NEPHROLOGY Flashcards
1
Q
Represents a stage of CKD where the accumulation of toxins, fluid, and electrolytes normally excreted by the kidneys leads to death unless the toxins are removed
A
end-stage renal disease
2
Q
The pathophysiology of CKD involves two broad sets of mechanisms of damage:
A
(1) initiating mechanisms specific to the underlying etiology
(2) hyperfiltration and hypertrophy of the remaining viable nephrons
3
Q
Most common inherited form of CKD
A
autosomal dominant polycystic kidney disease.
4
Q
The normal annual mean decline in GFR with age from the peak GFR (~120 mL/min per 1.73 m2) attained during _________ is _________ , reaching a mean value of _________ at age 70
A
the third decade of life
~1 mL/min per year per 1.73 m2
70 mL/min per 1.73 m2
5
Q
UACR above ________ in men and ________ in women serves as a marker not only for early detection of primary kidney disease, but for systemic microvascular disease as well
A
17 mg albumin/g creatinine
25 mg albumin/g creatinine
6
Q
Serves as a well-studied screening marker for the presence of systemic microvascular disease and endothelial dysfunction
A
presence of albuminuria
7
Q
T or F: The serum concentrations of urea and creatinine are readily measured complete surrogate markers for retained toxins in uremia
A
False. Accumulation of these two molecules themselves does not account for the many symptoms and signs that characterize the uremic syndrome in advanced renal failure
8
Q
T or F: CKD is associated with increased systemic inflammation
A
True
9
Q
The pathophysiology of the uremic syndrome can be divided into manifestations in three spheres of dysfunction:
A
(1) those consequent to the accumulation of toxins that normally undergo renal excretion;
(2) those consequent to the loss of other kidney functions,
(3) progressive systemic inflammation and its vascular and nutritional consequences
10
Q
Hyponatremia is not commonly seen in CKD patients but, when present, often responds to
A
Water restriction
As long as water intake does not exceed the capacity for renal water clearance, the ECFV expansion will be isotonic and the patient will have a normal plasma sodium concentration
11
Q
Medications that can inhibit renal potassium excretion and lead to hyperkalemia and must be cautiously used or avoided in CKD (2)
A
RAS inhibitors
Spironolactone and other potassium-sparing diuretics such as amiloride, eplerenone, and triamterene
12
Q
Certain causes of CKD can be associated with earlier and more severe disruption of potassium-secretory mechanisms in the distal nephron, out of proportion to the decline in GFR. These include conditions associated with (2)
A
Hyporeninemic hypoaldosteronism (diabetes) Renal diseases that preferentially affect the distal nephron (obstructive uropathy and sickle cell nephropathy)
13
Q
Alkali supplementation may, in addition, attenuate the catabolic state and possibly slow CKD progression and is recommended when the serum bicarbonate concentration falls below
A
20–23 mmol/L
14
Q
These changes that may lead to bone disease in CKD start to occur when the GFR falls below
A
60 mL/min
15
Q
Hyperparathyroidism stimulates bone turnover and leads to
A
osteitis fibrosa cystica
16
Q
Bone histology shows abnormal osteoid, bone and bone marrow fibrosis, and in advanced stages, the formation of bone cysts, sometimes with hemorrhagic elements so that they appear brown in color
A
osteitis fibrosa cystica
17
Q
Brown tumor is also known as
A
osteitis fibrosa cystica
18
Q
A devastating condition seen almost exclusively in patients with advanced CKD that is heralded by livedo reticularis and advances to patches of ischemic necrosis, especially on the legs, thighs, abdomen, and breasts
A
Calciphylaxis
19
Q
The optimal management of secondary hyperparathyroidism and osteitis fibrosa in CKD is
A
prevention
Once the parathyroid gland mass is very large, it is difficult to control the disease
20
Q
These are agents that are taken with meals and complex the dietary phosphate to limit its GI absorption
A
phosphate binders such as calcium acetate, calcium carbonate, sevelamer and lanthanum
21
Q
Non-calcium-containing polymers that also function as phosphate binders; they do not predispose CKD patients to hypercalcemia and may attenuate calcium deposition in the vascular bed (2)
A
sevelamer and lanthanum
22
Q
Enhance the sensitivity of the parathyroid cell to the suppressive effect of calcium, and produces a dose-dependent reduction in PTH and plasma calcium concentration in some patients
A
calcimimetic drugs such as cinacalcet
23
Q
Current National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines recommend a target PTH level between
A
150 and 300 pg/mL
24
Q
Very low PTH levels in CKD are associated with these conditions (3)
A
Adynamic bone disease
Fracture
Ectopic calcification
25
The leading cause of morbidity and mortality in patients at every stage of CKD
Cardiovascular disease
26
The CKD-related risk factors in the increased prevalence of cardiovascular disease are (6)
```
anemia
hyperphosphatemia
hyperparathyroidism
increased FGF-23
sleep apnea
generalized inflammation
```
27
The largest increment in cardiovascular mortality rate in dialysis patients is associated with (2)
congestive heart failure and sudden death
28
2 strongest risk factors for cardiovascular morbidity and mortality in patients with CKD that are thought to be related primarily, but not exclusively, to prolonged hypertension and ECFV overload
Left ventricular hypertrophy and dilated cardiomyopathy
29
The absence of hypertension in CKD may signify
poor left ventricular function
30
T or F, The use of exogenous erythropoiesis-stimulating agents do not have effect on the blood pressure
False. It can increase blood pressure and the requirement for antihypertensive drugs
31
The overarching goal of hypertension therapy in CKD is to
prevent the extrarenal complications of high blood pressure, such as cardiovascular disease and stroke
32
In CKD patients with diabetes or proteinuria >1 g per 24 h, blood pressure should be reduced to
<130/80 mmHg
33
First line of therapy in the management of hypertension in CKD
salt restriction
34
Antihypertensive drugs that appear to slow the rate of decline of kidney function in a manner that extends beyond reduction of systemic arterial pressure and that involves correction of the intraglomerular hyperfiltration and hypertension
ARBs and ACEi
35
Chest pain with respiratory accentuation, 2117 accompanied by a friction rub, is diagnostic of
pericarditis
36
T or F: In patients with uremic pericarditis/effusion, hemodialysis should be performed with heparin
False. Because of the propensity to hemorrhage in pericardial fluid.
