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Final FA review > 3/1 renal > Flashcards

3/1 renal Flashcards

1
Q

Renal tubular acidosis (RTA): type 1

  • Whats happening?
  • What will urine pH be?
A
  • H/K exchanger in the alpha intercalated cell does not work. You can’t secrete H in exchange for resorbing K. Leads to hypokalemia.
  • Also, if intercalated cell can’t secrete H that means it cant resorb bicarb into blood stream. B/c the acidity needs to be even.
  • urine pH will be more basic than normal, pH > 5.5
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2
Q

RTA 1

  • risk for what?
  • potential causes?
A
  • calcium phosphate kidney stones (due to  urine pH and  bone turnover).
  • acidic environment promotes bone resorption.

-amphotericin B toxicity, analgesic nephropathy, multiple myeloma (light chains), and congenital anomalies (obstruction) of the urinary tract.

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3
Q

What do all RTAs lead to?

A

Non-anion gap hyperchloremic metabolic acidosis.

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4
Q

RTA 2

  • whats happening?
  • does it cause hypo/hyperkalemia?
  • so whats the big problem?
  • urine pH?
A
  • defective bicarb resorption in PCT.
  • excess bicarb in PCT carries Cl (and thus Na) w/it down tubule. Macula densa senses this excess Cl & mistakes it for hypotension & inc. renin prod. Leads to high aldo state & aldo stimulates loss of protons & K in exchange for Na.
  • so leads to hypokalemia.
  • big problem = not enough phosphate = can’t buffer the acid = leads to metabolic acidosis.

-urine pH < 5.5. alpha intercalated cells acidify the urine.

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5
Q

RTA 2

  • inc risk for what?
  • causes?
A
  • inc. risk for hypophosphatemic rickets.
  • Fanconi syndrome (e.g., Wilson disease), chemicals toxic to proximal tubule (e.g., lead, aminoglycosides), and carbonic anhydrase inhibitors.
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6
Q

RTA 4

  • whats happening?
  • whats the big problem here?
A
  • hypoaldosteronism, aldo resistance, K sparing diuretics.
  • The resulting hyperkalemia impairs ammoniagenesis in the proximal tubule. Decreases the buffering capacity and dec. the H+ excretion into urine.
  • big problem is not enough ammonia, so not enough buffering for acid, so you can’t excrete as much acid, leads to metabolic acidosis.
  • pH < 5.5. Not enough ammonia.
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7
Q

What leads to acidification of urine?

A
  • if buffers are used up and you have to excrete straight up protons into the tubule, the pH will decrease fast. That will destroy the conc. gradient quickly and you wont be able to secrete any more protons. This can easily lead to a metabolic acidosis.
  • This explains why the pH of RTA 2 and 4 is acidic yet they’re both still causing a metabolic acidosis.

*you need ammonia and phosphate to get rid of your acid.

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8
Q

ammonium in your urine represents what?

A

2/3 of the acid lost in urine.

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9
Q

phosphoric acid in your urine represents what?

A

1/3 of the acid lost in urine

-titrateable acid.

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10
Q

Total acid lost in urine =

A

= (H2PO4-) + (NH4+)

*which equals the same amount of bicarb added to your body.

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11
Q

Possible causes of RBC casts

A

-Glomerulonephritis, ischemia, or malignant HTN.

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12
Q

Possible causes of WBC casts

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection.

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13
Q

Possible causes of waxy casts

A

Advanced renal disease/chronic renal failure.

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14
Q

Why do you get high hct in nephrotic?

A
  • its a relative polycythemia.

- fluid all leaving into interstitum. So RBCs get more concentrated.

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15
Q

How can you get anemia in nephrotic syndrome?

A

-spill transferrin.

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16
Q
  • Sizes of pores in glomerulus

- size of albumin

A
  • Endothelial cell fenestration: 40 nm
  • Glomerular basement membrane pore: 4 nm
  • Foot processes slit pore: 4 nm

-albumin = 3.5 nm, but repelled by neg. charge. If not it can pass.

