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USMLE: step 1 > Renal > Flashcards

Renal Flashcards

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USMLE® Step 1 flashcards
1
Q

Where is horseshoe kidney normally found? Why?

A
  • Lower abdomen

- Gets stuck on IMA as it ascends from pelvis

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2
Q

What is dysplastic kidney?

A
  • Non inherited, congenital malformation of renal parenchyma
  • With cysts and abnormal tissue eg: cartilage
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3
Q

Ddx with bilateral dysplastic kidney?

A

Inherited PKD “Polycystic kidney disease”

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4
Q

What is PKD?

A

“Polycystic kidney disease”

  • Inherited defect of bilaterally enlarged kidneys
  • Cysts in renal cortex and medulla
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5
Q

Associations with recessive PKD?

A
  • Hepatic fibrosis and cysts: portal HTN
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6
Q

Presentation of ARPKD?

A
  • Infantile presentation with HTN and worsening renal failure
  • Potter’s sequence
  • Hepatic fibrosis and cysts
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7
Q

ADPKD associations?

A
  1. Berry aneurysm
  2. Hepatic cysts
  3. Mitral valve prolapse
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8
Q

Presentation ADPKD?

A

Adults with HTN, hematuria, and renal failure

- Cysts in brain, heart, and liver

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9
Q

What is medullary cystic kidney disease?

A
  • Inherited AD defect
  • Cysts in medullary collecting ducts
  • Parenchymal fibrosis = shrunken kidneys with renal failure
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10
Q

What is hallmark of acute renal failure?

A
  1. Azotemia: increased nitrogenous waste products

2. Oliguria

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11
Q

What are the renal parameters indicative of prerenal failure?

A
  1. BUN:CR > 15

2. FeNa 500 (tubular function still in tact)

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12
Q

What is normal BUN:Cr?

A

15

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13
Q

Why does BUN:Cr increase in prerenal failure?

A
  • Low blood flow increases renin / aldosterone
  • Aldosterone increase Na / H2O absorption
  • Bun follows water and Na out of tubules
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14
Q

What is normal FENa and urine osmolality?

A

FENa: 500

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15
Q

Difference between ST / LT post renal azotemia?

A

ST: tubular function preserved to FENa and OSM normal and BUN:CR increases as bun pushed back
LT = tubular damage: FENA > 2%, osm

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16
Q

What is most common cause of ARF?

A
  • ATN
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17
Q

What happens in ATN?

A
  • Injury and necrosis of tubular epithelial cells
  • Necrotic cells plug tubules decreasing GFR
  • Brown casts will be seen in urine
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18
Q

What are brown casts in urine indicative of?

A

ATN

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19
Q

Urine parameters in ATN?

A
  1. BUN:CR 2%

3. Urine OSM

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20
Q

2 etiologies of ATN?

A
  1. Ischemic: preceded by prerenal azotemia

2. Nephrotoxic

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21
Q

Which part of kidney most susceptible to ischemic ATN?

A
  1. Proximal tubule

2. Medullary segment thick ascending limb

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22
Q

Part of kidney most affected in toxic ATN?

A

Proximal tubule

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23
Q

Causes of toxic ATN?

A
  1. Aminoglycosides
  2. Heave metals
  3. Myoglobinuria: crush injury
  4. Ethylene glycol: antifreeze
  5. Radiocontrast dye
  6. Urate: tumor lysis syndrome
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24
Q

How to prevent tumor lysis syndrome?

A
  • Hydrate patient

- Allopurinol to prevent formation of uric acid

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25
Q

Prognosis of ATN?

A
  • Damage is reversible but often requires dialysis due to deadly electrolyte imbalances that can ensue
  • Oliguria persists for 2 - 3 weeks
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26
Q

What is acute interstitial nephritis?

A
  • Drug induced HSR of interstitium and tubules

- Causes ARF

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27
Q

What can cause AIN?

A
  1. NSAIDs
  2. PCN
  3. Diuretics
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28
Q

Presentation of AIN?

A
  1. Rash
  2. Fever
  3. Oliguria
  4. EOSs in urine
    * **Days to weeks after drug
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29
Q

What are eosinophils in urine indicative of?

A

AIN

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30
Q

What can AIN progress to?

A

Renal papillary necrosis

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31
Q

Presentation of renal papillary necrosis?

A
  1. Flank pain

2. Gross hematuria

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32
Q

Causes of AIN?

A
  1. Chronic analgesic use
  2. TIIDM
  3. Sickle cell
  4. Severe pyelonephritis
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33
Q

Presentation of nephrotic syndrome? and why are they occurring?

A
  1. Proteinuria > 3.5 g / day
  2. HYPOalbuminemia = edema
  3. HYPOgammaglobulinemia = increased risk infx
  4. Hypercoagulable state = loss of ATIII
  5. Hyper lipids and cholesterol = liver drops fat to counteract thin blood
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34
Q

Most common cause of nephrotic syndrome in kids? Cause?