37
Type of anemia in CKD
normochromic, normocytic
38
Anemia in CKD can be observed in what stage of CKD
Stage 3
39
Anemia in CKD is universal in what stage of CKD
Stage 4
40
The primary cause of anemia in CKD
insufficient production of EPO
41
Current practice in management of CKD is to target a hemoglobin concentration of
100–115 g/L
42
Coexistence of bleeding disorders and a propensity to thrombosis is unique in patients with
CKD
43
Subtle clinical manifestations of uremic neuromuscular disease usually become evident at what stage of CKD
Stage 3
44
Peripheral neuropathy usually becomes clinically evident after the patient reaches what stage of CKD
stage 4 CKD
45
Characterized by ill-defined sensations of sometimes debilitating discomfort in the legs and feet relieved by frequent leg movement
restless leg syndrome
46
T or F: Evidence of peripheral neuropathy without another cause is an indication for starting renal replacement therapy
True
47
A urine-like odor on the breath, derives from the break- down of urea to ammonia in saliva and is often associated with an unpleasant metallic taste
Uremic fetor
48
A class of drugs that result in glucose lowering, accompanied by striking reductions in kidney function decline and in cardiovascular events
SGLT-2 inhibitors
49
In advanced CKD, even on dialysis, patients may become more pigmented, and this is felt to reflect the deposition of retained pigmented metabolites called
urochromes
50
Although many of the cutaneous abnormalities in CKD improve with dialysis, this particular manifestation is often tenacious
pruritus
51
Pruritus in CKD may be caused by this electrolyte abnormality
hyperphosphatemia
52
A skin condition unique to CKD patients consists of progressive subcutaneous induration, especially on the arms and legs
nephrogenic fibrosing dermopathy
seen in patients exposed to gadolinium contrast of MRI
53
Stage of CKD that is contraindicated for exposure with gadolinium contrast
Stage 4-5
Stage 3 - precaution or minimize exposure
54
The most useful imaging study in evaluation of CKD
Renal utrasound
55
CKD causes with normal or increased kidney size on ultrasound (4)
DM nephropathy
Amyloidosis
HIV nephropathy
Polycystic kidney disease
56
_____________ that has reached some degree of renal failure will almost always present with enlarged kidneys
Polycystic kidney disease
57
In the patient with bilaterally small kidneys, renal biopsy is not advised because (3)
(1) it is technically difficult and has a greater likelihood of causing bleeding and other adverse consequences
(2) there is usually so much scarring that the underlying disease may not be apparent
(3) the window of opportunity to render disease-specific therapy has passed
58
Contraindications to kidney biopsy (4)
```
bilaterally small kidneys
uncontrolled hypertension
active urinary tract infection
bleeding diathesis (including ongoing anticoagulation)
severe obesity
```
59
favored approach for kidney biosy
Ultrasound-guided percutaneous biopsy
60
In the CKD patient in whom a kidney biopsy is indicated (e.g., suspicion of a concomitant or super-imposed active process such as interstitial nephritis or in the face of accelerated loss of GFR), the bleeding time should be measured, and if increased,_________ should be administered immediately prior to the procedure
desmopressin
| or brief run of HD without heparin
61
The most important initial diagnostic step in approach to kidney disease management
to distinguish newly diagnosed CKD from acute or subacute renal failure
62
Among the calcium channel blockers, ______ and_______ may exhibit superior antiproteinuric and renoprotective effects
diltiazem and verapamil
63
Two human kidneys harbor nearly how many glomerular capillary tufts
1.8 million
64
The glomerular capillaries filter how many liters of plasma water
120–180 L/d
65
Humans with normal nephrons excrete on average how many mg of albumin in daily voided urine
8–10 mg
66
Persistent glomerulonephritis that worsens renal function is always accompanied by (3)
interstitial nephritis
renal fibrosis
tubular atrophy
67
T or F: Renal failure in glomerulonephritis best correlates histologically with the type of inciting glomerular injury
False. It best correlates histologically with the appearance of tubulointerstitial nephritis rather than with the type of inciting glomerular injury
68
Glomerular diseases often present as microscopic hematuria except for these 2 conditions wherein gross hematuria is common.
IgA nephropathy
| sickle cell disease
69
Microalbuminuria is how much albumin in the urine?
30–300 mg/24 h
70
Frank proteinuria is how much albumin in the urine?
