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USMLE/ Step ONE > Renal > Flashcards

Renal Flashcards

1
Q

What are the 3 embryological origin tissues for kidneys?

A

PROnephros
MESOnephros
METAnephros

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2
Q

What are the derivatives of PROnephros?

A

Nothing! Degenerates

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3
Q

What are derivatives & Fx of MESOnephros?

A

male genitals
Becomes the Wolffian ducts–» ductus deferns & epididymis

Female genitals: Gartner’s ducts
for 1st trimester, an interim kidney

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4
Q

What are the derivates and Fx of METAnephros?

A
  • Uteric bud (metanephric diverticulum)–> ureter, pelvises, calyces, collecting ducts
  • Metanephric mesenchyme–> glomerulus to CDT (following interaction between uteric bud)
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5
Q

What is time-frame of kidney development?

A

Propnephros- 4wks
Mesonephros- 1 trim
Metanephros- 5th wk, development goes until 32-36wks (uteric bud fully canalized by wk 10)

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6
Q

MC site of hydronephrosis (obstruction) in fetus?

A

Uteropelvic junction

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7
Q

What causes Potter Syndrome?

A

Oligohydramnios

ARPKD
Posterior Urethral valves
Bilateral Renal Agenesis

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8
Q

What are Sx of Potter syndrome?

A

Fetus has hypoplastic lungs (norm: lungs would grow w/ inhalation of fluid), absent kidneys, and

abnormal face features (face pressed against uterus): suborbital crease, depressed nasal tip, retrognathia, low-set ears.

limb defect (pressed against uterus)

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9
Q

what structure blocks ascension of Horse-shoe kidney?

A

Inferior Mesenteric Artery

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10
Q

What disease is associated w/ Horseshoe kidney?

A

Turner syndrome

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11
Q

What causes multicystic dysplastic kidney disease?

A

abnormal interaction between uteric bud & metanephric mesenchyme

Nonfunctional kidney w/ cysts and connective tissue (usually presents in one–> healthy kidney hypertrophies)

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12
Q

Looking at a glomerulus, how do you differentiate afferent and efferent arterioles?

A

Macula dense, Juxtaglomerular cells, and distal renal tubules next to afferent arteriole

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13
Q

draw a glomerulus:
Afferent & efferent arteriole, periteal layer of BC, Podocytes (visceral layer), Basement membrane, Mesengial cells, Juxtaglomerular cells, Macular densa, endothelial cells, distal renal tubule, PCT

A

pg 479

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14
Q

What brings negative charge to glomerulus? When is it lost, and what conditions result?

A

neg charge by fused BM w/ Heperan sulfate

Charge barrier lost in Nephrotic syndrome.
–> Albuminuria, Hypoproteinemia, edema, hyperlipidemia

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15
Q

components of glomerular filtration barrier

A

Fenestrated capillary endothelium (size)
Fused BM w/ heparan sulfate (charge)
Podocytes

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16
Q

What is normal osmolarity?

A

290 mOsm/L

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17
Q

Fluid breakdown in body!

total water, ECF, ECF

A

60-40-20 rule (% body weight)
60% of our body weight WATER =
40% ICF + 20% ECF

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18
Q

breakdown of ECF

A

1/4 plasma

3/4 is interstitial

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19
Q

How to measure plasma ad ECF

A

plasma: radiolabeled albumin
ECF: inulin

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20
Q

formula for clearance

A

Cx = (Ux*V)/Px

Cx = clearance of X (mL/min)
Ux = urine concentration of X
Px = plasma conentration of X
V = urine flow rate
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21
Q

relate Clearance to GFR

A

Cx = GFR : no net secretion or GFR
Cx > GFR : net tubular secretion of X
Cx < GFR : net tubular reabsorption of X

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22
Q

formula for GFR?

A 
(U*V)/P = Cx
X = inulin

or, Kf [Pgc- Pbs)-( πgc - πbs)]
πbs usually 0

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23
Q

Normal GFR? Change in levels indicate?

A

Normal level: 100mL/min

incremental reductions sign of chronic kidney disease

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24
Q

formula for renal blood flow

A

RBF = RPF/ (1- Hct)

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25
Q

how to measure effective renal plasma flow?