A
  • MCD

- Usually idiopathic but can be associated with hodgkin lymphoma

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35
Q

What do the podocytes sit on?

A

Epithelial layer

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36
Q

What is happening in MCD?

A
  • Flattening of podocyte foot processes from production of cytokines
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37
Q

MCD on imaging?

A

HE: normal
EM: podocyte foot effacement
IF: negative as no IC involved

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38
Q

Proteinuria characteristics in MCD?

A
  • Selective with loss of albumin but no loss of immunoglobulin
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39
Q

Rx for MCD?

A
  • Great response to steroids

- Makes sense as caused by cytokines

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40
Q

3 layers of filtration barrier?

A
  1. Endothelial layer: next to vessels
  2. Basement membrane
  3. Epithelial layers: podocytes
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41
Q

Who is FSGS common in?

A
  1. Hispanics

2. Blacks

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42
Q

What can cause FSGS?

A
  1. Idiopathic
  2. HIV
  3. Heroin
  4. Sickle cell disease
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43
Q

Imagine of FSGS?

A

HE: Focal / segmental pink sclerosis
EM: effacement of foot processes
IF: negative

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44
Q

What does MCD progress to?

A

FSGS if they do not respond to steroids

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45
Q

Prognosis of FSGS?

A
  • Poor response to steroids with progression to chronic renal failure
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46
Q

What are the nephrotic syndromes?

A
  1. MCD
  2. FSGS
  3. Membranous nephropathy
  4. Membranoproliferative glomerulonephritis
  5. TIIDM
  6. Amyloidosis
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47
Q

Most common cause of nephrotic syndrome in white people?

A

Membranous nephropathy

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48
Q

Causes of membranous nephropathy?

A
  1. Idiopathic
  2. HBV / HCV
  3. SLE
  4. Solid tumors
  5. Drugs
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49
Q

Most common cause of death in SLE?

A
  • Renal failure
  • Membranous nephropathy in nephrotic
  • Diffuse proliferative glomerulonephritis if nephritic
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50
Q

Imaging in membranous nephropathy?

A

HE: Thick basement membrane
EM: spike and dome
IF: granular, this is what is thickening membrane

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51
Q

What is spike and dome appearance on EM indicative of?

A

Membranous nephropathy

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52
Q

WHat is happening in all renal diseases with membranous in name?

A

Thickening of GBM from IC deposition

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53
Q

WHat is causing membranous nephropathy?

A
  • IC deposition under the podocytes
  • Leads to granular / spike and dome appearance
  • Podocyte does not like having IC under it so secretes more basement membrane on top of it leading to spike and dome
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54
Q

When is tram track appearance seen?

A

Membranoproliferative Glomerulonephritis

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55
Q

2 locations of IC deposit in membranoproliferative glomerulonephritis? How does it lead to imaging?

A

“Proliferative” mesangial cell is proliferating through IC

  1. Basement membrane: mesangial cell splits it in half with its cytoplasm
  2. Endothelium
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56
Q

Location in type 1 / 2 membranoproliferative? Associations?

A

Type 1: Subendothelial
- HBV / HCV
Type 2: Intramembranous
- C3 nephritic factor

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57
Q

What is C3 nephritic factor associated with?

A
  • Type II membranoproliferative glomerularnephritis
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58
Q

What is going on in type II membranoproliferative?

A
  • C3 convertase normally converts C3 -> C3a/b
  • Normally has short 1/2 life: in disease is stabilized by Ig
  • Leads to drop in C3 and overactive complement
  • Leads to inflammation in kidneys
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59
Q

Where are subepithelial deposits seen?

A

Membranous nephropathy

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60
Q

Pathogenesis of TIIDM nephrotic syndrome?

A
  • High glucose = non enzymatic glycosylation of vascular basement membrane = hyaline arteriolosclerosis
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61
Q

Does diabetic nephrotic system like afferent or efferent arterioles?

A
  • Efferent - this is why GFR increases
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62
Q

How to slow progression of diabetic nephrotic syndrome?

A

ACEIs

  • Angiotensin II is squeezing down on efferent as well
  • So if we stop this we decrease the already increased hyperfiltration that is occurring from the hyaline arteriolar sclerosis of efferent
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63
Q

Classic histology in diabetic nephropathy?

A
  • Sclerosis of mesangium

- Formation of kimmelstiel wilson nodules

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64
Q

What are kimmelstiel wilson nodules indicative of?

A

Diabetic nephropathy

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65
Q

Most common site of systemic amyloidosis?

A
  • Kidney where amyloid deposits in mesangium
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66
Q

Imaging of renal amyloidosis?

A

Apple green birefringence under polarized light

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67
Q

Presentation of nephrotic syndrome?

A

“Glomerular inflammation and bleeding”

  1. RBC casts and RBCs in urine
  2. Oliguria / azotemia
  3. Salt retention: periorbital edema
  4. HTN
  5. Proteinuria
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68
Q

What is periorbital edema associated with?

A

Nephritic syndrome

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69
Q

What is causing nephritic syndrome?