>300 mg/24 h
71
Sustained proteinuria value
>1–2 g/24 h
72
Foaming urine on voiding is indicative of
proteinuria
73
Class of proteinuria that is nonsustained, generally <1 g/24 h
benign proteinuria
sometimes called functional or transient proteinuria
caused by fever, exercise, obesity, sleep apnea, emotional stress, and congestive heart failure
74
Proteinuria only seen with upright posture
orthostatic proteinuria
benign prognosis
75
T or F: In children with minimal change disease (MCD), the proteinuria is non-selective and composed of albumin and a mixture of other serum proteins
False. selective, composed largely of albumin
Proteinuria in most adults with glomerular disease is nonselective, containing albumin and a mixture of other serum proteins
76
Glomerular syndrome producing 1–2 g/24 h of proteinuria, hematuria with red blood cell casts, pyuria, hypertension, fluid retention, and a rise in serum creatinine associated with a reduction in glomerular filtration
acute nephritic syndrome
77
If glomerular inflammation causes the serum creatinine rises quickly, particularly over a few days, this acute nephritis is called
rapidly progressive glomerulonephritis (RPGN)
78
Pathologic equivalent of the clinical presentation of RPGN
crescentic glomerulonephritis
79
When patients with RPGN present with lung hemorrhage from Goodpasture’s syndrome, antineutrophil cytoplasmic antibodies (ANCA)-associated small-vessel vasculitis, lupus erythematosus, or cryoglobulinemia, they are often diagnosed as
pulmonary-renal syndrome
80
Describes the onset of heavy proteinuria (>3.0 g/24 h), hypertension, hypercholesterolemia, hypoalbuminemia, edema/anasarca, and microscopic hematuria
Nephrotic syndrome
81
Only large amounts of proteinuria (>3.0 g/24 h) are present without clinical manifestations
nephrotic-range proteinuria
82
Describes patients with vascular injury producing hematuria and moderate proteinuria
Glomerular–vascular syndrome
Affected individuals can have vasculitis, thrombotic microangiopathy, antiphospholipid syndrome, or, more commonly, a systemic disease such as atherosclerosis, cholesterol emboli, hypertension, sickle cell anemia, and autoimmunity
83
The most common infectious causes of glomerulonephritis throughout the world (2)
subacute bacterial endocarditis
malaria and schistosomiasis
closely followed by HIV and chronic hepatitis B and C
84
The kidney biopsy uses this stain to assess cellularity and architecture
hematoxylin and eosin (H&E)
85
The kidney biopsy uses this stain to stain carbohydrate moieties in the membranes of the glomerular tuft and tubules
periodic acid–Schiff (PAS)
86
The kidney biopsy uses this stain to enhance basement mem- brane structure
Jones-methenamine silver
87
The kidney biopsy uses this stain for amyloid deposits
Congo red
88
The kidney biopsy uses this stain to identify collagen deposition and assess the degree of glomerulo- sclerosis and interstitial fibrosis
Masson’s trichrome
89
Ideal number of glomeruli that are reviewed individually for discrete lesions in kidney biopsy
20
90
How many percent of glomeruli is involved in focal lesion? diffuse lesion?
<50%
| >50%
91
When cells in the capillary tuft proliferate, it is called
endocapillary
92
when cellular proliferation extends into Bowman’s space
extracapillary
93
formed when epithelial podocytes attach to Bowman’s capsule in the setting of glomerular injury
Synechiae
94
develop when fibrocellular/ fibrin collections fill all or part of Bowman’s space
crescents
95
acellular, amorphous accumulations of proteinaceous material throughout the tuft with loss of functional capillaries and normal mesangium in the glomerulus
sclerotic glomer- uli
96
Histopathologic finding that is an ominous sign of irreversibility and progression to renal failure
Interstitial fibrosis
97
prototypical for acute endocapillary proliferative glomerulonephritis
Poststreptococcal glomerulonephritis
98
PSGN is common in what ages
2-14 years old
99
Infection prior to development of PSGN and the cause
Skin and throat infections with particular M types of streptococci (nephritogenic strains) antedate glomerular disease
100
Post- streptococcal glomerulonephritis due to impetigo develops ______ after skin infection and ________ after streptococcal pharyngitis
2–6 weeks
| 1–3 weeks
101
On renal biopsy, this condition demonstrates hypercellularity of mesangial and endothelial cells, glomerular infiltrates of polymorphonuclear leukocytes, granular subendothelial immune deposits of IgG, IgM, C3, C4, and C5–9, and subepithelial deposits (which appear as “humps”)
poststreptococcal glomerulonephritis
102
Acute nephritic syndrome with hematuria, pyuria, red blood cell casts, edema, hypertension, and oliguric renal failure, and manifests as headache, malaise, anorexia, and flank pain
PSGN
103
Increased titers of these antibodies can help confirm the diagnosis of PSGN (3)
ASO (30%)
anti-DNAse (70%)
antihyaluronidase antibodies (40%)
104
Kidneys have subcapsular hemorrhages with a “flea-bitten” appearance, and microscopy on renal biopsy reveals focal proliferation around foci of necrosis associated with abundant mesangial, subendothelial, and subepithelial immune deposits of IgG, IgM, and C3
Subacute bacterial endocarditis
105
Predominant organism causing glomerulonephritis in subacute bacterial endocarditis
Staphylococcus
106
The most common clinical sign of renal disease in lupus nephritis
proteinuria
107
Antibodies that correlate best with the presence of renal disease in lupus
Anti-dsDNA
108
the only reliable method of identifying the morphologic variants of lupus nephritis
renal biopsy
109
Class of lupus nephritis with minimal mesangial
Class I
110
Class of lupus nephritis with normal histology with mesangial deposits
Class I
111
Class of lupus nephritis with mesangial proliferation
Class II
112
Class of lupus nephritis with mesangial hypercellularity with expansion of the mesangial matrix
Class II
113
Class of lupus nephritis with focal nephritis
Class III
114
Class of lupus nephritis with focal endocapillary ± extracapillary proliferation with focal subendothelial immune deposits and mild mesangial expansion
Class III
115
Class of lupus nephritis with diffuse nephritis
Class IV
116
Class of lupus nephritis with diffuse endocapillary ± extracapillary proliferation with diffuse subendothelial immune deposits and mesangial alterations
Class IV
117
Class of lupus nephritis with membranous nephritis
Class V
118
Class of lupus nephritis with thickened basement membranes with diffuse subepithelial immune deposits; may occur with class III or IV lesions and is sometimes called mixed membranous and proliferative nephritis
Class V
119
Class of lupus nephritis with sclerotic nephritis
Class VI
120
Class of lupus nephritis with global sclerosis of nearly all glomerular capillaries
Class VI
121
Class of lupus nephritis that describes focal lesions with proliferation or scarring, often involving only a segment of the glomerulus
Class III
122
Class of lupus nephritis that have the most varied course
Class III
123
Class of lupus nephritis that describes global, diffuse proliferative lesions involving the vast majority of glomeruli
Class IV
124
Without treatment, this aggressive lesion has the worst renal prognosis among the classes of lupus nephritis
Class IV
125
Class of lupus nephritis that describes subepithelial immune deposits producing a membranous pattern
Class V
126
Patients with this class of lupus nephritis are predisposed to renal-vein thrombosis and other thrombotic complications
Class V
127
Lupus patients with this class of lupus nephritis have >90% sclerotic glomeruli and ESRD with interstitial fibrosis
Class VI
128
When do you do renal transplantation in renal failure from lupus?
