Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

FA note cards > Renal > Flashcards

Renal Flashcards

1
Q

most common site of obstruction

A

Ureteropelvic junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Potter sequence (syndrome) sx

A

Oligohydramnios → compression of developing fetus → limb deformities, facial anomalies (low-set ears, retrognathia, flattened nose), compression of chest and lack of amniotic fluid aspiration into fetal lungs pulmonary hypoplasia (cause of death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of Potter sequence

A

ARPKD, obstructive uropathy, bilateral renal agenesis, chronic placental insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

On what vessel does a horseshoe kidney get trapped?

A

Under IMA and remain low in the abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do you have increased risk of in duplex collecting system?

A

UTIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Course of ureters

A

Pass under uterine artery or under vas deferens (retroperitoneal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Best estimate of GFR

A

Creatinine clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Best estimate of RPF

A

PAH clearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Equation for filtration fraction

A

FF = GFR/RPF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Normal FF?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where is glucose reabsorbed?

A

In the proximal convoluted tubule (PCT) by Na+/glucose cotransport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Plasma glucose threshold for glucosuria? When are all transports saturated?

A

∼ 200 mg/dL

∼ 375 mg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is absorbed in the early PCT?

A

all glucose and amino acids and most HCO3, Na, Cl, PO43, K, H2O, and uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Effect of PTH at the PCT?

A

inhibits Na/PO43 cotransport → PO43 excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Effect of ATII at the PCT?

A

Stimulates Na/H exchange → ↑ Na, H2O, and HCO reabsorption (permitting contraction alkalosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tonicity of filtrate leaving the PCT?

A

Isotonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What occurs in the thin descending loop of Henle?

A

Passive reabsorbtion of H2O via medullary hypertonicity (impermeable to Na+) Concentrating segment. Makes urine hypertonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which section of the kidney is the “concentrating segment”

A

thin descending loop of Henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What occurs in the thick ascending loop of Henle?

A

Reabsorbs Na, K, and Cl

Indirectly induces paracellular reabsorption of Mg2+ and Ca2+ through ⊕ lumen potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens to the concentration of urine in the TAL?

A

Makes urine less concentrated as it ascends; impermeable to H2O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens to the concentration of urine in the DCT?

A

Makes urine fully dilute (hypotonic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

PTH effect on DCT?

A

↑ Ca2/Na exchange: Ca2+ reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Aldosterone regulation in the collecting tubule?

A

reabsorbs Na+ in exchange for secreting K+ and H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ADH effect in collecting tubule?