A
  • IC deposition activates complement

- C5a attracts neuts who mediate damage

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70
Q

Biopsy in nephritic syndrome?

A

Inflamed, hypercellular glomeruli

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71
Q

What causes PSGN?

A

Group A, beta hemolytic strep infx of skin or pharynx

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72
Q

What makes strep capable of causing PSGN?

A

M protein

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73
Q

PSGN presentation?

A
  1. 2 - 3 weeks post infx
  2. Cola colored urine
  3. Oliguria
  4. HTN
  5. Periorbital edema
  6. Subepithelial humps on imaging
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74
Q

When are subepithelial humps seen? What is happening?

A
  • PSGN

- IC is deposited endothelial then moves epithelial creating hump

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75
Q

PSGN prognosis?

A

Kids: rarely progress to failure
Adults: RPGN

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76
Q

What is characteristics of RPGN?

A

Crescents in bowman’s space

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77
Q

What are crescents indicative of?

A

RPGN

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78
Q

What are crescents composed of?

A

Fibrin and macrophages

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79
Q

When is linear IF seen? What is causing it?

A
  • Goodpasture’s

- Anti GBM Ig is binds membrane in linear fashion

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80
Q

Presentation and pathogenesis of goodpasture’s?

A
  • Ig against collagen in GBM and alveolar basement membrane
  • Presents as hematuria and hemoptysis
  • Classic in young males and adults
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81
Q

Causes of granular IF?

A
  1. PSGN
  2. Diffuse, proliferative glomerulonephritis
    * ***Caused by IC deposition in both cases
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82
Q

What is occurring in diffuse proliferative glomerulonephritis?

A
  • Most often seen in SLE

- Subendothelial IC deposition

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83
Q

Possible causes of pauci immune crescents?

A
  1. Wegener’s granulomatosis: c-ANCA
  2. Microscopic polyangiitis: p-ANCA
  3. Churg Strauss: p-ANCA
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84
Q

Presentation of wegener’s?

A
  1. Hemoptysis
  2. Hematuria
  3. Nasopharynx involvement
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85
Q

How do differentiate wegener’s from goodpasture’s?

A

Both: renal and pulm symptoms

Wegener’s also involves nasopharynx

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86
Q

How to tell churg strauss from microscopic polyangiitis?

A

Churg strauss has:

  1. Asthma
  2. Eosinophils
  3. Granulomatis inflammation
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87
Q

What happens in IgA nephropathy?

A
  • IgA, IC deposition in mesangium

- Most common worldwide nephropathy

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88
Q

Presentation of IgA nephropathy?

A
  • Episodic hematuria
  • Usually in kids following mucosal infx
  • Can slowly progress to renal failure
  • IgA IC deposition in mesangium
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89
Q

Imaging of IgA nephropathy?

A
  • Granular IF
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90
Q

Cause / presentation of Alports?

A

X linked defect in collagen Type IV:

  1. Thinning and splitting of GBM
  2. Sensory hearing loss
  3. Hematuria
  4. Ocular disturbances
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91
Q

What is cystitis?

A

Bladder infx

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92
Q

Presentation of cystitis?

A
  1. Dysuria
  2. Frequency / urgency
  3. Suprapubic pain
  4. No systemic signs
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93
Q

Labs in cystitis?

A

Urinalysis: cloudy, > 10 WPCs / hPF
Dipstick: Leukocyte esterase and nitrate +
Culture: > 100k colony forming units

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94
Q

What is sterile pyuria and what does it suggest?

A
  • Pyuria but culture does not meet 100k colony forming units
    Suggests URETHRITIS due to:
    1. Chlamydia
    2. Gonorrhea
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95
Q

Pyelonephritis symptoms?

A
  1. Cystitis symptoms
  2. Fever
  3. Flank pain
  4. WBC casts
  5. Leukocytosis
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96
Q

Most common causes of pyelonephritis?

A
  1. E Coli
  2. Klebsiella
  3. Enterococcus
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97
Q

What is chronic pyelonephritis?

A
  • Interstitial fibrosis and tubules atrophy from recurrent acute infx
  • Causes cortical scarring and blunted calyces
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98
Q

What is cortical scarring and blunted calyces characteristic of?

A

Chronic pyelonephritis

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99
Q

What is scarring at upper poles of kidneys indicative of?

A

Vesicoureteral reflux

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100
Q

What is the following indicative of:

  • Atrophic tubules w/ eosinophilic proteinaceous material
  • Reminiscent of thyroid follicles
  • Waxy casts in urine
A

“Thyroidization of kidney”

- Chronic pyelonephritis

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101
Q

What is the following indicative of:

  • Collicky pain
  • Hematuria
  • Flank tenderness
A

Nephrolithiasis

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102
Q

Rx for Ca stones?

A
  1. Hydrochlorothiazide and other Ca sparring diuretics

2. Citrate

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103
Q

What disease are Ca stones seen in?

A

Chrohns

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104
Q

What orgs cause AMP stones?