Usually performed after ~6 months of inactive disease
129
When anti-GBM disease present with lung hemorrhage and glomerulonephritis, they have a pulmonary-renal syndrome called
Goodpasture’s syndrome
130
The target epitopes for the anti-GBM disease lie in the quaternary structure of
α3 NC1 domain of collagen IV
131
T or F: In Goodpasture's syndrome, hemoptysis is largely confined to smokers
True
132
T or F: In Goodpasture's sydrome, those who present with lung hemorrhage as a group do better than older populations who have prolonged, asymptomatic renal injury
True
presentation with oliguria is often associated with a particularly bad outcome
133
Renal biopsies typically show focal or segmental necrosis that later, with aggressive destruction of the capillaries by cellular proliferation, leads to crescent formation in Bowman’s space
Goodpasture's syndrome / anti-GBM disease
134
Prognosis at presentation of anti-GBM disease is worse if (4)
- >50% crescents on renal biopsy with advanced fibrosis
- serum creatinine is >5–6 mg/dL
- oliguria is present
- need for acute dialysis
135
In the management of Goodpasture's syndrome, aside from dialysis, patients with advanced renal failure who present with hemoptysis should still be treated for their lung hemorrhage with
Plasmapheresis
can be life-saving
8-10 treatments
accompanied by oral prednisone and cyclophosphamide in the first 2 weeks
136
It is classically characterized by episodic hematuria associated with the deposition of IgA in the mesangium
IgA nephropathy
137
Henoch-Schönlein purpura is distinguished clinically from IgA nephropathy by (4)
- prominent systemic symptoms
- a younger age (<20 years old)
- preceding infection
- abdominal complaints.
138
An immune complex–mediated glomerulonephritis defined by the presence of diffuse mesangial Ig deposits often associated with mesangial hypercellularity
IgA nephropathy
139
In IgA nephropathy, IgA deposited in the mesangium is typically polymeric and of what subclass
IgA1
140
Recurrent episodes of macroscopic hematuria during or immediately follow- ing an upper respiratory infection often accompanied by proteinuria or persistent asymptomatic microscopic hematuria
IgA nephropathy
141
T or F: IgA nephropathy is a benign disease for the majority of patients
True
142
Renal failure seen in how many percent of patients with IgA nephropathy over 20–25 years
25–30%
143
Treatment of IgA nephropathy
ACE inhibitors
steroid and immunosuppressive therapy have conflicting results in the studies
Tonsillectomy and fish oil have also been suggested in small studies to benefit select patients
144
The 2 types of antibodies in ANCA small-vessel vasculitis
anti-proteinase 3 (PR3)
| anti-myeloperoxidase (MPO)
145
Vasculitis syndromes that are ANCA-positive and have a pauci-immune glomerulonephritis with few immune complexes in small vessels and glomerular capillaries (4)
Granulomatosis with polyangiitis
Microscopic polyangiitis
Churg-Strauss syndrome
Renal-limited vasculitis
146
Induction therapy of ANCA small-vessel vasculitis (3)
Glucocorticoids
| Rituximab or cyclophosphamide
147
Recommended treatment in rapidly progressive renal failure or pulmonary hemorrhage in ANCA small-vessel vasculitis
Plasmapheresis
148
Patients with this disease classically present with fever, purulent rhinorrhea, nasal ulcers, sinus pain, polyarthralgias/arthritis, cough, hemoptysis, shortness of breath, microscopic hematuria, and 0.5–1 g/24 h of proteinuria; occasionally there may be cutaneous purpura and mononeuritis multiplex
Granulomatosis with Polyangiitis
149
Biopsy of involved tissue will show a small-vessel vasculitis and adjacent noncaseating granulomas.