A

acts at V2 receptor to ↑ aquaporins on apical side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Order of Na reabsorption
Early PCT > TAL > DCT > CD
26
Fanconi syndrome
Generalized reabsorptive defect in PCT | ↑ excretion of all amino acids, glucose, HCO3, and PO4; leads to metabolic acidosis
27
Causes of Fanconi Syndrome
``` hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease, cystinosis), ischemia, multiple myeloma, nephrotoxins/drug, lead poisoning (Fanconi is First dx in renal tubule) ```
28
Bartter syndrome
AR reabsorptive defect in thick ascending loop of Henle Affects Na/K/2Cl cotransporter → hypokalemia and metabolic alkalosis with hypercalciuria Presents like loop diuretic use
29
Gitelman syndrome
AR reabsorptive defect of NaCl in DCT HypoK, hypoMg, metabolic alkalosis, hypocalciuria Presents like thiazide use
30
Liddle syndrome
GoF: ↑ Na+ reabsorption in collecting tubules d/t ↑ Na channel activity HTN, hyperK, metabolic alkalosis, ↓ aldosterone Looks like hyperaldosteronism except aldosterone is zero Treat w/ amiloride
31
Syndrome of Apparent Mineralocorticoid Excess
Hereditary deficiency of 11β-hydroxysteroid dehydrogenase: converts cortisol to cortisone in cells with MC-r ↑ MC activity: HTN, hypoK, metabolic alkalosis Can happen w/ too much licorice Treat with corticosteroids
32
Distal renal tubular acidosis
Type 1; pH > 5.5 Defect in ability of α intercalated cells to secrete H → no new HCO3 → metabolic acidosis Hypokalemia, Ca phosphate stones
33
Causes of Type 1 RTA
Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract
34
Proximal renal tubular acidosis
Type 2 Defect in PCT HCO reab Hypokalemia, hypophosphatemic stones
35
Causes of type 2 RTA
Fanconi syndrome and carbonic anhydrase inhibitors
36
Hyperkalemic renal tubular acidosis
Type 4 D/t Hypoaldosteronism Hyperkalemia
37
Casts in urine
Indicates glomerular or renal tubular | ie. not bladder cancer or infection or kidney stones
38
RBC casts
Glomerulonephritis, malignant hypertension
39
WBC casts
Tubulointerstitial in ammation, acute pyelonephritis, transplant rejection
40
Fatty casts (“oval fat bodies”)
Nephrotic syndrome. Associated with “Maltese cross” sign
41
Granular (“muddy brown”) casts
Acute tubular necrosis
42
Waxy casts
End-stage renal disease/chronic renal failure
43
Hyaline casts
Nonspecific, can be a normal finding, often seen in concentrated urine samples
44
PSGN on LM, IF and EM
LM: glomeruli enlarged and hypercellular IF: starry sky; granular EM: subepithelial immune complex humps
45
RPGN on LM and IF
Crescent moon shape; crescents consist of brin and plasma proteins with glomerular parietal cells, monocytes, macrophages
46
Diffuse proliferative glomerulonephritis on LM, EM and IF
``` LM—“wire looping” of capillaries EM—subendothelial and sometimes intramembranous IgG-based ICs with C3 deposition IF—granular ```
47
Dz associated with diffuse proliferative glomerulonephritis
SLE
48
IgA nephropathy on LM, EM and IF
LM: mesangial proliferation EM: mesangial IC deposits IF: IgA-based IC deposits in mesangium
49
Alport syndrome
Type IV collagen; Xlinked “Basket-weave” on EM Lens dislocations, glomerulonephritis, sensorineural deafness
50
Membrano- proliferative glomerulonephritis
Type I: subendothelial immune complex with granular IF; “tram-track”; GBM splitting Type II: DDD
51
Cause of type I Membrano- proliferative glomerulonephritis
2° to hepatitis B or C infection or idiopathic
52
Cause of type II Membrano- proliferative glomerulonephritis
C3 nephritic factor (IgG antibody that stabilizes C3 convertase)
53
FSGS on LM, IM and EM
LM: segmental sclerosis and hyalinosis IF: ⊝, but may be ⊕ for nonspecific focal deposits of IgM, C3, C1 EM: effacement of foot process like MCD
54
Most common cause of nephrotic syndrome in African Americans and Hispanics
FSGS
55
Membranous nephropathy on LM, IF, and EM
LM: diffuse capillary and GBM thickening IF: granular d/t immune complex deposition; nephrotic presentation of SLE EM: “spike and dome” appearance with subepithelial deposits.
56
Most common cause of 1° nephrotic syndrome in Caucasian adults
Membranous nephropathy
57
Diabetic glomerulo- nephropathy on LM
Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis
58
Most common cause of end-stage renal disease in the United States
Diabetic glomerulo- nephropathy
59
Ammonium magnesium phosphate stone
↑ pH; Radiopaque Coffin lid shaped Urease ⊕ bugs Form staghorn calculi
60
Uric acid stone
↓ pH; Radiolucent Rhomboid or rosettes Gout and ↑ cell turnover (leukemia)
61
Cystine stone
↓ pH; Radiolucent Hexagonal Hereditary: lost function of cystine reabsorbing PCT transporter Sodium cyanide nitroprusside test ⊕
62
Calcium stone
Most common; Radiopaqu oxalate > phosphate ↓ pH
63
Hydronephrosis
Distention/dilation of renal pelvis and calyces
64
Renal cell carcinoma
From PCT cells: polygonal clear cells filled with lipids and carbohydrates (golden-yellow) Most common 1° renal malignancy
65
RCC spread
Invades renal vein (may develop varicocele if left sided) then IVC and spreads hematogenously; metastasizes to lung and bone
66
Renal oncocytoma
Benign epithelial cell tumor from collecting ducts | Large eosinophilic cells with abundant mitochondria without perinuclear clearing
67
Nephroblastoma
Wilms tumor Contains embryonic glomerular structures LoF of WT1 or WT2 on 11 WAGR complex
68
Denys-Drash
Wilms tumor, early-onset nephrotic syndrome, male pseudohermaphroditism (WT1 mutation)
69
Beckwith-Wiedemann
Wilms tumor, macroglossia, organomegaly, hemihyperplasia (WT2 mutation)
70
Transitional cell carcinoma
``` Painless hematuria (no casts) Most common tumor of urinary tract system ```
71
Squamous cell carcinoma of the bladder
Squamous metaplasia → dysplasia and squamous cell carcinoma Risk: Schistosoma infection (Middle East), chronic cystitis, smoking, cx nephrolithiasis Painless hematuria
72
Stress incontinence
Urethral hypermobility or intrinsic sphincteric defciency Leak w/ ↑ intra-abdominal pressure ⊕ bladder stress test
73
Urgency incontinence
Overactive bladder (detrusor instability): leak with urge to void immediately
74
Over flow incontinence
Incomplete emptying (detrusor underactivity or outlet obstruction): leak with overfilling
75
Acute pyelonephritis histology
Neutrophils in ltrate renal interstitium; WBCs in urine +/− WBC casts Affects cortex with relative sparing of glomeruli/vessels
76
Acute pyelonephritis presentation
Fevers, flank pain, nausea/vomiting, chills
77
Chronic pyelonephritis appearance
Coarse, asymmetric corticomedullary scarring, blunted calyx | Tubules can contain eosinophilic casts resembling thyroid tissue
78
Chronic pyelonephritis risks
Predisposition to infection such as vesicoureteral reflux or chronically obstructing kidney stones
79
Xanthogranulomatous pyelonephritis
Rare; grossly orange nodules; mimic tumor nodules; widespread kidney damage due to granulomatous tissue containing foamy macrophages
80
Diffuse cortical necrosis
Acute generalized cortical infarction of both kidneys D/t vasospasm or DIC Strong association w/ obs problems
81
Acute tubular necrosis
Seen in hospitalized patients Granular (“muddy brown”) casts Spontaneously resolves
82
Renal papillary necrosis
Sloughing of necrotic renal papillae; gross hematuria and proteinuria

FA note cards (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions