Checkpoint Notes: Renal Diseases Flashcards
1
Q
Sodium carbonate Uric acid reagent (Folin reagent with PTA)
A
URIC ACID
2
Q
HCl upon addition of MnO2
A
CARBONATE OXALATE
3
Q
Ammonium molybdate in nitric acid
A
PHOSPHATE
4
Q
HCl and NaOH
A
CALCIUM
5
Q
HCl, NaOH, and p-nitrobenzeneazoresorcinol in NaOH
A
MAGNESIUM
6
Q
HCl, NaOH and Nessier’s solution
A
AMMONIUM
7
Q
NH4OH, NaCN, and Na nitroprusside
A
CYSTINE
8
Q
Deep blue color
A
URIC ACID
9
Q
Formation of tiny bubbles
A
CARBONATE OXALATE
10
Q
Distinct yellow color after heating
A
PHOSPHATE
11
Q
White cloud
A
CALCIUM
12
Q
Blue color
A
MAGNESIUM
13
Q
Orange-brown ppt.
A
AMMONIUM
14
Q
Beet red color
A
CYSTINE
15
Q
Clinical representation of glomerular diseases
A
Nephrotic syndrome
Nephritic syndrome
16
Q
Immune-mediated
A
Nephritic syndrome
17
Q
Acute onset of usually grossly visible hematuria
A
Nephritic syndrome
18
Q
Presence of rbc casts
A
Nephritic syndrome
19
Q
Mild-to-moderate proteinuria
A
Nephritic syndrome
20
Q
Oluguria
A
Nephritic syndrome
21
Q
Disruption of the filtration barrier because of the damage to the membrane and changes in the electrical charges in the basal lamina and podocytes, producing a less tightly connected barrier
A
Nephrotic syndrome
22
Q
Heavy proteinuria [> 3.5 gm/day]
A
Nephrotic syndrome
23
Q
Hyporalbuminuria
A
Nephrotic syndrome
24
Q
Severe edema
A
Nephrotic syndrome
25
Hyperlipidemia
Nephrotic syndrome
26
Lipiduria
Nephrotic syndrome
27
Glomerulopathies presenting as nephritic syndrome
Acute poststreptococcal glomerulonephritis
Rapidly progressive or crescentic glomerulonephritis
Membranous glomerulonephritis
Membranoproliferative glomerulonephritis
IgA nepheropathy (Berger disease)
Chronic glomerulonephritis
28
Two types of Rapidly progressive or crescentic glomerulonephritis
Goodpasteur syndrome
Wegener granulomatosis
29
Glomerulopathies presenting as nephrotic syndrome
Minimal change disease
Google segmental glomerulosclerosis
30
Deposition of immune complexes, formed in conjunction with a group a streptococcus infection, on glomerular membranes
Acute poststreptococcal glomerulonephritis
31
Deposition of immune complexes from systemic immune disorders on the glomerular membrane
Rapidly progressive or crescentic glomerulonephritis
32
Thickening of the glomerular membrane following IgG immune complex deposition associated with systemic disorders
Membranous glomerulonephritis
33
Cellular proliferation affecting the capillary walls or the glomerular basement membrane, possibly immune-mediated
Membranoproliferative glomerulonephritis
34
Deposition of IgA on the glomerular membrane resulting from increased levels of serum IgA
IgA nepheropathy (Berger disease)
35
Most common cause of glomerulonephritis
IgA nepheropathy (Berger disease)
36
Marked decrease in renal function resulting from glomerular damage precipitated by other renal disorders
Chronic glomerulonephritis
37
Attachment of a cytotoxic antibody formed during viral respiratory infections to glomerular and alveolar basement membranes
Goodpasteur syndrome
38
Initial pulmonary complaints or hemoptysis and dyspnea, followed by the development of hematuria
Goodpasteur syndrome
39
(+) ANTI GLOMERULAR BASEMENT MEMBRANE ANTIBODY
Goodpasteur syndrome
40
Antineutrophilic cytoplasmic autoantibodies binds to neutrophils and vascular walls producing damage to small vessels in the lungs and glomerulus
Wegener granulomatosis
41
(+) ANTI NEUTROPHILIC CYTOPLASMIC AUTO-ANTIBODY (ANCA)
Wegener granulomatosis
42
Disruption of podocytes occurring primarily in children following allergic reactions and immunizations
Minimal change disease
43
Disruption of podocytes in certain areas of glomeruli associated with heroin and analgesic abuse and AIDS
Focal segmental glomerulosclerosis
44
Occurs primarily in children following viral respiratory infections
Henoch-Schonlein Purpura
45
Decrease in platelets disrupts a vascular integrity
Henoch-Schonlein Purpura
46
Also known as Kimmelstiel-Wilson disease
Diabetic nephropathy
47
Currently the most come on cause of end-stage renal disease
Diabetic nephropathy
48