A

Urease positive orgs:

  1. Proteus vulgaris
  2. Klebsiella
    * **The alkaline urine is leading to formation of stone
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105
Q

Which stones cause staghorn calculi?

A
  1. AMP: adult

2. Cysteine: kid

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106
Q

Which stone is radiolucent?

A

Uric acid = not visible on xray

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107
Q

Risk factors for uric acid stones?

A
  1. Hot / arid climate
  2. Low urine volume
  3. Low PH
  4. Gout
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108
Q

Rx for uric acid stone?

A
  1. Hydration
  2. Alkalization of urine: K/bicarb
  3. Allopurinol: if gout
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109
Q

Types of Ca stones and environment they prefer?

A
  1. Oxalate: acidic

2. Phosphate: basic

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110
Q

Which stones are envelope or dumbbell shaped?

A

Ca

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111
Q

Some causes of Ca stones?

A
  1. Antifreeze
  2. Hypocitraturia
  3. Chrons
  4. Vitamin C abuse
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112
Q

Which stone looks like coffin lid?

A

AMP

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113
Q

Which stones are rhomboids or rosettes?

A

Uric acid

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114
Q

Which stones are hexagonal?

A

Homocystinuria: ‘cyxteine’ six sides

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115
Q

Most common causes of renal failure?

A
  1. TIIDM
  2. HTN
  3. Glomerular disease
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116
Q

What is uremia?

A

Increased nitrogenous products in blood causing:

  1. Nausea
  2. Anorexia
  3. Pericarditis
  4. Platelet dysfunction
  5. Encephalopathy + asterixis
  6. Urea deposition in skin
    * *Cause by end stage renal failure
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117
Q

Where is EPO made?

A

Renal peritubular interstitial cells

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118
Q

Signs of end stage renal failure?

A
  1. Uremia
  2. HTN from salt and water retention
  3. Hyper K with metabolic acidosis
  4. Anemia - decrease EPO
  5. HYPOcalcemia: decreased 1-a-hydroxylation of vit. D
    - Also cannot excrete P - increased P
  6. Renal osteodystrophy
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119
Q

3 components of renal osteodystrophy?

A
  1. Osteitis fibrosis cystica
  2. Osteomalacia
  3. Osteoporosis
120
Q

What is osteitis fibrosis cystica?

A
  • Low Ca = increased PTH pulling more Ca out

- Leads to fibrosis and cysts in bone

121
Q

What is osteomalacia?

A
  • Cannot mineralize osteoid being make by osteoblasts
122
Q

What do osteoblasts do?

A

Lay down osteoid that needs to be mineralized by Ca and P

123
Q

What leads to osteoporosis?

A

Metabolic acidosis seen in renal failure being buffered b lead of Ca from bone

124
Q

Negative impact of dialysis on kidneys?

A
  1. Renal cell carcinoma
  2. Cysts
  3. Shrunken kidneys
125
Q

Renal tumor at increased risk in tuberous sclerosis?

A

Angiomyolipoma

126
Q

What is renal cell carcinoma?

A
  • Malignant epithelial tissue arising from kidney tubules
127
Q

Presentation of renal cell carcinoma?

A
  1. Hematuria
  2. Palpable mass
    3 Flank pain
  3. Fever / weight loss
  4. Many paraneoplastic syndromes
128
Q

Appearance of RCC?

A

Gross: yellow mass
Micro: clear cytoplasm if clear cell type

129
Q

Pathogenesis of RCC?

A
  • Loss of VHL tumor suppressor gene causing:
  • ***IN both sporadic and herediatary
    1. Increase IGF 1
    2. Increased HIF: TF increasing VEGF and PDGF
130
Q

Who is sporadic RCC most commonly seen in?

A
  • Adult spoker

- Single tumor in upper pole

131
Q

What is VHL disease?

A

Increased risk of:

  1. RCC
  2. Hemangioblastoma of cerebellum
    * Autosomal dominant inactivation of VHL suppressor
132
Q

What nodes does RCC spread to?

A

Retroperitoneal

133
Q

Presentation of wilms tumor?

A
  1. Unilateral flank mass in kid
134
Q

Composition of wilms tumor?

A
  • Blastema
  • Stromal cells
  • Primitive glomeruli and tubules
135
Q

Mutation in wilms tumor?

A

WT1 mutation

136
Q

What is WAGR syndrome?

A
  1. Wilms tumor
  2. Aniridia
  3. Genital abnormalities
  4. Mental / motor retardation
137
Q

What is beckwith wiedeman syndrome?

A
  1. Wilms tumor
  2. Neonatal HYPOglycemia
  3. Muscular hemihypoertrophy
  4. Organomegaly - tongue
138
Q

What makes up lower renal tract?

A

Everything past kidney:

  1. Bladder
  2. Renal pelvis
  3. Ureter
  4. Urethra
139
Q

Where does urothelial cancer usually arise and from what does it?

A
  • Usually in bladder

- Arises from urothelial lining

140
Q

What lines the lower urinary tract?

A

Urothelium

141
Q

Risk factors for urothelial carcinomas?

A
  1. Cigarettes
  2. Naphthylamine
  3. Azo dyes
  4. Cyclophosphamide
  5. Phenacetin
142
Q

What is painless hematuria indicative of?

A

Urothelial carcinoma

143
Q

2 pathways of urothelial carcinoma? How do they progress? Mutations?

A
  1. Flat: starts as high grade
    - Early p53
  2. Papillary: low grade, to high grade, to invasion
144
Q

Prognosis of urothelial carcinoma?

A
  • Many tumors with frequent recurrence

“Field effect:” urothelium has been hit by so many toxins for so long that it is grossly mutated

145
Q

Risk factors for Squamous cell carcinoma of lower tract?1

A
  1. Chronic cystitis
  2. S. haematobium: middle eastern males
  3. Long standing kidney stones
    * usually seen in bladder
146
Q

Risks of lower tract adenocarcinoma?

A
  1. Urachal remnant - dome of bladder
  2. Cystitis glandularis
  3. Exstrophy
147
Q

What does PS innervation cause relative to urination?

A
  1. Detrusor contraction
  2. Sphincter relaxation
    * **Sympathetic does opposite
148
Q

What does ADH cause to be resorbed other than water?

A

Urea

149
Q

Blood supply to proximal ureter?

A

Renal artery

Distal: vesicular

150
Q

Presentation of henoch Schonlein purpura?

A
  1. Abdominal pain
  2. Arthralgia
  3. Palpable purpura
  4. Hematuria
151
Q

Pathogenesis of Henoch?

A
  • IgA IC vasculitis following URI
152
Q

What does PAH clearance estimate?

A

RPF

153
Q

Handling of PAH?

A

Some is freely filtered but most is secreted in PCT

154
Q

Where is PAH lowest in kidney?

A

Bowman’s Space

155
Q

Another name for goodpasture’s?

A

Anti GBM disease

156
Q

What is attacking in anti GBM disease?

A

IgG and C3 complex

157
Q

Impact of angiotensin II?

A
  1. Efferent arteriole constriction

2. Systemic constriction

158
Q

Where is angiotensinogen produced?

A

Liver

159
Q

What does RCC originate from?

A

Epithelium of PCT

160
Q

Which diuretic can cause hearing deficits?

A

Loops

161
Q

What causes uric acid to precipitate?

A

Low PH

162
Q

Lowest PH in kidney?

A

Distal tubules

Collecting duct

163
Q

What is the most potent diuretic?

A

IV loops

164
Q

What are antiphospholipid Igs and what do they cause?

A
  • From SLE
  • Falsely elevate PTT when actually hypercoag
  • False RPR for syphillis
165
Q

What layer are kidneys derived from?

A

Mesoderm

- Muscle, bone, connective tissue as well

166
Q

When is pronephros around?

A

Until 4 weeks: degenerates to become mesonephros

167
Q

What is the first functional unit of fetal kidney?

A
  • Mesonephros which is functional during the first trimester
168
Q

What becomes permanent kidney and when does it develop?

A

Metanephros developing in 5th week

- Metanephric mesenchyme, ureteric bud

169
Q

What is WT1 mutation involved in?

A

Wilms tumor

170
Q

What does the mesonephros turn into?

A
  1. Collecting duct
  2. Calyces
  3. Pelvis
  4. Ureters
  5. Vas def
171
Q

Vertebral level of kidneys?

A

“1,2,3 is where you find kidneys”

T12 - L3

172
Q

Which anterior branch of aorta are kidneys next to?

A

SMA

173
Q

Where do horseshoe kidneys get stuck?

A

IMA

- Commonly seen in turner’s syndrom

174
Q

Is multicystic kidney disease hereditary?

A

No

175
Q

How to ureteric bud progress?

A

Grows laterally from mesonephric duct connecting to mesonephric mesenchyme forming metanephros

176
Q

How would one kidney have 2 ureters?

A

“Duplex collecting system”
Ureteric bud bifurcates before reaching mesonephros in embryogenesis
*High risk for vesicoureteral reflux and infx

177
Q

What results in unilateral renal agenesis

A

Aberrant interaction between ureteric bud and metanephric mesenchyme

178
Q

What are the retroperitoneal structures?

A

“SAD PUCKER”
Suprarenal glands
Aorta + IVC
Duodenum 2 - 4th

Pancreas (except tail)
Ureters
Colon (ascending / descending)
Kidneys 
Esophagus (lower 2/3)
Rectum
179
Q

Where do Renal arteries branch?

A

L1

180
Q

Where do renal veins run?

A

Anterior to renal arteries and aorta

181
Q

Which renal vein is longer?

A

Left: because IVC is right of aorta so left vein has further to go

182
Q

Where do right and left gonadal veins drain?

A

Right: directly into IVC
Left: Renal vein - > IVC

183
Q

Relation to ureter and gonadal vessels?

A
  • Runs under them “water under the bridge”

- Also is running under vas def

184
Q

Are autonomic and somatic voluntary or involuntary and how does this related to the two urethral sphincters?