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17
Q

Focal segmental glomerulosclerosis

  • nephrotic/nephritic?
  • IC? If so, where?
  • risk factors?
  • do steroids work?
A
  • nephrotic
  • no immune complex
  • Black, mexican, idiopathic, HIV, sickle cell, heroin use, obesity, interferon treatment.
  • inconsistence response to steroids.
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18
Q
  • Most common cause of death in SLE pts?
  • more common glomerular problem?
  • second most common glomerular problem?
A
  • renal failure
  • # 1 common = diffuse proliferative glomerulonephritis (nephritic).

-#2 = membranous nephropathy (nephrotic).

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19
Q

Membranous nephropathy

  • nephrotic/nephritic?
  • IC? If so, where?
  • EM presentation?
  • Risk factors?
  • response to steroids?
A
  • nephrotic
  • yes. IgG & C3. Subepithelial.
  • spike & dome
  • Caucasian, Ab to phospholipase A2 receptor, drugs (ie. NSAIDs, penicillamine), infection (HBV, HCV), SLE, any solid tumors.
  • poor response to steroids.
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20
Q

Ab to phospholipase A2 receptor

-risk factor for which glomerular disease?

A

Membranous nephropathy.

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21
Q

Membranous nephropathy

-what are the “spikes”?

A

-IgG & C3.

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22
Q

Effacement of podocytes seen in which diseases?

A

Minimal change & focal segmental glomerulosclerosis.

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23
Q

Minimal change disease

  • nephrotic/nephritic?
  • IC?
  • EM?
  • cause?
  • which cancer is it associated with?
A
  • nephrotic
  • no ICs.
  • effacement of podocytes
  • problem w/immunologic function. Hence its association w/resp.infections, immunizations, atopic disorders, & excellent response to steroids. Thus, dmg to podocytes probly immuno as well, most likely IL-13 mediated.
  • Hodgkins lymphoma (massive overprod of cytokines).
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24
Q

Hodgkin lymphoma associated w/which glomerular disease?

A

Minimal change disease

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25
Q

What is lipoid nephrosis and why is it called that?

A

In Minimal Change Disease, the defective glomerular filtration charge barrier results in increased filtration and subsequent tubular resorption of lipoproteins, ultimately leading to lipid-laden proximal tubular cells—hence the name “lipoid nephrosis”.

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26
Q

Which is the only nephrotic syndrome w/excellent response to treatment?

A

minimal change disease, steroids.

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27
Q

amyloidosis

-what visualization technique do you use to visualize the apple green birefringence?

A

-light microscope.

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28
Q

6 causes of nephrotic syndrome: in pairs.

A
  • minimal change + FSGS = effacement of foot process
  • Membranous + MPGN = IC deposition
  • 2 systemic disease that affect glomerulus (DM + amyloidosis)
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29
Q
  • subepithelial immune complex deposits =
  • subendothelial deposits =
  • deposits w/in basement membrane =
A
  • membranous glomerulonephritis
  • type 1 MPGN
  • type 2 MPGN
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30
Q

Type 1 MPGN

  • nephrotic or nephritic?
  • where are ICs?
  • associated w/what?
A
  • mixed, both nephrotic & nephritic.
  • sub-endothelial: tram tracks
  • HBV, HCV
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31
Q

Type 2 MPGN

  • nephrotic or nephritic?
  • where are ICs?
  • associated w/what?
A
  • mixed, both nephrotic & nephritic.
  • membranous IC deposits “dense deposits”.
  • associated with C3 nephritic factor (stabilizes C3 convertase dec. serum C3 levels).
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32
Q

C3 convertase

-type 2 MPGN

A

C3 =C3 convertase=> C3a + C3b

  • you usually get rid of C3 convertase right after you use it b/c you only want it active for a very limited amount of time.
  • but in type 2 pts - they have Ab that stabilizes the c3 convertase. Will overactivate complement.
  • you’ll get a decreased serum C3.
  • you’ll get inflammation and damage in the glomerulus.
  • The C3 is the immune complex thats being deposited in the basement membrane and causing the damage!
  • inflammation in glomerulus is more so a nephritic syndrome than a nephrotic syndrome. This disease can cause both nephritic and nephrotic
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33
Q

Which glomerular disease has the lowest serum C3 levels?