A

measure PAH (plug into Cx formula)

PAH filtered and actively secreted (all PAH entering kidney excreted)

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26
Q

How is GFR maintained?

A

1) myogenic response to SM stretch

2) Tubular glomerualr feedback. Macula densa cells detect increase Na –> afferent contriction

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27
Q

Filtration fraction formula? normal %?

A

GFR/ RPF

normal is 20%

GFR can be estimated w/ creatinine clearance
RPF estimated w/ PAH

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28
Q

Which drugs effect afferent & efferent arterioles of kidney?

A

Afferent affected by NSAIDS

Efferent by ACE (-)

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29
Q

specific effect of NSAIDS on kidney?

A

Affects afferent arteriole

Prostaglandins dilate it, increasing RPG & GFR (so FF is same)

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30
Q

Effects of Ace (-) on glomerulus?

A

ANgiotensin II constricts efferent arteriole (decrease RPF, increase GFR, so FF increases)

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31
Q

effect of renal agenesis?

A

hypertrophy of healthy kidney. In time, hyperfiltration can cause renal failure

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32
Q

which disease has cysts unilaterally or bilaterally, congenital, and is NOT inherited?

A

dysplastic kidney

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33
Q

What are contents of cysts in dysplastic kidney?

A

abnormal tissue like cartilage

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34
Q

REMINDER SLIDE!

A

dont assume a bilateral kidney disease of cysts is only PKD. It can also be dysplastic kidney disease (not inherited)

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35
Q

Describe PKD presentation

A
  • always bilateral

- enlarged kidneys, due to cysts in renal cortex & medulla

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36
Q

What are forms of PKD?

A

AR- “juvenile”, more in infants

AD- Adult form (“ADult”)

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37
Q

Describe AR of PKD? Associations of other tissue?

A

Newborns may have Potter sequence (PKD kidneys so bad; non-Fx)

Worsening renal failure & HTN

Associated w/ hepatic cysts –> congenital hepatic fibrosis (has** Portal HTN!!!)***.

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38
Q

Describe AD PKD Sx?

A

HTN (increased renin)
hematuria
worsening renal failure
Abdominal pain

Present from birth, but Sx worsen w/ time

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39
Q

Associations w/ AD

A

Berry aneurysm (“cyst” in brain, balloon dilation), MVP, hepatic cysts

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40
Q

C/C: Family w/ renal disease & death due to this or brain hemorrhage, think of what?

A

AD PKD

Cysts in the liver, brain, and kidney

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41
Q

What genes associated w/ AD PKD?

A

mutation of APKD1 or APKD2

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42
Q

Describe Medullary cystic kidney disease

A

cysts in medullarary collecting duct,

Shrunken kidney

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43
Q

differentiate Medullary cystic kidney disease from AD PKD?

A

Both at AD

Medullary cystic kidney:
Smaller kidney
cysts in collecting duct

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44
Q

Key presentation of Acute Renal Failure? What tests are indicative?

A

Azotemia (increased BUN & Cr)

Oliguria

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45
Q

What is azotemia?

A

Azotemia is a medical condition characterized by abnormally high levels of nitrogen-containing compounds, such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds in the blood

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46
Q

Normal BUN: Cr ratio?

A

15

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47
Q

What is BUN: Cr ratio in Prerenal Azotemia and why?

A

> 15

In Prerenal, GFR reduced. Leads to Angiotensin response –> Increase Na/H2O reabsorb, causing more BUN to be reabsorbed

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48
Q

Renal tubule function in Prerenal azotemia? What tests are indicative of this?

A

Normal function
fractional excretion of Na (FENa) < 1%
Urine Osm> 500mOsn/kg

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49
Q

describe progression of Postrenal azotemia

A

early: BUN: Cr >15 (backpressure from ureters)
Normal FENa, Urine osm >500…normal tubular function

after time: ratio < 15, FENa>2%, unable to concentrate urine (urine Osm <500)…poor tubular Fx

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50
Q

MCC of Acute renal failure?

A

Injury and necrosis of tubular epithelial cells

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51
Q

Pathophysiology of Acute tubular necrosis? Site of damage?

A

necrosis of tubular epithelial cells. This cells slough off and block off; plug tubulues–> back pressure–> decrease GFR

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52
Q

Urinalysis of Acute tubular necrosis?

A

Urine: Brown granular casts

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53
Q

How is tubular function in Acute tubular necrosis?

A

Goes down
BUN: Cr < 15
FENa >2%
Urine Osm <500

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54
Q

What is ischemic Acute tubular necoris? Sites of damage?

A
  • decreased blood to tubules
  • preceded by Prerenal Azotemia*

Sites: Proximal tubule & medullary part of Thick ascending limb

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55
Q

What is nephrotoxic Acute tubular necrosis?

A

necorosis of tubular epithelial due to TOXIC agents. Proximal tubules mostly affected

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56
Q

What are causes of nephrtotoxic acute tubular necrosis?

A 
Aminoglycosides
Heavy metals
Myoglobinuria
Ethylene glycol (Anti-Freeze), kids may drink
Radiocontrast dye
Urate (tumor lysis syndrome)
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57
Q

Urine presentation of drinking anti-freeze (ethylene glycol)?

A

Oxalate crystals

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58
Q

C/C: Patient has Tumor Lysis syndrome and is going through chemotherapy. How can this be a risk damage to kidneys?

Prevention?

A

Chemo –> massive cell breakdown in blood–> increase uric acid levels–> tubular damage

Prevention: Allopurinol to prevent uric acid + drink a lot of water

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59
Q

Clinical presentation of ATN?

A

Hyperkalemia w/ Metabolic acidosis
Elevated BUN & Cr
Oliguria w/ brown granular casts

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60
Q

What causes Acute interstitial nephritis? Give pathophys too!

A

Drug induced Hypersensitivity, affects interstitium (conenctive tissue) between tubules

causes: NSAIDS, PCN, diuretics

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61
Q

How to diagnose acute interstitial nephritis? Tx?

A

Fever & rash
Eosinophils
Oliguria

Tx: stop drug therapy

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62
Q

Renal papillary necrosis presentation.

A

gross hemeturia and flank pain

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63
Q

Causes of Renal papillary necrosis?

A

-Diabetes mellitus
-chronic analgesic abuse (aspirin, phenacetin, etc)
-Acute interstitial nephritis
-Severe acute pyelonephritis
Sickle disease/trait

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64
Q

Key abnormal level in nephrOtic syndrome? Characteristics?

A

Proteinuria (>3.5g/day)

Hypoalbuminemia-pitting edema
Hypogammaglobinemia- infection
Hypercoagulable state- loss of AT3
Hyperlipidemia
Hypercholesterolemia
(blood "thins out" due to protein loss, so liver spits out fat to thicken)

FATTY CASTS!!!!!!!!!!

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65
Q

MCC of nephrotic syndrome in kids? Associations?

A

Minimal change disease

Hodgkin’s disease

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66
Q

pathophys of Minimal change disease

A

loss; effacement of podocyte foot processes. Due to cytokines (like by Reedsternberg cells in Hodgkin lymphoma)

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67
Q

How does Minimal Change disease on H&E stain? EM? IF?

A

H&E: normal
EM: effacement of foot processes
IF: negative (no immune complexes involved anyways)

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68
Q

What protein loss in Minimal change disease?

Tx?

A

Albumin (NOT Abs!)

Tx: Steroids (only nephrotic syndrome to responds to this)

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69
Q

Who is affected by Focal Segmental Glomerulosclerosis?

Associations?

A

Blacks & Spanish

HIV, heroin, sickle cell

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70
Q

How dose Focal Segmental Glomerulosclerosis present on H&E?

A

Only portions of a glomerulus (segmental) & a few glomeruli affected (focal)

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71
Q

What diseases are a pre and postcursor of Focal Segmental Glomerulosclerosis?

A

Pre: Minimal Change Disease
Post: Chronic renal failure

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72
Q

MCC of nephrotic disease in Causcasian adults?

A

Membranous Nephropathy

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73
Q

What is associated w/ Membranous Nephropathy?