Damage to the glomerular membrane occurs as a result of glomerular membrane thickening, increase proliferation of mesangial cells, and increase deposition of cellular and non-cellular material within the glomerular matrix resulting in accumulation of solid substances around the capillary tufts
Diabetic nephropathy
49
This is believed to be associated with the the position of glycosylated proteins resulting from poorly controlled blood glucose levels
Diabetic nephropathy
50
The vascular structure of the glomerulus also develops sclerosis
Diabetic nephropathy
51
Tubulointerstitial Diseases
ACUTE TUBULAR NECROSIS
52
Damage to the renal tubular cells caused by ischemia or toxic agents
ACUTE TUBULAR NECROSIS
53
Inherited in association with cystinosis and Hartnup disease or acquired through exposure to toxic agents
Fanconi's Sysndrome
54
Inherited defect of tubular response to ADH or acquired from medications
Nephrogenic Diabetes Insipidues
55
Inherited autosomal recessive traits
Renal Glycosuria
56
Infection of the renal tubules and intestitium related to interference of urine flow to the bladder, reflux of urine from the bladder, and untreated cystitis
Acute Pyelonephritis
57
Recurrent infection of the tubules and interstitium caused by structural abnormalities affecting the flow of urine
Chronic Pyelonephritis
58
Allergic inflammation of the renal interstitium in response to certain medications
Acute Interstitial Nephritis
59
Ascending bacetrial infection of the bladder
Cystitis
60
May be acute or chronic
Renal Failure
61
may be a gradual progression from the original disorder to chronic renal failure or end-stage renal disease
Renal Failure
62
A marked decrease in glomerular filtration rate (< 25mL/min)
progression to end-stage renal disease
63
Steadily rising serum BUN and creatinine values (azotemia)
progression to end-stage renal disease
64
Electrolyte imbalance
progression to end-stage renal disease
65
Lack of renal concentrating ability producing an isosthenuric
progression to end-stage renal disease
66
Proteinuria
progression to end-stage renal disease
67
Renal glycosuria
progression to end-stage renal disease
68
Abundance of granular, waxy, and broadcast, often referred to as telescope urine sediment
progression to end-stage renal disease
69
Exhibits sudden loss of renal function and is frequently reversible
Acute renal failure
70
Decrease blood pressure
PRERENAL
71
Cardiac output
PRERENAL
72
Hemorrhage
PRERENAL
73
Burns
PRERENAL
74
Surgery
PRERENAL
75
Septicemia
PRERENAL
76
Acute glomerulonephritis
RENAL
77
Acute tubular necrosis
RENAL
78
Acute pyelonephritis
RENAL
79
Acute interstitial nephritis
RENAL
80
Renal calculi
POSTRENAL
81
Tumors
RENAL
82
Crystallization of ingested substances
RENAL
83
Kidney stones
Renal calculi
84
May form in the calyces and pelvis of the kidney. ureters, and bladder
Renal calculi
85
They may be small and be passed in the urine or large and obstract the urinary tract
Renal calculi
86
A procedure using high-energy shock waves, can be used to break stones located in the upper urinary tract into pieces that can then be passed in the urine
LITHOTRIPSY
87
Conditions favoring the formation of renal calculi
pH
Chemical concentration
Urine stasis
88
PRIMARY CALCULI CONSTITUENTS
Calcium oxalate or phosphate
Magnesium ammonium phosphate
Uric acid
Cystine
89
Frequently associated with metabolic calcium and phosphate disorders and occasionally diet
~75 CALCIUM OXALATE OR PHOSPHATE
90
Frequently accompanied by urinary infections involving the splitting-bacteria
Magnesium ammonium phosphate
91
Urine pH usually > 7
Magnesium ammonium phosphate
92
Associated with increased intake of food with high purine content
Uric acid
93
Urine ph is acidic
Uric acid
94
Seen in conjunction with hereditary disorders of cysteine metabolism
Cystine
95
Increase crystalluria has been noted during the summer months in person known to form renal calculi
Renal lithiasis
96
Analysis can be performed chemically, but examination using x-ray crystallography provides a more comprehensive analysis
Renal lithiasis
97
Patient management technique include maintaining the urine at a compatible pH with crystallization of particular chemicals, maintaining adequate hydration to lower chemical concentration, and suggesting possible dietary restrictions
Renal lithiasis
