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
About when relative to the original illness does poststrep GN show up?
2 to 3 weeks
26
What is the serum finding in acute poststrep GN?
Decreased C3 in serum
27
What do glomerular crescents consist of?
Fibrin and plasma proteins (eg C3b)
28
3 main causes of RPGN
Goodpasture, Wegeners, Microscopic Polyangiitis
29
What is the most common cause of death in SLE?
Diffuse proliferative GN
30
How long after the original illness does Bergers disease occur?
About 2 days
31
Nerve disorders, ocular disorders, deafness, nephritic syndrome
Alport syndrome. X-linked
32
What is a quick way to differentiate between Wegeners and Goodpasture
Wegeners can involve upper respiratory (eg nasal) ulcerations while Goodpasture does not
33
Immunofluorescence findings in diffuse membranous glomerulopathy type 1
Granular depositions. C1q (or might be IgE if due to SLE)
34
What is the most common cause of adult nephrotic syndrome
FSGS
35
Main causes of membranous glomerulonephritis (diffuse membranous glomerulopathy)
Drugs, infections, SLE, solid tumors
36
What type of glomerular disease may be triggered by atopic disorders?
Minimal change
37
Treatment for minimal change disease
Corticosteroids. Will usually resolve, especially with treatment
38
Key associations for the appearance of MPGN
Type 1 - Tram track on LM. Type 2 - Dense deposits on EM
39
Kimmelstiel-Wilson lesion
Eosinophilic nodular glomerulosclerosis (really really pink) seen in diabetic glomerulonephropathy
40
What is the most common calcium status of pts with calcium kidney stones?
Normocalcemic with idiopathic hypercalciuria
41
Which type of renal stone precipitates at a different pH than the others
Staghorn (ammonium magnesium phosphate) precipitates at alkaline pH (others are all acidic or neutral)
42
Which type of renal stone has a different appearance on x-ray than the others
Uric acid stones. They are radiolucent, others are all radioopaque
43
Microorganisms causing staghorn calculi (3)
Proteus mirabilis, staph, klebsiella
44
Test of choice for suspected cystine stones
Sodium cyanide-nitroprusside test. If they are cystine stones, they will turn red-purple
45
What is hydronephrosis a common complication of?
Pelvic surgery (eg hysterectomy)
46
What does hydronephrosis look like grossly and what is the difference?
Looks like ADPKD, but has a less bumpy surface
47
What is the cell of origin for RCC?
Renal tubular cell
48
Hematuria, palpable mass, polycythemia, flank pain, fever, weight loss
RCC
49
How does RCC spread and where does it go?
Hematogenously (via IVC). Goes to lung and bone mostly
50
Ectopic hormones produced by RCCs
epo, ACTH, PTHrP, prolactin
51
Histologic appearance of Wilms tumor (nephroblastoma)
Looks like immature glomerular structures
52
WAGR
Wilms tumor, Aniridia, Genitourinary malformation, mental-motor Retardation
53
What is the best indicator of the malignant potential of a transitional cell carcinoma?
Involvement of the bladder wall (muscular layer)
54
What is transitional cell carcinoma associated with?
Phenacetin, Smoking, Aniline dyes, Cyclophosphamide
55
Painless hematuria without casts
Suggestive of bladder cancer
56
What condition is white cell casts classic for?
Acute pyelonephritis
57
Eosinophilic casts (thyroidization of kidney)
Chronic pyelonephritis
58
Findings and timing of drug-induced interstial nephritis
1-2 weeks after administration. Pyuria (eosinophils) and azotemia
59
Drugs that cause interstitial nephritis
NSAIDs, penicillin derivatives, sulfas, rifampin
60
Diffuse cortical necrosis
Acute generalized cortical infarction of both kidneys
61
What is the most common outcome of ATN?
Re-epithelialization and restoration of function
62
Describe the recovery phase of ATN
Polyuric. BUN and serum creatinine fall. Risk of hypokalemia
63
Renal osteodystrophy
Failure to make active Vit D leads to Ca wasting and PO4 retention (due to hyperparathyroidism). Subperiosteal thinning of bones
64
What is ADPKD associated with?
Polycystic liver disease, berry aneurysms (HTN), MVP
65
Clinical consequences of simple cysts
Benign. Occur in more than 40 percent of elderly
66
Medullary cystic disease
Cysts lead to fibrosis and renal failure. Small kidney on ultrasound, 70 percent develop kidney stones. Poor prognosis
67
Mannitol
Osmotic diuretic. Use in shock, drug overdose, also high ICP or IOP. May cause pulmonary edema
68
Acetazolamide
Carbonic anhydrase inhibitor. Use in glaucoma, urinary alkalinization, met alk, and altitude sickness. Is a sulfa drug
69
Furosemide
Loop diuretic. Stimulates PGE release (dilates aff art). Inhibited by NSAIDs.
70
Toxicities of furosemide
Ototoxicity, hypokalemia, dehydration, sulfa allergy, interstitial nephritis, gout
71
Ethacrynic acid
Basically same as furosemide but not a sulfa drug. Can cause gout, do not use to treat gout
72
HCTZ
Thiazide diuretic. Use in HTN, CHF, hypercalciuria, nephrogenic DI
73
Toxicities of HCTZ
Met alk, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy
74
Which diuretic has significant lipid effects and what are they?