A

SLE
Hepatitis B
Tumors
Drugs

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74
Q

Patient w/ lupus can present with what nephrotic syndrome?

A

Membranous nephropathy

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75
Q

Describe histo of Membranous nephropathy

A

thick BM of glomerulus
Immune complex deposition (granualr IF)
subendothelial deposits w/ * SPIKE & DOME* appearance on EM

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76
Q

Relate Membranous nephropathy & Memnraoproliferative glomerulonephritis

A

Thickening of BM due to immune complex deposition. Podocytes respond to complexes by thickening the BM.

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77
Q

H&E stain shows glomerulus w/ “tram-track” appearance. Name disease?

Cause of this pattern

A

Membranoproliferative glomerulonephritis

proliferation of cytoplasm of Mesangial cells cuts immune deposit into 1/2 (tram track)

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78
Q

Key difference of types of Membranoproliferative glomerulonephritis?

A

Location!

Type I- Subendothelial
Type II- intramembranous; w/n BM

79
Q

Describe Type I Membranoproliferative glomerulonephritis

A

Immune complexes under endothelium (subendothelium)

  • *associated w/ HCV**
  • More associated w/” tram-track” appearance*
80
Q

What immune substance associated w/ Type II Membranoproliferative glomerulonephritis ?

A

C3 nephritic factor- an auto-Ab that stabilizes C3 convertase

causes compliment over-activation–>inflammation

81
Q

How long C3 convertase active normally? Abnormally in nephrotic syndrome?

A

short time

w/ Membranoproliferative glomerulonephritis, an Ab, C3 nephritic factor, stabilizes it to prevent its degradation –> continuous inflammation –> damage (too much compliment activated)

82
Q

What type of renal disease is Membranoproliferative glomerulonephritis?

A

NephrOtic, Nephritic

83
Q

What diseases associated w/ Type I Membranoproliferative glomerulonephritis?

A

HBV & HCV

84
Q

locations of immune complex deposition in glomerulus filtration layers?

A
  • Below epithelium (podocytes)- Membranous Nephropathy
  • w/n BM: Type II Membranoproliferative glomerulonephritis
  • below endothelium: Type I Membranoproliferative glomerulonephritis
85
Q

REMINDER SLIDE!

How to categorize Nephrotic syndromes
test yourself if you know!

A

Effacement of podocyte foot processes: Minimal change disease & Focal segment glomerulosclerosis

Deposition of immune complexes: Membranous Nephropathy; MPGN Typie I & TypII

Systemic- DM & Systemic Amyloidosis

86
Q

Effect of adding sugar to BM w/o enzyme (Non enzymatic glycosylation)?

What diseases associated?

A

BM becomes leaky–> protein leaks into wall–> hyaline arteriolosclerosis (which occurs w/ DM & HTN!!!)

87
Q

What tissue affected by DM in glomerulus? Effect?

A

Efferent arteriole

Lumen decreases–> hyperfiltration–>

Microalbuminuria, then sclerosis of mesangium

88
Q

How to Tx hyperfiltration of glomerulus?

A

ACE (-)

89
Q

First change of kidney in DM?

A

non-enzymatic glycosylation of BM–> hyaline arteriolosclerosis

90
Q

Hallmark of nephrotic syndrome in DM patient?

A

Kimmelstiel-Wilson nodules
(dense sclerosis)

looks like large golf balls

91
Q

MC organ affected by systemic amyloidosis?

A

Kidneys

92
Q

Site of amyloid despoition in systemic amyloidosis? What is resulting disease?

A

Mesangium

Nephrotic syndrome

93
Q

How to identify systemic amyloidosis?

A

apple-green birefringence under polarized light

94
Q

hallmark of Nephritic syndrome?

A

glomerular inflammation & bleeding

proteinuria <3.5g.day

95
Q

Characteristics of nephritic syndrome

A
  • salt retention–> edema around eyes & HTN
  • Oliguria & azotemia
  • RBC casts and hematuria

HTN!!!!!!! RBC Casts!!!!!!!

96
Q

Biopsy of nephritic syndrome?

A

inflammed glomeruli, & hypercellular

Neutrophils!