A

Somatic: voluntary, external sphincter
Autonomic: involuntary, internal sphincter

185
Q

Where does the vasa recta come off?

A

“peritubular capillaries”

Efferent arteriols

186
Q

Functions of angiotensin II?

A
  1. Enhances aldosterone release
  2. Vasoconstriction
  3. Constricts efferent arteriole
  4. Increased Na absorption in PCT
187
Q

Where is renin secreted

A

JG cells: Modified smooth muscles cells in afferent tunica media

188
Q

3 things increasing renin?

A
  1. Decreased flow
  2. Decrease Na
  3. Increased sympathetic tone
189
Q

Where does collecting duct drain?

A

Minor calyx at the renal papillae

190
Q

Arterial suppel of ureters?

A

Upper 1/3: Renal artery
Middle: gonadal / common iliac
Lower: Internal iliac

191
Q

What is the break out of water in the body?

A 
60 - 40 - 20
60% total body weight is water
- 2/3 of this is ICF (40%)
- 1/3 of this is ECF (20%)
40% of body weight is non water mass
192
Q

How is volume of ECF measured?

A

Inulin

- Moves out of vasculature but cells do not take up

193
Q

Break out of ECF?

A

Plasma: 1/4 (volume of fluid inside vascular system)
- Measured by albumin
Interstitial fluid: 3/4

194
Q

How are plasma levels measured?

A

Radio labeled albumin: moves into vasculature but too large to move into ECF as inulin does

195
Q

Major cations in ICF and ECF?

A

“The cell is like a banana in the open sea”
ICF: K
ECF: Na

196
Q

What is the charge barrier of the GFR?

A
  • Heparan sulfate in the basement membrane blocks negative molecules
  • Lost in nephrotic syndrome which is why albumin is now able to cross barrier as it is a negatively charged molecule
197
Q

Layers of glomerulus from in to out?

A

Endothelium: size barrier
Basement membrane: heparan charge barrier
Epithelium: podocytes

198
Q

3 things that are freely filtered?

A
  1. AAs
  2. Glucose
  3. Electrolytes
    * Majority resorbed in PCT
199
Q

What is clearance?

A

Volume of plasma in ml cleared of substance in minutes
C = UV/P

U: urine[x]
V: urine flow rate
P: plasma [x]

200
Q

How is GFR measured?

A

Inulin clearance: freely filtered neither reabsorbed, nor secreted

  • **Creatinine is used clinically and it overestimates since a small amount is secreted in tubules
  • Inulin is also measure of ECF fluid volume)
201
Q

What does inulin measure?

A

GFR - freely filtered and neither secreted nor reabsorbed

- Cr is actually used in practice

202
Q

What is EPRF, how is it measure?

A

“Effective renal plasma flow”

  • Measured by PAH
  • PAH is both filtered and secreted
203
Q

What does PAH measured?

A

RPF

204
Q

Equation for RBF?

A

RPF / (1 - hematocrit)

***This includes both plasma and cell mass

205
Q

What part of CO do the kidneys receive?

A
  1. 2 L / Min

- This is 25% of resting CO

206
Q

Filtration fraction equation?

A

FF = GFR / RPF

- Normally 20%

207
Q

Effects of angiotensin II and prostaglandins on GFR?

A

Angiotensin: constricts efferent so increase GFR
Prostaglandins: Dilate afferent increasing BOTH GFR and RPF

208
Q

Effects of dehydration on kidney dynamics?

A

Decreased in GFR and even greater decrease in RPF

**Leads to increase in filtration fraction

209
Q

Equation for filtered load?

A

= GFR x [plasma]

210
Q

Equation for excretion rate?

A

= V x [U]

Urine flow x urine [ ]

211
Q

What what plasma glucose is it seen in urine?

A
  • 200

- PCT transporters are fully saturated at 375

212
Q

What type of drug is acetazolamide? Major indication?

A
  • Carbonic anhydrase inhibitor

- High altitude pulmonary and cerebral edema “acute mountain sickness”

213
Q

What is permeability of thin ascending limb?

A
  • Impermeable to Na
  • Water is passively absorbed
  • Urine is being concentrated
  • **Being caused by hypertonicity of medulla
214
Q

What is permeability of thick ascending limb?

A
  • Impermeable to water
  • Allows for solute resorption
  • **Urine is being diluted
215
Q

Transporter found in thick ascending limb?

A

NaK2Cl

- Mg/Cl also reabsorbed paracellularly

216
Q

Which diuretics increase renal excretion of Ca?

A

Loops: Eg, furosemide

217
Q

Contraindication of loops?

A
  • Ca kidney stones as loops are increasing excration / tubular [Ca] which will lead to more stones
218
Q

What diuretics lead to decreased Ca excretion?

A
  • Thiazides
219
Q

Transporter in distal tubule?

A

NaCl

- No water being absorbed so filtrate is being diluted

220
Q

Where is PTH functioning?