A

-type 2 MPGN

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34
Q

hyaline arteriolosclerosis

-preferetially affects which vessel?

A
  • efferent arteriole

- hence the role of ACE inibitors in DM.

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35
Q

eosinophilic nodular glomerulosclerosis

A

aka DM glomerulo-nephropathy & kimmelsteil wilson nodules.

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36
Q

Oliguria & HTN

-nephrotic or nephritic?

A
  • nephritic

- nephrotic doesn’t get oliguria or HTN.

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37
Q

PSGN

  • after pharyngitis, impetigo, or both?
  • inc or dec complement levels?
A
  • both

- dec. complement levels

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38
Q

PSNG

-how long after infection will it occur?

A
  • 2-3 weeks after.

* IgA nephropathy just a few days after.

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39
Q

Goodpastures

-hemoptysis or hematuria usually first?

A

-hemoptysis.

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40
Q

“wire looping” of capillaries?

  • seen in what?
  • most associated w/what extra-renal disease?
A
  • Diffuse proliferative GN

- SLE

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41
Q

IgA nephropathy

-where are the ICs deposited?

A

-mesangium

42
Q

Alport syndrome

  • inheritance patttern
  • what other problems associated w/it?
A
  • X-linked

- Glomerulonephritis, deafness, and, less commonly, eye problems.

43
Q

Which is the only nephritic syndrome you aren’t familiar with?

A

Diffuse proliferative GN

  • IC deposition
  • SLE associated.
44
Q

Membranous nephropathy

-doesnt end w/itis, so how do we know its IC mediated?

A
  • b/c its associated w/SLE.

- and SLE is an immune complex disease.

45
Q
  • Calcium phosphate precips at what pH?

- Calcium oxalate precips at what pH?

A

-Calcium phosphate = inc pH

  • Calcium oxalate = dec pH
  • think oxalic acid, acids precip in acid.
46
Q

Ca stone shape

A

envelope/X tic tac toe

47
Q

Crohns disease can lead to what type of stones?

A
  • Calcium oxalate

- causes inc. resorption of oxalate.

48
Q

Ca stone

-Tx?

A

-thiazides and citrate.

49
Q

Most common kidney stone presentation:

A

-calcium oxalate stone in a patient with hypercalciuria and normocalcemia.

50
Q

Ammonium magnesium phosphate (AMP) stone

  • precip in inc or dec pH?
  • shape?
A
  • inc. pH. form in alkaline urine.

- coffin lid

51
Q

AMP stone

  • aka?
  • causes?
A
  • struvite stone: can form staghorn calculi.
  • urease + bugs
  • Proteus mirabilis, Staphylococcus, Klebsiella: that hydrolyze urea to ammonia = urine alkalinization.
52
Q

Uric acid

  • precips in inc or dec pH?
  • shape?
A
  • acids precip in acidic pH.
  • radiolucent! Only stone thats radiolucent.
  • rhomboid or rosettes
53
Q

Cystine

  • precips in inc or dec pH?
  • shape?
  • test for cystine in urine?
A
  • dec. pH.
  • hexagonal
  • Can form staghorn calculi.
  • Sodium nitroprusside test +
54
Q

Which kidney stones can cause staghorn calculi?

A
  • ammonium magnesium phosphate 9adults

- cystine stones (kids)

55
Q

Mnemonic for paraneoplastics of RCC?

A

PEAR: PTHrP, EPO, ACTH, renin

-the tumor looks like a yellow pear.

56
Q
  • RCC associated w/gene deletion on which chrom?

- does it respond well to chemo/radiation?

A
  • chrom 3
  • sporadic or inherited as Von-Hippel Lindau syndrome
  • does NOT respond to chemo/radiation.
57
Q

Renal oncocytoma

  • what is it?
  • whats it’s cells look like?
  • Tx?
A
  • Benign epithelial cell tumor.
  • Large eosinophilic cells with abundant mitochondria without perinuclear clearing.
  • well circumscribed mass w/central scar
  • Presents with painless hematuria, flank pain, and abdominal mass (same presentation as RCC).
  • Tx: nephrectomy
58
Q

Well circumscribed renal mass w/central scar

A

-Renal oncocytoma

59
Q

Can you use acetazolamide to alkalinize the urine to treat calcium stones?

