Renal Flashcards

1
Q

What is the arterial supply of the first 1/3 of the ureter?

A

Renal artery

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2
Q

What two major arteries do the ureters pass between?

A

The external and internal iliac arteries

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3
Q

Calculation for interstitial volume

A

ECF volume (inulin space) - Plasma volume

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4
Q

Formula for renal clearance

A

C = U x V/P. U is urine concentration, V is urine flow rate, P is plasma concentration

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5
Q

Normal GFR

A

About 100 ml/min

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6
Q

Does creatinine clearance slightly overestimate or underestimate GFR?

A

Overestimate (creatinine is moderately secreted)

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7
Q

Formula for RBF

A

RPF/(1-Hct)

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8
Q

What substance is used to estimate RBF and does it underestimate or overestimate RBF?

A

PAH clearance. Underestimates RPF by about 10 percent

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9
Q

Normal filtration fraction

A

20 percent

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10
Q

At what plasma concentration of glucose does glucosuria begin?

A

Around 160-200 mg/dL

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11
Q

Where is digoxin excreted?

A

Kidneys

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12
Q

Where in the tubule is tonicity lowest when ADH is present?

A

Early DCT

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13
Q

Two things that cause increased ANP and BNP release

A

LV hypertrophy and volume overload

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14
Q

Where in the kidney is the sodium sensor? Where is renin secreted from?

A

Macula densa is sodium sensor, JG cells secrete renin

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15
Q

Serum sodium levels can be normal in hyperaldosteronism. Why is this and what other labs should you look at to make the diagnosis?

A

Increased ANP release can normalize serum sodium even in hyperaldosteronism. However, potassium will still be low and bicarb will still be high

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16
Q

What cells produce epo?

A

Tubular interstitial cells

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17
Q

What receptors do JG cells have and what is the pharmacotherapy implication of this?

A

Beta receptors. B1 stimulation there leads to increased renin release. Beta blockers thus lower renin levels and reduce BP

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18
Q

ADH increases reabsorption in the collecting duct of water and what other substance?

A

Urea

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19
Q

Signs of ethylene glycol poisoning

A

Acute renal failure, calcium oxalate crystals, AG metabolic acidosis, increased osmolar gap

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20
Q

What is the defect in Type 1, Type 2, and Type 4 RTA respectively?

A

Type 1 - Collecting tubules ability to excrete acid, Type 2 - Proximal tubules ability to reabsorb biacrb, Type 4 - Hypoaldosteronism or lack of aldosterone response (you get inhibition of ammonium excretion in prox tubule)

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21
Q

What causes granular, waxy, and hyaline casts respectively?

A

Granular - ATN, Waxy - ARF/CRF, Hyaline - nonspecific

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22
Q

Findings in SIADH

A

Dec plasma Na and osmolality, inappropriately concentrated urine, increased urinary sodium, normal total body water volume

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23
Q

Immunofluorescence findings in acute poststreptococcal GN

A

Granular appearance of IgG, IgM, and C3 along GBM and mesangium

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24
Q

What is the most important prognostic factor in acute poststrep GN?

A

Age. Kids do best

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25
Q

About when relative to the original illness does poststrep GN show up?

A

2 to 3 weeks

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26
Q

What is the serum finding in acute poststrep GN?

A

Decreased C3 in serum

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27
Q

What do glomerular crescents consist of?

A

Fibrin and plasma proteins (eg C3b)

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28
Q

3 main causes of RPGN

A

Goodpasture, Wegeners, Microscopic Polyangiitis

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29
Q

What is the most common cause of death in SLE?

A

Diffuse proliferative GN

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30
Q

How long after the original illness does Bergers disease occur?

A

About 2 days

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31
Q

Nerve disorders, ocular disorders, deafness, nephritic syndrome

A

Alport syndrome. X-linked

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32
Q

What is a quick way to differentiate between Wegeners and Goodpasture

A

Wegeners can involve upper respiratory (eg nasal) ulcerations while Goodpasture does not

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33
Q

Immunofluorescence findings in diffuse membranous glomerulopathy type 1

A

Granular depositions. C1q (or might be IgE if due to SLE)

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34
Q

What is the most common cause of adult nephrotic syndrome

A

FSGS

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35
Q

Main causes of membranous glomerulonephritis (diffuse membranous glomerulopathy)

A

Drugs, infections, SLE, solid tumors

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36
Q

What type of glomerular disease may be triggered by atopic disorders?

A

Minimal change

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37
Q

Treatment for minimal change disease

A

Corticosteroids. Will usually resolve, especially with treatment

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38
Q

Key associations for the appearance of MPGN

A

Type 1 - Tram track on LM. Type 2 - Dense deposits on EM

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39
Q

Kimmelstiel-Wilson lesion

A

Eosinophilic nodular glomerulosclerosis (really really pink) seen in diabetic glomerulonephropathy

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40
Q

What is the most common calcium status of pts with calcium kidney stones?