C5a (inflammation) attractios Neutrophils

97
Q

What glomerular disease caused by Group A, beta hemolytic strep infection of skin or pharynx?

A

Poststreptococcal glomerulonephritis

98
Q

Cause of Poststreptococcal glomerulonephritis? Pathophysiology?

A

Strep pyogenes

G.A.S. strains that carry M protein virulence factor. M protein defines nephritogenic strains

99
Q

Presentation of Poststreptococcal glomerulonephritis

A

Hematuria (coke color)
Oliguria
HTN
periorbital edema

100
Q

Sx presentation of Poststreptococcal glomerulonephritis infection?
Demographics?

A

Kids, sometimes adults

Sx present 2-3 wks after infection

101
Q

Hallmark on biopsy of Poststreptococcal glomerulonephritis?

A

subepithelial HUMPs on EM

immune complexes start Subendothelial

102
Q

Severity of poststreptococcal glomerulonephritis?

A

kids, no biggie

adults, sometimes progress to RPGN (progresses to renal failure in wks to months)

103
Q

how to characterize Rapidly progressive glomerulonephritis?

A

Crescents in bowman space (H&E stain)

made of *fibrin and macrophages, inflammatory debris

104
Q

Content of cresents in RPGN?

A

made of *fibrin and macrophages, inflammatory debris

105
Q

IF test patterns of RPGN? Cause of pattern and disease association?

A

Linear (Abs to collagen in BM)- Goodpasture syndrome

Granular (immune complex depoistion)- PSGN or diffuse prolifferative glomerulonephritis (subendothelial)

negative (pauci-immune), do ANCA!

106
Q

MC type of renal disease in lupus?

A

diffuse proliferative glomerulonephritis

107
Q

MC cause of renal disease in lupus, Nephrotic Vs. Nephritic syndrome?

A

Nephrotic: Membranous nephropathy

Nephritic: Diffuse proliferative glomerulonephritis

108
Q

What do you do w/ a negative IF in RPGN?

describe patterns p-ANCA, c-ANCA

A

Do ANCA!

c-ANCA: Wegners granulomatosis
p-ANCA: Churg-Strauss, microscopic polyangilitis

109
Q

C/C: Patient w/ hemoptisis, hematuria, and RPGN w/ cresents, and nasal symtoms.

A

Wegners granulomatosis

!!!!!!!! Watch out for knee jerk to pick Goodpasture, as here nasal Sx mentioned!!!!!

110
Q

differentiate positive p-ANCA Churg-Strauss, microscopic polyangilitis

A

Churg-Strauss:

1) granulomatous inflammatoion
2) Asthma
3) eosinophilia

111
Q

IgA nephropathy deposition site?

A

mesangium of glomeruli

112
Q

Whom and how does IgA nephropathy present clinically?

A

Following mucosal infections (IgA…)
RBC casts
Microscopic hematuria

113
Q

IF of IgA nephropathy?

A

granular in mesangium

114
Q

What is Alport syndrome?

A

X-linked defect in Type 4 collagen–> causes thinning and splitting of glomerular BM

115
Q

Sx of Alport syndrome>

A

Isoalted hematuria
Sensory hearing loss
Ocular disturbances

all due to BM membrane damage.

116
Q

Sites of infection for UTI? common infection source location and causes?

A

Urethra, bladder, or kidney

Mostly starts from urethra and goes up. Catheters, sex, and stasis of urine

117
Q

What is term for bladder infection? Sx of this?

A

Cystitis

Sx: Dysuria, urine frequency and urgency increases, suprapubic pain

118
Q

Lab diagnosis of Cystitis?

A
  • Cloudy urine (>10WBC/hpf)
  • Dipstick: positive for leukocyte esterase (due to pyuria) & nitrites
  • **Culture: >100,000 cfu **
119
Q

What bug is MCC of cytitis?

A

E. coli

120
Q

List bugs that cause UTI?

A 
E coli
Staph saprophyticus
Klebsiella pneumonia
Proteus mirabilis- causes alkoline urine (ammonia scent)
Enterococcus faecalis

“KEEP Safe” (safe = saphrophyticus)

121
Q

Pyuria w/ neg urine culture is indicative of what?

causes?