A
  • NO
  • acetazolamide will cause metabolic acidosis which causes bone resorption and hypercalcemia which can potentially cause calcium stones.
60
Q

kid w/hematuria/flank mass thats big =

*unilateral

A

Wilms tumor

61
Q

Wilms tumor

  • mutation?
  • risk factor?
A
  • “Loss of function” mutations of tumor suppressor genes WT1 or WT2 on chromosome 11.
  • horseshoe kidney (ie. can be seen in turners syndrome)
62
Q

Beckwith–Wiedemann syndrome

-what tumor is often present?

A
  • overgrowth disorder

- wilms tumor often seen.

63
Q

WAGR complex

A 
-Wilms tumor, Aniridia, Genitourinary malformation, and 
mental Retardation (intellectual disability).
*aniridia = absence of iris.
64
Q

Transitional cell carcinoma

  • mnemonic for risk factors
  • what type of growth?
A

Pee SAC:
Phenacetin (tylenol), Smoking, Aniline dyes, and Cyclophosphamide.

  • papillary growth (better prognosis)
  • flat growth (worse prognosis)
65
Q

Squamous cell carcinoma of the bladder

  • whats required before the carcinoma?
  • risk factors
A
  • squamous metaplasia (epithelium in bladder is normally transitional).
  • Schistosoma haematobium infection (Middle East), chronic cystitis, smoking, and chronic nephrolithiasis.
  • chronic inflammation basically.
66
Q

sexually active young women

-most common cause of cystitis?

A

-E. coli and then s. saprophyticus.

67
Q

Causes of acute infectious cystitis

A
  • E. coli (most common).
  • Staphylococcus saprophyticus
  • Klebsiella.
  • Proteus mirabilis—urine has ammonia scent.
  • Adenovirus—hemorrhagic cystitis.
68
Q

Urine has ammonia smell = which bug?

A

Proteus.

69
Q

nitrites in urine =

A

gram (-) organisms, especially E. coli.

70
Q

Sterile pyuria and (-) urine cultures suggest:

A

-Urethritis by N. gonorrhoeae or C. trachomatis.

71
Q

what does CT of acute pyelo show?

A

striated parenchymal enhancement

72
Q

acute pyelo

-mainly affects what part of kidney?

A

-Affects cortex with relative sparing of glomeruli/
vessels.
-Glomerular injury is not the major consequence of renal infections.

73
Q

chronic pyelo

-whats kidney look like?

A
  • Coarse, asymmetric corticomedullary scarring
  • blunted calyx
  • Tubules can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney).
74
Q

thyroidization of kidney seen in what disease?

A

-chronic pyelo.

75
Q

eosinophilic casts seen in what disease?

A

-chronic pyelo

76
Q

ATN: Hyper or hypokalemia?

  • maintenance phase:
  • recovery phase:
A
  • maintenance phase: hyperkalemia

- recovery phase: hypokalemia

77
Q

Radiocontrast agents

-can predispose to what?

A

ATN

-they are nephrotoxic.

78
Q

Most common cause of renal papillary necrosis?

A

DM

79
Q

Consequences of renal failure

-mnemonic:

A

MAD HUNGER

  • Metabolic Acidosis
  • Dyslipidemia (especially  triglycerides)
  • Hyperkalemia
  • Uremia—clinical syndrome marked by
  • Na+/H2O retention (CHF, pulmonary edema, HTN)
  • Growth retardation and developmental delay (in children)
  • Erythropoietin failure (anemia)
  • Renal osteodystrophy
80
Q

What can uremia cause?

*uremia = inc. BUN & creatinine

A

-platelet dysfunction
-pericarditis
-

81
Q

Renal osteodystrophy

A
  • Osteitis fibrosa cystica = too much PTH
  • Osteomalacia = not enough vit D
  • Osteoporosis = met. acidosis causes leeching of Ca from bone.
82
Q

Mitral valve prolapse associated w/which hereditary kidney disease?