Granulomatosis with Polyangiitis
150
Renal biopsies during active disease demonstrate segmental necrotizing glomerulonephritis without immune deposits and have been classified as focal, mixed, crescentic or sclerotic
Granulomatosis with Polyangiitis
151
Small-vessel vasculitis that is more common in patients exposed to silica dust and those with α1-antitrypsin deficiency, which is an inhibitor of PR3
Granulomatosis with Polyangiitis
152
Αmong the ANCA small-vessel vasculitis, relapse is most common in
Granulomatosis with Polyangiitis
153
Clinically, these patients look somewhat similar to those with granulomatosis with polyangiitis, except they rarely have significant lung disease or destructive sinusitis
Microscopic Polyangiitis
154
Small-vessel vasculitis is associated with peripheral eosinophilia, cutaneous purpura, mononeuritis, asthma, and allergic rhinitis, often accompanied by hypergammaglobulinemia, elevated levels of serum IgE, or the presence of rheumatoid factor
Churg-Strauss Syndrome
155
Lung inflammation, including fleeting cough and pulmonary infiltrates, often precedes the systemic manifestations of this small-vessel vasculitis by years; lung manifestations are rarely absent
Churg-Strauss Syndrome
156
Small-vessel vasculitis and focal segmental necrotizing glomerulonephritis can be seen on renal biopsy, usually absent eosinophils or granulomas
Churg-Strauss Syndrome
157
defined morphologically with dense deposits forming ribbons in the GBM
dense deposit disease
158
sometimes called mesangiocapillary glomerulonephritis or lobar glomerulonephritis
membranoproliferative glomerulonephritis
159
It is an immune-mediated glomerulonephritis characterized by thickening of the GBM with mesangioproliferative changes; 70% of patients have hypocomplementemia
membranoproliferative glomerulonephritis
160
MPGN that is commonly associated with persistent hepatitis C infections, autoimmune diseases like lupus or cryoglobulinemia, or neoplastic diseases
Type I
161
The most proliferative of the three types of MPGN
Type I
162
Shows mesangial proliferation with lobular segmentation on renal biopsy and mesangial interposition between the capillary basement membrane and endothelial cells, producing a double contour sometimes called tram-tracking
Type I MPGN
163
Low serum C3 and a dense thickening of the GBM containing ribbons of dense deposits and C3
type II MPGN, dense deposit disease
164
Classically, the glomerular tuft has a lobular appearance; intramesangial deposits are rarely present and subendothelial deposits are generally absent. What type of MPGN?
Type II
165
MPGN that has the least proliferation and is often focal; mesangial interposition is rare, and subepithelial deposits can occur along widened segments of the GBM that appear laminated and disrupted.
Type III
166
MPGN that is secondary to glomerular deposition of circulating immune complexes or their in situ formation
Type I
167
____ percent of patients with MPGN develop ESRD 10 years after diagnosis, and ____ percent have renal insufficiency after 20 years
50%
| 90%
168
Characterized by expansion of the mesangium, sometimes associated with mesangial hypercellularity; thin, single contoured capillary walls; and mesangial immune deposits.
Mesangioproliferative glomerulonephritis
169
Mesangioproliferative disease may be seen in what conditions (4)
IgA nephropathy
Plasmodium falciparum malaria
Resolving postinfectious glomerulonephritis
Class II nephritis from lupus
170
Nephrotic syndrome classically presents with (6)
```
Heavy proteinuria
Minimal hematuria
Hypoalbuminemia
Hypercholesterolemia
Edema
Hypertension
```
171
Minimal change disease is sometimes known as
nil lesion
172
Renal biopsy shows no obvious glomerular lesion by light microscopy and is negative for deposits by immunofluorescent microscopy, or occasionally shows small amounts of IgM in the mesangium
Minimal change disease
173
Electron microscopy demonstrates an effacement of the foot processes supporting the epithelial podocytes with weakening of slit-pore membranes.
Minimal change disease
174
Presents clinically with the abrupt onset of edema and nephrotic syndrome accompanied by acellular urinary sediment. Average urine protein excretion reported in 24 h is 10 g with severe hypoalbuminemia.
Minimal change disease
175
In minimal change disease, adults are not considered steroid-resistant until after ______ of therapy
4 months
176
First-line therapy for minimal change disease
Prednisone
177
Refers to a pattern of renal injury characterized by segmental glomerular scars that involve some but not all glomeruli
FOCAL SEGMENTAL GLOMERULOSCLEROSIS
178
the clinical findings of FSGS largely manifest as
proteinuria
179
The pathologic changes of FSGS are most prominent in glomeruli located at the
corticomedullary junction
so if the renal biopsy specimen is from superficial tissue, the lesions can be missed, which sometimes leads to a misdiagnosis of MCD
180
T or F: Steroids and other immunosuppressive agents may be used in the treatment of both primary and secondary FSGS
False. There is no role for steroids or other immunosuppressive agents in secondary FSGS
181
Accounts for ~20% of cases of nephrotic syndrome in adults, with a peak incidence between the ages of 30 and 50 years and a male to female ratio of 2:1
Membranous glomerulonephritis
182
Most common cause of nephrotic syndrome in the elderly
Membranous glomerulonephritis
rare in children
183
Uniform thickening of the basement membrane along the peripheral capillary loops is seen by light microscopy on renal biopsy
Membranous glomerulonephritis
184
Immunofluorescence demonstrates diffuse granular deposits of IgG and C3, and electron microscopy typically reveals electron-dense subepithelial deposits
Membranous glomerulonephritis
185
T or F: The stage of glomerular disease in membranous glomerulonephritis is predictive of its progression
False. degree of tubular atrophy or interstitial fibrosis is more predictive of progression than is the stage of glomerular disease
186
Factors that are associated with worse prognosis in membranous glomerulonephritis (4)
Male gender
older age
hypertension
persistence of proteinuria
187
Nephrotic syndrome that has the highest reported incidences of renal vein thrombosis, pulmonary embolism, and deep-vein thrombosis
Membranous glomerulonephritis
188
The single most common cause of chronic renal failure
Diabetic nephropathy
189
A sensitive indicator for the presence of diabetes but correlates poorly with the presence or absence of clinically significant nephropathy
Thickening of the GBM
190
Some DM nephropathy patients develop eosinophilic, PAS+ nodules called
nodular glomerulosclerosis or Kimmelstiel-Wilson nodules
191
Microalbuminuria appears ____ years after the onset of diabetes
5–10
192
Feature of DM nephropathy that is a potent risk factor for cardiovascular events and death in patients with type 2 diabetes
Microalbuminuria
193
The absence of this condition in type 1 patients with proteinuria should prompt consideration of a diagnosis other than diabetic nephropathy
retinopathy
90% of patients with type 1 diabetes and nephropathy have diabetic retinopathy
194
It usually takes ____ years for DM nephropathy to reach ESRD
10–20
195
Specific pattern of renal injury caused by nephrotoxic light chain that causes renal failure but not heavy proteinuria or amyloidosis
cast nephropathy
196
Specific pattern of renal injury caused by nephrotoxic light chain that produces nephrotic syndrome with renal failure
light chain deposition disease
197
Result of primary fibrillar deposits of immunoglobulin light chains known as amyloid L (AL), or secondary to fibrillar deposits of serum amyloid A (AA) protein fragments
renal amyloidosis
198
T or F. Primary and secondary amyloidosis may both present as nephrotic syndrom
True
199
The treatment for primary amyloidosis that can delay the course of renal amyloidosis in about 30% of patients
melphalan
also autologous hematopoietic stem cell transplantation
200
Characterized by glomerular accumulation of nonbranching randomly arranged fibrils.