A

Urethritis, due to

Chlamydia trachomatis or Neisseria gonorrhoeaea

122
Q

Patient has flank pain, fever, WBC casts, and leukocytosis. Also complains of increased urinary frequency and pain upon urination. What is condition?

A

Pyelonephritis

123
Q

increased risk of pyelonephritis?

A

ascending infection and VESICOURETERAL REFLUX (from bladder to kidney)

124
Q

explain flank pain in pyelonephritis

A

nerves of kidney capsule sensitized

125
Q

What results from chronic pyelonephritis in tissues?

A

Interstitial fibrosis &
atrophy of tubules- “Thryoidization”

cortical scarring w/ blunted calyces

126
Q

Common group for pyelonephritis and why?

A

Kids w/ Vesicoureteral reflux

angle of ureters and bladder help prevent reflux of urine. If abnormal, VUR can happen–> scarring

127
Q

Affect on kidney w/ VUR?

A

scarring at upper and lower poles

128
Q

Explain “Thyroidization” in chronic pyelonephritis

A

Tubules undergo atrophy, and fileld with a red material w/ proteub that makes tubules look like thyroid follices

129
Q

Risk factors for nephrolithiasis?

A

high urine concentration of solute among low urine volume

130
Q

Nephrolithiasis Sx?

A

Colicky pain w/ blood in urine & unilateral flank tenderness

131
Q

MC nephtolithiasis type? MC cause?

A

Calcium oxalate and or calcium phosphate

Cause: idiopathic hypercalciuria (Ca levels in blood normal though)

132
Q

Tx of calcium kidney stones?

A

Hydrochlorothiazide (Ca-sparing diuretic)

133
Q

Cause of Ammonium magnesium phosphate nephrolithiasis?

A

Infection by Proteus vulgaris or Klebsiella–> alkaline urine –> stone

134
Q

Class presentation w/n tissues in Ammonium Magnesium stones?

A

Staghorm calculi in renal calyces

135
Q

Kidney stones visible on Xray?

A

All visible except Uric acid stone

136
Q

risk factors for Uric acid kidney stones?

A 
Hot weather
Low urine volume
Acidic pH of urine
Gout
Myeloproliferative diseases (more cells made--> more nuclear turnover--> uric acid high)
137
Q

Allopurinol can help in Tx of what type of kidney stone condition?

A

Uric acid

138
Q

Cysteine nephrolithiasis cause?

A

genetic defect in tubules, cannot reabsorb cysteine

139
Q

When do you see staghorn calculi?

A

kids- Cysteine stones

adults- Ammonium Mg PO4 stones

140
Q

MCC causes of end stage renal failure

A

1) DM
2) HTN
3) glomerular diseases

141
Q

describe uremia Sx

A 
Nausea
Anorexia
Pericaditis
PLT dysfunction- uria (-) PLT adhesion and grouping
Encephalopathy w/ asterixis
Urea crystals in skin
142
Q

Presentation of end stage renal disease

A

Uremia
Salt and water retention–> HTN!
Metabolic acidosis (anion gap) and hyperkalemia
Anemia (cant make EPO!)
Hypocalcemia (decrease alpha1 hydroxylation of Vit D by Prox tubule)
Phosphatemia
Renal osteodystrophy

143
Q

Where is EPO made?

A

Renal peritubular interstitial cells

144
Q

Explain causes of Renal osteodystrophy

A
  • Damage to bone due chronic renal failure
  • Due to secondary hyperparathyroidism

present with:

  • osteitis fibrosa cystica: reabsorbing Ca from bone-> bones develop cysts and damage (bones burn out)
  • Osteomalacia-cannot mineralize osteoid by osteoblast (done by Ca & PO4)
  • Osteoporosis- leak Ca from bones (due to Metabolic acidosis)
145
Q

Tx of end stage renal failure

A

transplant

dialysis (S/E: kidney shrinks –> cysts form–> *****increase risk of renal cell carcinoma)

146
Q

What’s are the types of Acute tubular necrosis

A

Ischemic and Nephrotoxic

147
Q

Normal RPF?