A

ADPKD

83
Q

ADPKD

-mutations

A

-Mutation in PKD1 (85% of cases, chromosome 16) or PKD2 (15% of cases, chromosome 4).

84
Q

ADPKD or ARPKD

-which one associated w/HTN?

A

-both

85
Q

ARPKD

-associated sxs?

A
  • hepatic fibrosis
  • portal HTN
  • HTN
  • oligohydramnios
86
Q

ARPKD

-whats kidney look like?

A

bilat. sym. enlarged.

87
Q

Medullary cystic disease appearance vs PKD?

A

Medullary cystic kidneys are SHRUNKEN.

88
Q

Simple vs. complex renal cyst

-which one has potential for RCC?

A

-complex renal cyst

89
Q

Clinical uses for mannitol?

A

-Drug overdose,  intracranial/intraocular pressure.

90
Q

Why is acetazolamide used in glaucoma?

A

-It inhibit aqueous humor formation

91
Q

What causes Sxs of altitude sickness?

A

-resp. alkalosis from hyperventilation.

92
Q

How do carbonic anhydrase inhibitors work?

A
  • PCT has Na/H exchanger.
  • PCT cells have carbonic anhydrase which makes the H needed for this exchange.
  • Also, once the H has been exchanged for Na and it in the tubule, its used to resorb bicarb.
  • So no CA = no intracellular H = no Na or bicarb resorption.
  • NaHCO3 diuresis!
93
Q

Acetazolamide: how does it cause

  • hyperchloremia
  • hyperammonemia
A
  • if you lose bicarb you resorb extra Cl.
  • ammonium easily excreted in acidic urine. But if urine is alkalinized, it can form ammonium gas then readily diffuses out of tubules and into blood stream.
94
Q

Acetazolamide

-can it cause sulfa allergy?

A

-yes, its a sulfa drug.

95
Q

Loops

-effects?

A
  • inhibits Na/K/2Cl channel
  • abolish hypertonicity of medulla
  • stimulate PGE release & dilate afferent arteriole
96
Q

Loops

  • side effects
  • mnemonic?
A

OH DANG!

  • Ototoxicity
  • Hypokalemia
  • Dehydration
  • Allergy (sulfa)
  • Nephritis (interstitial)
  • Gout.
97
Q

Hydrochlorothiazide

-how does this help nephrogenic DI?

A

nephrogenic DI:
ADH channels not working. Can’t resorb any free water.
thiazides prevent NaCl resorption in DCT, so this water is no longer free. And can be resorbed by Aldo effect in beginning of collecting duct.

also
Thiazides increase renal Na excretion → ECF volume contraction → ↓ GFR → ↑ proximal tubular reabsorption of water and Na ∴ less water and Na are lost as urine.
*slows shit down.

98
Q

Hydrochlorothiazide

  • side effects
  • mnemonic
A
  • Hypokalemic metabolic alkalosis
  • hyponatremia

HyperGLUC.

  • hyperGlycemia,
  • hyperLipidemia
  • hyperUricemia
  • hyperCalcemia

-Sulfa allergy.

99
Q

Which diuretic most often causes hyponatremia?

A

hydrochlorothiazide

100
Q

Why are ACE inhibitors C/I in C1 esterase inhibitor deficiency?

A

-C1 esterase inhibitor suppresses activation of C1. It
also inactivates kallikrein. Leads to less bradykinin.
-So in this disease, kallikrein and bradykinin are increased.
-Bradykinin, C3a, and C5a mediate angioedema by inc. vascular permeability & vasodilation.

*ACE inhibitors also inc. bradykinin and can also cause angioedema.

101
Q

ACE inhibitors side effects

-mnemonic

A

Captopril’s CATCHH.

  • Cough
  • Angioedema (c/i in C1 esterase inhibitor def.)
  • Teratogen (fetal renal malformations)
  • inc. Creatinine (dec. GFR)
  • Hyperkalemia
  • Hypotension.

Final FA review (52 decks)

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