Fibrillary-Immunotactoid Glomerulopathy
201
Fibrillar/microtubular deposits of oligoclonal or oligotypic immunoglobulins and complement appear in the mesangium and along the glomerular capillary wall, and stain negative to Congo red
Fibrillary-Immunotactoid Glomerulopathy
202
An X-linked inborn error of globotriaosylceramide metabolism secondary to deficient lysosomal a-galactosidase A activity, resulting in excessive intracellular storage of globotriaosylceramide
Fabry’s disease
203
Presents in childhood in males with acroparesthesias, angiokeratoma, and hypohidrosis
Fabry’s disease
204
Renal biopsy reveals enlarged glomerular visceral epithelial cells packed with small clear vacuoles containing globotriaosylceramide; vacuoles may also be found in parietal and tubular epithelia
Fabry’s disease
205
Vacuoles of electron-dense materials in parallel arrays (zebra bodies) are seen on electron microscopy
Fabry’s disease
206
Fabry's disease renal biopsy reveal features of
FOCAL SEGMENTAL GLOMERULOSCLEROSIS
207
Urinalysis may reveal oval fat bodies and birefringent glycolipid globules under polarized light (Maltese cross)
Fabry’s disease
208
Empiric and temporizing treatment for pulmonary-renal syndrome until results of testing are available (2)
plasmapheresis and methylprednisolone
209
Classically, patients with this condition develop hematuria, thinning and splitting of the GBMs, mild proteinuria (<1–2 g/24 h), which appears late in the course, followed by chronic glomerulosclerosis leading to renal failure in association with sensorineural deafness.
Alport's syndrome
210
Approximately 85% of patients with Alport’s syndrome have an X-linked inheritance of mutations in the
α5 (IV) collagen chain on chromosome Xq22–24
15% of patients have autosomal recessive disease of the α3(IV) or α4(IV) chains on chromosome 2q35–37
211
Τypically have thin basement membranes on renal biopsy, which thicken over time into multilamellations surrounding lucent areas that often contain granules of varying density—the so-called split basement membrane
Alport's syndrome
212
Characterized by persistent or recurrent hematuria and is not typically associated with proteinuria, hypertension, or loss of renal function or extrarenal disease
Thin basement membrane disease (TBMD)
213
Thin basement membrane disease (TBMD) is also known as
benign familial hematuria
it usually presents in childhood in multiple family members
214
Thin basement membrane disease (TBMD) is caused by a defect in what collagen
Collagen type IV
215
Develop iliac horns on the pelvis and dysplasia of the dorsal limbs involving the patella, elbows, and nails, variably associated with neural-sensory hearing impairment, glaucoma, and abnormalities of the GBM and podocytes, leading to hematuria, proteinuria, and FSGS
nail-patella syndrome
216
The syndrome is autosomal dominant, with haploinsufficiency for the LIM homeodomain transcription factor LMX1B
nail-patella syndrome
217
On renal biopsy there is focal sclerosing glomerulonephritis with specific lucent damage to the lamina densa of the GBM, an increase in collagen III fibrils along glomerular capillaries and in the mesangium, and damage to the slit-pore membrane, producing heavy proteinuria not unlike that seen in congenital nephrotic syndrome
nail-patella syndrome
218
Approximately ___ of glomeruli are normally sclerotic by age 40, rising to ___ by age 60 and ___ by age 80
10%
20%
30%
219
The lesion associated with HIV-associated nephropathy is
FSGS
220
HIV patients with FSGS typically present with nephrotic-range proteinuria and hypoalbuminemia, but unlike patients with other etiologies for nephrotic syndrome, they do not commonly have (3)
hypertension
edema
hyperlipidemia.
221
The lesion associated with syphilis-associated nephropathy is
membranous glomerulonephritis
222
Schistosoma that is most commonly associated with clinical renal disease
Schistosoma mansoni
223
Most common kidney stone
Calcium oxalate
224
2nd most common kidney stone
Calcium phosphate
225
T or F. A UTI in the setting of an obstructing stone requires urgent intervention to reestablish drainage
True. A UTI in the setting of an obstructing stone is a urologic emergency
226
The point at which the concentration product exceeds the solubility product
Supersaturation
227
The most clinically important inhibitor of calcium-containing stones
Urine citrate
228
The majority of calcium oxalate stones grow on calcium phosphate at the tip of the renal papilla forming
Randall’s plaque
229
Dietary factors that are associated with an increased risk of nephrolithiasis (6)
* Animal protein
* Oxalate
* Sodium
* Sucrose
* Fructose
230
Dietary factors associated with a lower risk of nephrolithiasis (4)
* Calcium
* Potassium
* Magnesium
* Phytate
231
T or F. Higher dietary calcium intake is related to a higher risk of stone formation
False. Lower risk. May be due to a reduction in intestinal absorption of dietary oxalate that results in lower urine oxalate
232
T or F. Supplemental calcium may increase the risk of kidney stone formation
True. May be due to the timing of supplemental calcium intake or to higher total calcium consumption leading to higher urinary calcium excretion
233
T or F. Dietary oxalate is a strong risk factor for kidney stone formation.