HCTZ causes increased LDL and cholesterol
75
List the K sparing diuretics (4)
Spironolactone, triamterene, amilioride, eplerenone
76
Side effects of spironolactone
Hyperkalemia (arrhythmias). Also gynecomastia and antiandrogen effects (can be used to decrease hirsutism)
77
Blood pH changes in diuretic therapy
Acidemia - carbonic anhydrase inhibitors, K+ sparings. Alkalemia - Loops and Thiazides
78
Captopril, enalapril, lisinopril
ACE inhibitors
79
Main difference in side effects between ACE-inhibitors and ARBs
No cough with ARBs (do not increase kallikrein)
80
What effect do ACE inhibitors have on GFR and why?
Significantly decrease it because they block angiotensin II, which constricts the efferent arteriole (thus ACE-Is dilate eff art)
81
Toxicities of ACE inhibitors
CAPTOPRIL. Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II. Also hyperkalemia
82
About when do cysts start appearing in ADPKD?
10-12 years of age
83
History of hypertension, abnormal ultrasound of the abdomen, and click murmur
ADPKD
84
What GI condition is ADPKD associated with?
Diverticulosis
85
What type of hypersensitivity is involved in any glomerulonephritis?
Type 3
86
What is responsible for the strong negative of the GBM which keeps albumin out of the urine?
Heparan Sulfate (a GAG)
87
Where are the deposits in SLE and post strep GN respsectively?
SLE - subendothelial (too big to get through BM), post strep - subepithelial (can fit past BM)
88
Appearance of fatty casts (nephrotic syndrome) on polarization
Maltese cross
89
Why do pts with nephrotic syndrome always have hypercholesterolemia?
When you start to lose protein the liver starts making cholesterol for some reason
90
Most common cause of nephrotic syndrome in AIDS patients
FSGS
91
Epimembranous spike like lesions on the outside of the GBM seen with silver stain
Diffuse membranous glomerulonephritis
92
Which glomerular diseases have a relationship with hepatitis and which hepatitis?
Membranous Glomerulonephritis with Hep B and Type 1 Membranoproliferative GN with Hep C
93
Where are the deposits in Type 1 Membranoproliferative GN?
Subendothelial
94
What causes Type 2 Membranoproliferative GN?
Auto antibodies against C3 (C3 nephritic factor)
95
In what glomerular disease will you see the lowest complement levels?
Type 2 Membranoproliferative GN (because autoantibody to C3)
96
First vessel hyalinized in diabetes
Efferent arterioles
97
What happens to the GFR and Cr clearance in early diabetic nephropathy?
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
Periodic episodes of hematuria and or proteinuria
IgA glomerulonephritis (Bergers)
99
Where are the deposits in IgA GN (Bergers)?
Mesangium
100
Key finding in diagnosing prerenal azotemia
Elevated BUN and Creatinine with a greater than 15 to 1 BUN to Creatinine ratio
101
BUN to Creatinine ratio in intrarenal (not prerenal) failure
Normal (10 to 1)
102
Separating renal from postrenal failure
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
Parts of the tubule that experience sloughing first in ATN
Proximal tubule and Medullary Thick Ascending Limb
104
Where does nephrotoxic tubular necrosis take place?
Proximal tubule. Often caused by gentamycin and other aminoglycosides
105
Do you see fever, flank pain, and WBC casts in cystitis or pyelonephritis?
Pyelonephritis (but not cystitis)
106
Type of hypersensitivity in acute drug induced interstitial nephritis
Combination of Type 1 and Type 4
107
Most common cause of sterile pyuria
Chlamydia. Tb is another
108
Hypospadias and epispadias respectively are defects of what?
Hypo - closure of urethral fold, Epi - genital tubercle
109
In what disorder is priapism commonly seen?
Sickle Cell
110
Most common cancer of the penis and the cause
SCC because of lack of circumcision (the smegma that accumulates with poor hygeine is carcinogenic)
111
What is responsible for the two phases of testicular descent?
Part 1 - MIF, Part 2 - Testosterone and dihydrotestosterone
112
If a testicle hasnt descended by two years, what are you at increased risk for?
Seminoma (the other one will also be at risk)
113
Streak gonad
An ovary without an follicles (eg Turners)
114
What does a streak gonad in Turners predispose to?
Dysgerminomas (the equivalent of a seminoma in a woman)
115
Most common cause of epididymitis
Less than 35 y/o - gonorrhea and chlamydia. Over 35 - pseudomonas
116
How can you differentiate hydrocele from testicular cancer?
Hydrocele will transilluminate, cancer wont
117
Most common testicular tumors in adult and children respectively
Adults - Seminoma. Children - Yolk sac tumor
118
Most aggressive testicular cancer
Choriocarcinoma
119
Why does a choriocarcinoma in a man cause gynecomastia?
Because b-HCG works like LH and thus stimulates progesterone
120
In what age population does testicular cancer often metastasize to become a malignant lymphoma?
Older men
121
What hormone is responsible for the prostate?
Dihydrotestosterone