacia

51

effectsof high serum Phosphate?

renal stones, metastatic calcifications

52

Compensatory response to respiratory acidosis or alkalosis?

--> 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!)

53

Causes of metabolic acidosis with a high anion gap?

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

54

Causes of normal anion gap metabolic acidosis?

-Diarrhea
-Glue sniffing
-Renal tubular acidosis (RTA)
-Hyperchloremia

55

Causes of Respiratory alkalosis:

-Hyperventilation (early high-altitude exposure)
-Initially after aspirin ingestion (then becomes anion-gap metabolic acidosis)

56

Causes of metabolic alkalosis with compensation (Hypoventilation):

-Diuretics
-Vomiting
-Antacids
-Hyperaldosteronsim (increases H+ secretion)

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

57

Causes of Respiratory Acidosis:

*any time can't get rid of CO2!
-airway obstruction
-acute lung disease
-chronic lung disease
-opiods, narcotics, sedatives
-weakened respiratory muscles

58

How to calculate anion gap:

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

59

3 types of RTA (Renal Tubular Acidosis)

*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

RBC casts

Glomerulonephritis
-Also: ischemia, malignant HTN

61

WBC casts

-Acute pyelonephritis
-Tubulointerstitial inflammation
-Also: transplant rejetion

62

"muddy brown"/Granular casts

Acute tubular necrosis

63

Waxy casts

advanced/chronic renal disease

64

Hyaline casts

nonspecific

65

What does the presence of casts in urine indicate?

-->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

Nephritis vs Nephrotic syndromes:

*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

Lumpy bumby appearance of glomeruli on LM?

Acute PSGN

68

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

Acute PSGN

69

supepithelial humps on EM

Acute PSGN

70

Wegener's vs Goodpasture

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

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

Diffuse Proliferative GN

72

wire looping of capillaries on LM

Diffues Proliferative GN
-->see in SLE or MPGN (Membranoproliferative GN)

73

most common cause of death in SLE?

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

74

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

Berger's disease = IgA nephropathy
-->related to Henoch-Schonlein disease (vasculitis, also have IgA immune complexes)

75

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

Alport syndrome = "can't see, can't pee, can't hear"
-->have nerve disorders, ocular disorders, deafness

76

most common glomerular disease in HIV pts?

Focal Segmental Glomerulosclerosis

77

Most common cause of adult nephrotic syndrome?

Membranous GN

78

Spike and dome appearance on EM with subepithelial deposits

Membranous GN

79

Foot process effacement on EM

Minimal Change Disease

80

Treatment for Minimal Change Disease?

Corticosteroids

81

Selectively lose albumin, but not globulins:

Minimal Change Disease

82

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

Associated w/chronic conditions:
-multiple myeloma
-TB
-Rheumatoid arthritis

83

Tram-track appearance on LM with GBM splitting

Type I Membranoproliferative GN

84

Glomerulonephritis associated with HBV, HCV

Type I Membranoproliferative GN

85

"dense deposits" on EM

Type II Membranoproliferative GN

86

Pathology behind Diabetic Glomerulonephropathy:

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

Kimmelstein-Wilson lesion:

-Diabetic glomerulonephropathy

88

Most common type of kidney stones?

Calcium (Calcium oxalate, Calcium phosphate, or both)

89

Calcium kidney stones:
-ph they precipitate at?
-x-ray appearance?
-what conditions may cause them?

-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

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

Calcium oxalate crystals

91

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

Calcium-oxalate kidney stones

92

Staghorn calculi

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

93

Ammonium-Magnesium-Phosphate kidney stones:
-ph precipitate at?
-X-ray appearance?
-Caused by?

-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

Uric acid kidney stones:
-precipitates at what pH?
-x-ray appearance?
-associated with?

-low pH
-radio-lucent
-assoc with hyperuricemia (ie gout); also diseases with high cell turnover, like leukemia

95

Cystine kidney stones:
-precipitate at what pH?
-x-ray appearance?
-causes?
-treatment?

-low pH
-radioopaque
-usually secondary to cystinuria
-treat by alkalinizing urine

96

What causes hydronephrosis?