False Dietary oxalate is a weak risk factor for stone formation, BUT urinary oxalate is a strong risk factor
234
Vitamin C supplements will increase risk of what type of kidney stone?
Calcium oxalate
235
Urine output which doubly increase the risk of stone formation
<1L/day
236
T or F. Higher urine citrate excretion increases the risk of stone formation
False. Lower urine citrate
237
Urine pH that promotes uric acid stones formation
≤ 5.5
238
Urine pH that promotes calcium phosphate stone formation
≥6.5
239
Formation of this stone is not influenced by urine pH
Calcium oxalate stones
240
2 most common monogenic disorders that lead to stone formation
Primary hyperoxaluria
| Cystinuria
241
Sudden onset of unilateral flank pain then intensity of pain increase rapidly often accompanied by nausea and vomiting that radiate to ipsilateral testicle in men or ipsilateral labium in women
Renal colic
242
2 most common presentation of acute stone event
* Renal colic
| * Painless gross hematuria
243
Nephrolithiasis mimic acute cholecystitis if stone is at the
right ureteral pelvic junction
244
Nephrolithiasis mimic acute appendicitis if stone is at the
blocks the ureter as it crosses over the right pelvic brim
245
Nephrolithiasis mimic acute diverticulitis if stone is at the
left pelvic brim
246
T or F: Absence of hematuria exclude the diagnosis of stone
False
247
Preferred imaging and highly sensitive for nephrolitiasis
Helical computed tomography
248
Drugs that may increase the rate of spontaneous kidney stone passage
Alpha blocker
249
Indications for urologic intervention (3)
```
• Evidence of UTI
• Low probability of spontaneous stone passage
o Stone measuring ≥6 mm
o Anatomic abnormality
• Intractable pain
```
250
The least invasive option for nephrolithiasis
Extracorporeal shockwave lithotripsy (ESWL)
251
Uses shock waves generated outside the kidney body to fragment the stone
Extracorporeal shockwave lithotripsy (ESWL)
252
Serve as the cornerstone on which therapeutic recommendations for nephrolithisis are based
24-h urine collection
253
The “gold standard” diagnostic test for nephrolithiasis
Helical CT without contrast
254
For all kidney stone types, consistently _____ reduces the likelihood of crystal formation
diluted urine
Urine volume should be at least 2 L/d
255
Antihypertensive drugs that can lower urine Ca in doses higher than those used to treat HPN
Thiazide diuretic (Most commonly chlorthalidone)
256
The only strategy that reduces endogenous oxalate production
Avoiding high-dose Vit C supplements
257
Supplemental alkali that may be given to kidney stone patients (2)
potassium citrate or bicarbonate
258
2 main risk factors for uric acid stone formation
* Persistently low urine pH
| * Higher uric acid excretion
259
The focus for cystine kidney stone prevention
Increasing cystine solubility
260
Medication that covalently binds to cystine (2)
Tiopronin
| Penicillamine
261
Preferred medication that covalently binds to cystine
Tiopronin
262
AKA infection stones
Struvite
263
AKA triple-phosphate stones
Struvite
264
Struvite forms only when the upper urinary tract is infected with
urease-producing bacteria
265
3 bacteria that most commonly cause struvite
* Proteus mirabilis
* Klebsiella pneumoniae
* Providencia species
266
Urease produced by urease-producing bacteria hydrolyzes urea and may elevate the urine pH to
>8.0
267
Struvite stones may grow quickly and fill the renal pelvis causing
staghorn calculi
268
2 management for staghorn calculi
Complete removal
| Acetohydroxamic acid
269
Imaging that is often used for long-term follow-up of nephrolithiasis
Plain abdominal radiography (KUB)
270
The first tolerable and effective agent for the treatment of UTI
Nitrofurantoin
271
The most common manifestation of UTI
Acute cystitis
272
Refers to acute cystitis or pyelonephritis in nonpregnant outpatient women without anatomic abnormalities or instrumentation of the urinary tract
Uncomplicated UTI
273
Prevalence of UTI during the neonatal period according to sex
male>female
274
Prevalence of UTI after 50 years of age according to sex
male=female
275
Prevalence of UTI between 1-50 years of age
female > male
276
How many percent of women in the general population acquire at least one UTI during their lifetime
50–80%
277
Independent risk factors for acute cystitis (3):
* Recent use of a diaphragm with spermicide
* Frequent sexual intercourse
* History of UTI
278
Risk factors of UTI in healthy postmenopausal women (3):
* Sexual activity
* Diabetes mellitus
* Incontinence
279
Factors independently associated with pyelonephritis in young healthy women (6)
* Frequent sexual intercourse
* New sexual partner
* A UTI in the previous 12 months
* Maternal history of UTI
* Diabetes
* Incontinence
280
Independent risk factors of UTI recurrence in premenopausal women (5)
* Frequent sexual intercourse
* Use of spermicide
* New sexual partner
* First UTI before 15 years of age
* Maternal history of UTI
281
Major risk factors of recurrent UTI in postmenopausal women (2)
* History of premenopausal UTI
| * Anatomic factors affecting bladder emptying
282
Most common cause of UTI in men
urinary obstruction secondary to prostatic hypertrophy
283
UTI due to lack of circumcision is due to what organism
Escherichia coli
284
Most common organisms causing UTI
enteric gram-negative rods (most common: E. coli)
285
Most common route of infection in UTI
Ascending from the urethra to the bladder
286
Hematogenous route is present in how many % of documented UTIs