A

Normocalcemic with idiopathic hypercalciuria

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41
Q

Which type of renal stone precipitates at a different pH than the others

A

Staghorn (ammonium magnesium phosphate) precipitates at alkaline pH (others are all acidic or neutral)

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42
Q

Which type of renal stone has a different appearance on x-ray than the others

A

Uric acid stones. They are radiolucent, others are all radioopaque

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43
Q

Microorganisms causing staghorn calculi (3)

A

Proteus mirabilis, staph, klebsiella

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44
Q

Test of choice for suspected cystine stones

A

Sodium cyanide-nitroprusside test. If they are cystine stones, they will turn red-purple

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45
Q

What is hydronephrosis a common complication of?

A

Pelvic surgery (eg hysterectomy)

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46
Q

What does hydronephrosis look like grossly and what is the difference?

A

Looks like ADPKD, but has a less bumpy surface

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47
Q

What is the cell of origin for RCC?

A

Renal tubular cell

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48
Q

Hematuria, palpable mass, polycythemia, flank pain, fever, weight loss

A

RCC

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49
Q

How does RCC spread and where does it go?

A

Hematogenously (via IVC). Goes to lung and bone mostly

50
Q

Ectopic hormones produced by RCCs

A

epo, ACTH, PTHrP, prolactin

51
Q

Histologic appearance of Wilms tumor (nephroblastoma)

A

Looks like immature glomerular structures

52
Q

WAGR

A

Wilms tumor, Aniridia, Genitourinary malformation, mental-motor Retardation

53
Q

What is the best indicator of the malignant potential of a transitional cell carcinoma?

A

Involvement of the bladder wall (muscular layer)

54
Q

What is transitional cell carcinoma associated with?

A

Phenacetin, Smoking, Aniline dyes, Cyclophosphamide

55
Q

Painless hematuria without casts

A

Suggestive of bladder cancer

56
Q

What condition is white cell casts classic for?

A

Acute pyelonephritis

57
Q

Eosinophilic casts (thyroidization of kidney)

A

Chronic pyelonephritis

58
Q

Findings and timing of drug-induced interstial nephritis

A

1-2 weeks after administration. Pyuria (eosinophils) and azotemia

59
Q

Drugs that cause interstitial nephritis

A

NSAIDs, penicillin derivatives, sulfas, rifampin

60
Q

Diffuse cortical necrosis

A

Acute generalized cortical infarction of both kidneys

61
Q

What is the most common outcome of ATN?

A

Re-epithelialization and restoration of function

62
Q

Describe the recovery phase of ATN

A

Polyuric. BUN and serum creatinine fall. Risk of hypokalemia

63
Q

Renal osteodystrophy

A

Failure to make active Vit D leads to Ca wasting and PO4 retention (due to hyperparathyroidism). Subperiosteal thinning of bones

64
Q

What is ADPKD associated with?

A

Polycystic liver disease, berry aneurysms (HTN), MVP

65
Q

Clinical consequences of simple cysts

A

Benign. Occur in more than 40 percent of elderly

66
Q

Medullary cystic disease

A

Cysts lead to fibrosis and renal failure. Small kidney on ultrasound, 70 percent develop kidney stones. Poor prognosis

67
Q

Mannitol

A

Osmotic diuretic. Use in shock, drug overdose, also high ICP or IOP. May cause pulmonary edema

68
Q

Acetazolamide

A

Carbonic anhydrase inhibitor. Use in glaucoma, urinary alkalinization, met alk, and altitude sickness. Is a sulfa drug

69
Q

Furosemide

A

Loop diuretic. Stimulates PGE release (dilates aff art). Inhibited by NSAIDs.

70
Q

Toxicities of furosemide

A

Ototoxicity, hypokalemia, dehydration, sulfa allergy, interstitial nephritis, gout

71
Q

Ethacrynic acid

A

Basically same as furosemide but not a sulfa drug. Can cause gout, do not use to treat gout

72
Q

HCTZ

A

Thiazide diuretic. Use in HTN, CHF, hypercalciuria, nephrogenic DI

73
Q

Toxicities of HCTZ

A

Met alk, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

74
Q

Which diuretic has significant lipid effects and what are they?

A

HCTZ causes increased LDL and cholesterol

75
Q

List the K sparing diuretics (4)

A

Spironolactone, triamterene, amilioride, eplerenone

76
Q

Side effects of spironolactone

A

Hyperkalemia (arrhythmias). Also gynecomastia and antiandrogen effects (can be used to decrease hirsutism)

77
Q

Blood pH changes in diuretic therapy

A

Acidemia - carbonic anhydrase inhibitors, K+ sparings. Alkalemia - Loops and Thiazides

78
Q

Captopril, enalapril, lisinopril

A

ACE inhibitors

79
Q

Main difference in side effects between ACE-inhibitors and ARBs

A

No cough with ARBs (do not increase kallikrein)

80
Q

What effect do ACE inhibitors have on GFR and why?

A

Significantly decrease it because they block angiotensin II, which constricts the efferent arteriole (thus ACE-Is dilate eff art)

81
Q

Toxicities of ACE inhibitors

A

CAPTOPRIL. Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II. Also hyperkalemia

82
Q

About when do cysts start appearing in ADPKD?

A

10-12 years of age

83
Q

History of hypertension, abnormal ultrasound of the abdomen, and click murmur

A

ADPKD

84
Q

What GI condition is ADPKD associated with?

A

Diverticulosis

85
Q

What type of hypersensitivity is involved in any glomerulonephritis?

A

Type 3

86
Q

What is responsible for the strong negative of the GBM which keeps albumin out of the urine?

A

Heparan Sulfate (a GAG)

87
Q

Where are the deposits in SLE and post strep GN respsectively?

A

SLE - subendothelial (too big to get through BM), post strep - subepithelial (can fit past BM)

88
Q

Appearance of fatty casts (nephrotic syndrome) on polarization

A

Maltese cross

89
Q

Why do pts with nephrotic syndrome always have hypercholesterolemia?

A

When you start to lose protein the liver starts making cholesterol for some reason

90
Q

Most common cause of nephrotic syndrome in AIDS patients

A

FSGS

91
Q

Epimembranous spike like lesions on the outside of the GBM seen with silver stain

A

Diffuse membranous glomerulonephritis

92
Q

Which glomerular diseases have a relationship with hepatitis and which hepatitis?

A

Membranous Glomerulonephritis with Hep B and Type 1 Membranoproliferative GN with Hep C

93
Q

Where are the deposits in Type 1 Membranoproliferative GN?

A

Subendothelial

94
Q

What causes Type 2 Membranoproliferative GN?

A

Auto antibodies against C3 (C3 nephritic factor)

95
Q

In what glomerular disease will you see the lowest complement levels?

A

Type 2 Membranoproliferative GN (because autoantibody to C3)

96
Q

First vessel hyalinized in diabetes

A

Efferent arterioles

97
Q

What happens to the GFR and Cr clearance in early diabetic nephropathy?

A

They are increased (because efferent arteriole is hyalinized and thus narrowed). It is the increased pressure on the glomerulus which causes problems in the long run

98
Q

Periodic episodes of hematuria and or proteinuria

A

IgA glomerulonephritis (Bergers)

99
Q

Where are the deposits in IgA GN (Bergers)?

A

Mesangium

100
Q

Key finding in diagnosing prerenal azotemia

A

Elevated BUN and Creatinine with a greater than 15 to 1 BUN to Creatinine ratio

101
Q

BUN to Creatinine ratio in intrarenal (not prerenal) failure

A

Normal (10 to 1)

102
Q

Separating renal from postrenal failure

A

Urine Na - Above 20 in renal, above 40 in postrenal. FeNA - Above 2 percent in renal, above 4 percent in postrenal. BUN to Creatinine ratio - Below 15 in renal, Above 15 in postrenal

103
Q

Parts of the tubule that experience sloughing first in ATN

A

Proximal tubule and Medullary Thick Ascending Limb

104
Q

Where does nephrotoxic tubular necrosis take place?

A

Proximal tubule. Often caused by gentamycin and other aminoglycosides

105
Q

Do you see fever, flank pain, and WBC casts in cystitis or pyelonephritis?

A

Pyelonephritis (but not cystitis)

106
Q

Type of hypersensitivity in acute drug induced interstitial nephritis

A

Combination of Type 1 and Type 4

107
Q

Most common cause of sterile pyuria

A

Chlamydia. Tb is another

108
Q

Hypospadias and epispadias respectively are defects of what?

A

Hypo - closure of urethral fold, Epi - genital tubercle

109
Q

In what disorder is priapism commonly seen?

A

Sickle Cell

110
Q

Most common cancer of the penis and the cause

A

SCC because of lack of circumcision (the smegma that accumulates with poor hygeine is carcinogenic)

111
Q

What is responsible for the two phases of testicular descent?

A

Part 1 - MIF, Part 2 - Testosterone and dihydrotestosterone

112
Q

If a testicle hasnt descended by two years, what are you at increased risk for?

A

Seminoma (the other one will also be at risk)

113
Q

Streak gonad

A

An ovary without an follicles (eg Turners)

114
Q

What does a streak gonad in Turners predispose to?

A

Dysgerminomas (the equivalent of a seminoma in a woman)

115
Q

Most common cause of epididymitis

A

Less than 35 y/o - gonorrhea and chlamydia. Over 35 - pseudomonas

116
Q

How can you differentiate hydrocele from testicular cancer?

A

Hydrocele will transilluminate, cancer wont

117
Q

Most common testicular tumors in adult and children respectively

A

Adults - Seminoma. Children - Yolk sac tumor

118
Q

Most aggressive testicular cancer

A

Choriocarcinoma

119
Q

Why does a choriocarcinoma in a man cause gynecomastia?

A

Because b-HCG works like LH and thus stimulates progesterone

120
Q

In what age population does testicular cancer often metastasize to become a malignant lymphoma?

A

Older men

121
Q

What hormone is responsible for the prostate?

A

Dihydrotestosterone