Results for complete or partial obstruction of urinary tract

97

polygonal clear cells on histology

Renal cell carcinoma
-->cells are filled with lipids and carbohydrates

98

2 main sites of metastasis of renal cell carcinoma?

lung and bone

99

Most common renal malignancy of childhood?

Wilm's tumor = Nephroblastoma
-->2-4 yo

100

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

Wilm's tumor = Nephroblastoma

101

WAGR complex:

-Wilm's tumor
-Aniridia (no iris)
-Genitourinary malformation
-mental-motor Retardation

*d/t deletion on chromosome 11
*often obese too

102

Squamous cell cancer of the bladder associated with?

Schistosomiasis

103

Painless hematuria, no casts:

Bladder cancer --> Transitional cell carcinoma

104

most common tumor of urinary tract system?

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

105

Problems associated with Transitional Cell Carcinoma?

Pee SAC:
-Phenacetin (analgesic; acetaminophen=phenacetin derivative)
-Smoking
-Aniline dyes
-Cyclophosphamide (alkylating agent, used to treat cancers/immunosuppressant)

106

Histology of Acute vs Chronic Pyelonephritis?

-Acute --> neutrophil infiltration ito renal interstitium
-Chronic --> lymphocytic invasion with fibrosis

107

Thyroidization of kidney (eosinophilic casts in tubules)

Chronic pyelonephritis

108

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

Drug-induced / Acute Interstitial Nephritis

109

What causes Acute Interstitial Nephritis?

*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

Most common cause of acute renal failure in hospital?

Acute tubular necrosis
-->can be reversible, but fatal if left untreated

111

3 stages of Acute Tubelar Necrosis:

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

Definition of Acute Renal Failure = Acute Kidney Injury:

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

113

Pre-Renal Azotemia: Acute Renal Failure

--> 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

Intrinsic Renal: Acute Renal Failure

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

Postrenal: Acute Renal Failure

-->d/t outflow obstruction (ie stones, BPH, neoplasia, congenital anomalies)
-->only have bilateral obstruction with postrenal...

116

2 most common causes of chronic renal failure?

-Hypertension
-Diabetes

117

Renal Osteodystrophy:

*get this with chronic renal failure

*failure of vitamin D hydroxylation --> Calcium wasting and Phosphate retention --> secondary hyperparathyroidism

*causes subperiosteal thinning of bones

118

Autosomal dominant mutation in PKD1 or PKD2 gene?

ADPKD

119

What conditions are associated with ADPKD?

-polycystic liver disease
-berry aneurysms
-mitral valve prolapse

120

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

-->ARPKD

121

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

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

Osmotic diuretic

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

123

Diuretic with Pulmonary edema side effect?

Mannitol

124

Diuretic used to treat altitude sickness?

Acetazolamide
-->Carbonic anhydrase inhibitor --> helps get rid of HCO3
-->can also be used for glaucoma
-->may cause hyperchloremic metabolic acidosis....

125

Diuretics used to treat Glaucoma?

-Acetazolamide --> for long-term treatment
-Mannitol --> for emergencies

126

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

Furosemide (loop diuretic)

127

Side effects of Furosemide?

"OH DANG"
-Ototoxicity
-Hypokalemia
-Dehydration
-Allergy (sulfa)
-Nephritis (Acute Interstitial Nephritis)
-Gout

128

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

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

129

Drugs that are both Ototoxic and Nephrotoxic?

-Aminoglycosides
-Loop diuretics (Furosemide)
-Cisplatin and Carboplatin (anti-cancer drugs)
-Vancomycin

130

Ethacrynic acid

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

131

K+ sparing diuretics:

"K+ STAES"
-Spironolactone
-Triamterene
-Amiloride
-Eplerenone

132

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

-->all, EXCEPT for K+sparing

133

Which diuretics may lead to decrease pH --> acidemia?

-->Carbonic anhydrase inhibitors
-->K+ sparing diuretics

134

Which diuretics may lead to increase pH --> alkalemia?

-->Loop diuretics
-->Thiazides

135

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

-->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