A

600-700 mL/min

148
Q

What are effects of hypovolemia (dehydration, diarrhea, vomiting) on filtration fraction and its factors?

A

RPF drops significantly
GFR drops, but not as substantially due to compensatory mechanisms (JG apparatus) to maintain filtration levels

FF will increase (GFR/RPF)

149
Q

Patient has Metabolic Acidosis. How do you access respiratory compensation?

A

Use WINTER’S FORMULA

PaCO2 = (1.5*HCO3-) + 8 +/-2

If PaCO2 > predicted, then concurrent resp acidosis & failure

If PaCO2 < predicted, then concurrent resp alkalosis (compensation…Kussmaul respirations, hyperpnea)

150
Q

What is the MOA of Thiazide diuretics and site of action?

A

(-) Na/Cl symporter–> (-)NaCl reabsobtion in early distal tubule

151
Q

S/E of Thiazide diuretics

A

Hypokalemic metabolic acidosis
Hyponatremia
hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (more activity of Na/Ca exchanger)

“hyperGLUC”

152
Q

Where is most of K reabsorbed? How do levels change along tubules?

A

2/3 reab in Prox tub, then 30% in Thick Ascend Loop

Levels fluctuate in late distal & Collecting tubules (principal & intercalated cells)

153
Q

Key mediators in K regulation in renal tubule?

A

Principal cells (Na/K pump) and H/K ATPase on alpha-intercalated cells in late distal and cortical collecting tubules.

Hyper or Hypokalemia affect K secretion or reabsorb (respect) here, unlike rest of tubules (which K reab rates unaffected)

154
Q

Causes of increased K excretion?

A

1) High ECF K levels
2) Increased aldosterone
3) Alkalosis, promotes K cell entry (K/H exchange). High K in principal and IC cells –> secretion in pee
4) Diuretics

155
Q

Acyclovir IV administration risk on kidneys?

Prevention?

A

Can cause crystalline nephropathy, where [drug] exceeds solubility in collecting duct–> drug crystallizes –? renal tube damage

Prevent w/ agressive IV hydration & dose adjustment

156
Q

Amphotericin B effect on kidneys?

A

S/E of renal toxicity

Hypokalemia & hypomagnesemia common

157
Q

While a patient in surgery for organ transplant, the organ becomes cyanotic soon after vessels connected. What is immunological condition?

A

Hyperacute rejection (Type II HS) w/ preformed Abs

Examples: ABO blood tranfusion, anti-HLA Abs

158
Q

MOA of Loop diuretics

What drug can interfere w/ them?

A

1) (-) Na/K/2C; symporters in ascending limb of LOH
2) Stimulate prostaglandin (PGE) release–> increase GFR

NSAIDs can (-) PGE

159
Q

Patient has ingested toxic substance, complains of flank pain, & shows oxalate crystals in urine. What other Sx to present?

A

Patient ingested anti-freeze; Ethylene glycol.

Oliguria
high anion-gap metabolic acidosis
flank pain

160
Q

At a fixed GFR and constant hydration rate, compare [urea] filtered to [urea] excreted

A

Roughly 40-50% of filitered urea is reabsorbed by PT. If value of filtered urea = X, 0.55X is excreted

161
Q

What makes BM in glomerulus? Damage to this has what effect on BM?

A

Podocytes

Any damage to podocytes automatically damages BM

162
Q

Linear pattern on BM for IF test. No gaps. What disease?

A

Goodpasture syndrome

163
Q

Granular, Sub-endothelial pattern. Nephritic disease. What condition?

A

Diffuse proliferative glomerulonephritis of SLE

164
Q

Granular pattern indicates of what HS?

Anti-BM linear pattern, what type of HS?

A

Type III- granular pattern in IF of glomerulus = Immune complexes

Linear pattern of IF: a type 2 HS

165
Q

C/C: 35 yo F, pos serum ANA w/ rim pattern. Indicative of ?

A

Anti-dsDNA Abs present

Lupus!

166
Q

Maltese cross sign of what condition?

A

Nephrotic syndrome

167
Q

Fusion of podocytes seen in …

A

any nephrotic syndrome!

168
Q

Alternate name of Minimal change disease?