A

DCT increasing Ca absorption via Na/Ca apical transporter

221
Q

Where does ADH function?

A
  • V2 receptor on principal cell of collecting tubule leading to aquaporin insertion in lumen
222
Q

K sparing diuretics?

A
  1. Triamterene
  2. Amiloride
    * **Inhibit Na reabsorption making lumen more positive driving K into cells
223
Q

Impact of aldosterone?

A
  • Mineralocorticoid receptor in both Principal and A cells in collecting duct
  • Causes Na channel insertion on lumen increasing its resorption
  • Increases K / H loss
224
Q

What is Cohns syndrome?

A

“Primary hyperaldosteronism”

  1. Hypertension from increase Na/H2O Resorption
  2. Hypokalemia
  3. Metabolic alkalosis
225
Q

How to remember the renal tubular defects?

A

The kidneys make “FABulous Glittering LiquidS”
FAnconi syndrome
Bartter syndrome
Gitelman syndrome
Liddle syndrome
Syndrome of apparent mineralocorticoid excess

226
Q

What happens in fanconi?

A
  • Non functional cells in PCT leading to loss of:
    1. Glucose
    2. AAs
    3. Bicarb
    4. Phosphate
227
Q

What is bartter’s syndrome?

A 
Resorption defect in thick limb of NaK2Cl causing:
1. HYOP Ca
2. HYPO K 
3. Metabolic alkalosis 
Increased: renin / aldosterone
Normal BP
228
Q

What is Gitelman syndrome?

A
  • DCT issue, similar to bartter but less severe

HYPO: Mg/Ca

229
Q

What is liddle syndrome? Treatment?

A
  • Increased Na reabsorption in distal / convoluted tubules
  • Increased activity of Na channel here
  • Causes HTN and reflex decrease in aldosterone
    Rx: Amiloride (K sparing)
230
Q

What happens in syndrome of apparent mineralocorticoid excess?

A
  • 11-B-Hydroxysteroid Dehydrogenase which normally converts cortisol into cortisone
  • If enzyme absent, excess cortisol begins to activate mineralocorticoid receptors
231
Q

What causes release of ANP?

A
  • Stretching of cardiac atria from increased BV

- Can be caused by volume overload or aortic stenosis

232
Q

How does ANP work?

A
  1. Relaxes vascular smooth muscle to lower BP
  2. Dilates afferent increasing GFR
  3. Decreases renin
233
Q

What does the macula densa do? JG?

A

MD: Sense [Na] in distal tubule
- MD can stimulate JG to release renin
JG: Sense pressure in afferent

234
Q

What is an endocrine hormone?

A

Something that acts at a distant site

235
Q

What is a paracrine hormone?

A

Hormone that acts locally

236
Q

What causes secondary polycythemia?

A

COPD

237
Q

Processing of vitamin D?

A
  1. Liver 25-a-hydroxylase: vitamin d -> 25-H-vitamin D

2. Kidney 1-a-hydroxylase 25-H-vitamin D -> 1-25-OH-2-D

238
Q

What enzyme activated vitamin D and where is it found?

A

1 alpha hydroxylase in PCT

- Stimulated by PTH

239
Q

Functions of vitamin do?

A
  1. Increased GI absorption Ca/P
  2. Decrease renal absorption P
  3. Increased renal reabsorption Ca
240
Q

Drug often associated with renal papillary necrosis?

A

Chronic NSAID use: stops creation of prostaglandins constricting efferent leading to ischemia

241
Q

Effect of De on kidney?

A

Low dose: dilates afferent

High dose: vasoconstrictor via A1 action

242
Q

4 things shifting K into cells?

A
  1. Insulin
  2. Adrenergic agonists
  3. Alkalosis - exchanging for H
  4. HYPOsmolality
243
Q

What do flattened and peak T waves indicated?

A

Flattened: HYPO K
Peaked: HYPER K

244
Q

Normal PH of blood?

A

7.4

245
Q

Values in metabolic acidosis?

A

PH: decreased
CO2: Decreased
Bicarb: Decreased
Response: HYPERventilation

246
Q

Values in metabolic alkalosis?

A

PH: Increased
CO2: Increased
Bicarb: Increased
Response: HYPOventilation

247
Q

Values in respiratory acidosis?

A

PH: Decreased
CO2: Increased
Bicarb: Increased
Response: increased renal bicarb

248
Q

Values in respiratory alkalosis?

A

PH:
CO2:
Bicarb:
Response: decreased renal bicarb

249
Q

What does opiated OD cause relative to acid base?

A

Respiratory acidosis from respiratory depression

250
Q

Difference in onset between compensatory metabolic / respiratory mechanisms?

A 
Respiratory = immediate
Metabolic = delayed
251
Q

What is the normal PCO2?

A

40

252
Q

How to calculate anion gap?

A

[Na] - ([Cl] + [bicarb])

**Normal is between 8 and 12

253
Q

What is normal anion gap?

A

8 - 12

254
Q

Causes of increased anion gap metabolic acidosis?