A

Lipoid nephrosis. Lipids can be seen in Prox tubule cells

169
Q

What vascular condition associated w/ HBV?

A

Polyarthritis nodosa

170
Q

Dense deposit disease, aka?

A

Type II membranoproliferative glomerulonephritis

171
Q

Long term consequence of Non enzymatic glycosylation on glomerulus?

A

Hyaline arteriolosclerosis more on efferent arteriole –> Increased GFR–> Hyperfiltration for years in kidney

172
Q

Tx of glomerular disease w/ DM, w/ HTN?

A

ACE (-)

Decrease constriction of efferent arteriole, PLUS decrease BP

173
Q

Most potent diuretic for maximum diuresis in shortest time? Site of action?

A

Loop diuretics

Act on ascending limb of loop of Henle

174
Q

When are Loop diuretics used?

A 
Edamatous states: 
CHF
Cirrhosis
Nephrotic syndrome
Pulmonary edema
Peripheral edema

HTN

175
Q

S/E of Loop diuretics?

A

OH DANG!

Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout

HypoCalcemia

176
Q

Patient is missing VHL on chromosome 3p. What conditions are associated?

A

Von Hippel-Lindau disease

Renal cell carcinoma

177
Q

Fx of DNA ligase?

A

repair single stranded breaks in duplex during DNA replication and repair

178
Q

Fx of DNA polymerase III?

A

make DNA daughter strands

proofreading

179
Q

Compare and contrast DNA polymerase I & III?

A

I: has 5’->3’ exonuclease activity to remove RNA primers & damaged DNA

Both I & III have 3’->5’ proofreading ability

180
Q

Fx of DNA polymerase I?

A

replace RNA primer

181
Q

How much fluid filtered in prox tubule, and how? Does hydration status affect this?

A

60% fluid reab isosmotically w/ solute

hydration status doesnt affect this

182
Q

What is max osmolarity kidneys can concentrate urine?

A

1200mOsm/L

183
Q

Minimal urine body needs to make to remove wastes?

A

0.5L

184
Q

What is the 2X2 table for relative risk?

A

Outcome No outcome
Exposure a b
no Exposure c d

RR = [a/(a+b)]/[c/(c+d)]

185
Q

End stage renal disease has what metabolic effects?

A

1) Decreased 1,25-(OH)2 vit D made
2) Hyperphotphatemia (more phosphate retained)

both lead to low Ca-> increased PTH made -> Secondary hyperparathyroidism –>

renal OSTEODYSTROPHY

186
Q

Patient w/ renal artery stenosis (hypoperfusion) can have hyperplasia result where?

A

JG apparatus hypertrophies and has hyperplasia–> more renin made.

187
Q

What is JG apparatus made of? Where are they?

A

Macula densa cells, w/n distal tubule, transmit info to JG cells (drops in NaCl)

JG cells- modified SM cells, by eff & aff. arterioles

188
Q

High load of cell lysis can have what effect in renal tubules in acidic pH in renal tubules?

A

Lysis of tumor cells causes increased:
Uric acid
Potassium
Phosphorus

Uric acid soluble at normal pH, but precipitates in acidic environment–> UA crystals (blocking tubules)

189
Q

In dehydration & higher levels of ADH, which site of renal tubules is most dilute? Highest osmolality?

A

Most concentrated: Collecting tubules

Lead concentrated: thick ascending of LOH & DCT

190
Q

S/E of Amphotericin B on kidney?

Presenting Sx?

A
  • drops GFR
  • toxic effects on tubular epithelium
  • Hypokalemia
  • Hypomagnesemia

Hypokalemia: weakness & arrhythmias.
premature Atrial and ventricular contractions.

If severe hypo-K-> V-tachy or V-fib

191
Q

ECG presentation of Hypokalemia?

A

ECG: flatter Twaves. ST segment depression, strong U-waves

192
Q

What molecules are absorbed less during pregnancy and spill over into urine?

A

amino acids

Glucose

193
Q

Defiency in amino acid, tryptophan, transporters causes pellagra. Name the disease.

A

Hartnup’s disease

USMLE/ Step ONE (20 decks)

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