A

“MUD PILES” - think, you are piling the anions up
Methanol - formic acid
Uremia
Diabetic Ketoacidosis

Propylene glycol 
Iron / Isoniazid (INH)
Lactic acidosis
Ethylene Glycol
Salicylates
255
Q

Causes of Normal anion gap metabolic acidosis?

A 
"HARD ASS"
Hyperalimentation
Addison's 
RTA
Diarrhea - Losing both Na / bicarb in stool

Acetazolamide
Spironolactone
Saline infusion

256
Q

Causes of hyperventilation?

A
  1. Hysteria
  2. Hypoxemia
  3. Salicylates
  4. Tumor
  5. Pulmonary Embolism
257
Q

Causes of metabolic alkalosis?

A
  1. Dehydration
  2. Vomit
  3. Antacids
  4. Hyperaldosteronism
  5. Loops / thiazides
258
Q

Other names for type 1, 2, and 4 RTA? What happens to urine PH?

A

1: Distal: PH > 5.5
2: Proximal: PH

259
Q

Causes of Type I RTA?

A
  1. Amphotericin
  2. Analgesics
  3. Multiple myeloma
260
Q

Cause of Type I RTA?

A

Inability of a-intercalated cells in distal to secret H:

  1. Leads to HYPO K: decreased lumen charge pulls K
  2. Increase lumen PH: Ca/P stones
261
Q

What happens in type II RTA?

A

PCT can not resorb bicarb, distal secretes H to compensate = Decreased PH
1. K being secreted with H = HYPOkalemia

262
Q

Causes of type II RTA?`

A
  1. Fanconi
  2. Lead
  3. Aminoclydosides
263
Q

Cuase of Type IV RTA?

A

HYPOaldosteronism: normally causes Na resorp and K dumb

- without, K is being held in

264
Q

DDx for RBC casts?

A
  1. Glomerulonephritis
  2. Ischemia
  3. Malignant Htn
265
Q

Ddx for granular casts?

A

ATN

266
Q

DDx for fatty casts?

A

Nephrotic syndrome

267
Q

Ddx WBC casts?

A
  1. Interstitial inflammation
  2. Pyelonephritis
  3. Transplant rejection
268
Q

What is being disrupted in nephritic/rotic syndromes?

A

Nephritic: GBM
Nephrotic: Podocytes

269
Q

What type of hypersensitivity is PSGN?

A

III

270
Q

What hypersensitivity is goodpasture’s?

A

II`

271
Q

What is wire looping of capillaries indicative of?

A

DPGN: most common cause of death in SLE

LOOPus for LOOPing

272
Q

Another name for IgA nephropathy?

A

Bergers

273
Q

RBC casts in kidney stones?

A

No, problem is after tubules

274
Q

When most likely to die during ATN?

A

Oliguric / maintenance phase

- Recovery phase is polyuric

275
Q

Renal drug causing gynecomastia?

A

Spirinolaction

276
Q

More water resorbed in collecting duct or PCT?

A

PCT

277
Q

What is hyperacute rejection?

A
  • Occurs immediately upon insertion of transplant

- Type II IgG mediated

278
Q

First step in working up a metabolic alkalosis?

A

Volume status and urine chloride

279
Q

What is a positive Na-cyanide-nitroprusside test indicative of?

A

Homocysteinuria

280
Q

What does hypo K do to muscles?

A
  1. Cramps
  2. Weakness
  3. Rhabdo
    * **Can be caused by thiazides
281
Q

Where in nephron does lowest osmolality occur?

A

DCT

282
Q

Which diuretic leads to increase in Cr upon administration?

A

Ace inhibitors as they are dilating the efferent decreasing GFR

283
Q

Most serious complication during recovery phase of ATN?

A

HYPOk as diuresis but epithelial cells of tubules can not yet function

284
Q

What are phospholipase A2 Receptor (PLAR2) Ig indicative of?

A

Membranous nephropathy

285
Q

Secondary effect of loops?

A

Stimulation of Pg release

286
Q

Side effect of aggressive osmotic diuretic therapy?

A

Pulmonary edema

287
Q

What type of hypersensitivity is serum sickness?

A

Type II: Ig mediated complement activation

288
Q

What leads to meckel’s diverticulum?

A

Persistence of the vitelline / omphalomesenteric duct

- Think VITTTTTY for SHITTTTY

289
Q

What does the allantois become?

A
  • The urachus, a duct between bladder and yolk sac

- Think UUUUUrine, for UUUUURACHUS

290
Q

When is serum C3 decreased?

A

PSGN

291
Q

What is starry sky appearance indicative of?

A

PSGN

292
Q

Which vessels cross under and over the ureter?

A

Over: Gonadal artery and vein
Under: interior iliac artery

293
Q

How do EOSs kill parasites?

A

Ig dependent, cell mediated toxicity

294
Q

IF in PSGN?

A

Granular deposits in lumpy bumpy formation

295
Q

Prevalence of posterior urethral valves?

A

Only seen in males

USMLE: step 1 (15 decks)

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