<2%
287
Hematogenous route of UTI is most commonly seen in these 3 organisms
* Salmonella
* S. aureus
* Candida
288
The critical initial step in the pathogenesis of UTI among women
Colonization of the vaginal introitus and periurethral area with organisms from the intestinal flora
289
Inhibition of ureteral peristalsis and decreased ureteral tone leads to this condition which is important in the pathogenesis of pyelonephritis in pregnant women
Vesicoureteral reflux
290
The primary reason why UTI is predominantly an illness of young women rather than of young men
Distance of the urethra from the anus
291
Virulence factor of E. coli that mediate binding to specific receptors on the surface of uroepithelial cells
Surface adhesins
292
Virulence factor of E. coli described as hair-like protein structures that interact with a specific receptor on renal epithelial cells
P fimbriae
293
Virulence factor of E. coli that is important in the pathogenesis of pyelonephritis and subsequent bloodstream invasion from the kidney
P fimbriae
294
Play a key role in initiating E. coli bladder infection that mediate binding to mannose on the luminal surface of bladder uroepithelial cells
Type 1 pilus
295
The most important issue to be addressed when a UTI is suspected is the
characterization of the clinical syndrome
296
An indication that the upper urinary tract is involved in UTI
Unilateral back or flank pain
297
An indication of invasive infection of either the kidney or the prostate
Fever
298
Severe pyelonephritis is characterized by these clinical manifestations (5)
* High fever
* Rigors
* Nausea
* Vomiting
* Flank and/or loin pain
299
the main feature distinguishing cystitis from pyelonephritis
Fever
300
Fever in pyelonephritis typically exhibits this pattern
high spiking “picket-fence” pattern
301
Complication of pyelonephritis seen in patients with diabetes that present as obstructive uropathy when sloughed papillae obstruct the ureter
Acute papillary necrosis
302
A particularly severe form of the pyelonephritis that is associated with the production of gas in renal and perinephric tissues
Emphysematous pyelonephritis
303
Emphysematous pyelonephritis occurs almost exclusively in what group of patients
Diabetic patients
304
Occurs when chronic urinary obstruction (often by staghorn calculi) together with chronic infection causes this suppurative destruction of renal tissue
Xanthogranulomatous pyelonephritis
305
Causes yellow coloration of kidney with infiltration by lipid-laden macrophages
Xanthogranulomatous pyelonephritis
306
When to you suspect the abscess as complication of pyelonephritis?
when a patient has continued fever and/or bacteremia despite antibacterial therapy
307
Presents as fever, chills, dysuria, frequency, and pain in the pelvic or perineal area in men
Acute bacterial prostatitis
308
In women presenting with at least one symptom of UTI (dysuria, frequency, hematuria, or back pain) and without complicating factors, the probability of acute cystitis or pyelonephritis is
50%
309
If vaginal discharge and complicating factors are absent and risk factors for UTI are present, then the probability of UTI is close to___, and no laboratory evaluation is needed
90%
310
Combination of dysuria and urinary frequency (in the absence of vaginal discharge) increases the probability of UTI to
96%
311
Laboratory tests that provide point-of-care information for UTI
Urine dipstick test
| Urinalysis
312
Only members of the family ______ convert nitrate to nitrite that can be detected in urine dipstick test
Enterobacteriaceae
313
Enough ______ must accumulate in the urine to reach the threshold of detection
Nitrite
314
Diagnostic gold standard for UTI
Urine culture
315
In symptomatic women, colony count threshold of ______ can be diagnostic of UTI
≥10^2 bacteria/mL
316
T or F. Men with febrile UTI for the first time should have imaging performed
True
CT or ultrasound
317
Microbiologic criterion for asymptomatic bacteriuria
≥10^5 bacterial CFU/mL of urine
318
The predominant multilocus sequence type found worldwide as the cause of multidrug-resistant UTI
E. coli ST131
319
previously recommended as first-line treatment for acute cystitis
TMP-SMX
320
Organisms that are intrinsically resistant to this nitrofurantoin (5)
* Proteus
* Pseudomonas
* Serratia
* Enterobacter
* Yeasts
321
T or F. Nitrofurantoin may be used in the treatment of pyelonephritis
False
322
Most fluoroquinolones are highly effective as short-course therapy for cystitis, except
moxifloxacin – may not reach adequate urinary levels
323
Rare but potentially serious adverse effects of fluoroquinolones in >60 years of age
Increased risk of Achilles tendon rupture
324
Widely used urinary analgesics but can cause significant nausea
Phenazopyridine
325
First-line therapy for acute uncomplicated pyelonephritis
Fluoroquinolones
Oral ciprofloxacin (500 mg twice daily, with or without an initial IV 400-mg dose)
326
UTI medications that are relatively safe in early pregnancy (3)
* Nitrofurantoin
* Ampicillin
* Cephalosporins
327
2 drugs of choice for UTI in pregnancy
Ampicillin
| Cephalosporins
328
Standard of care for overt pyelonephritis in pregnancy
parenteral β-lactam therapy with or without aminoglycosides
329
For acute bacterial prostatitis, what is the recommended treatment and duration?
fluoroquinolone or TMP-SMX
| 2-4 weeks
330
For chronic bacterial prostatitis, what is the recommended treatment and duration?
fluoroquinolone or TMP-SMX
| 4-6 weeks
331
For recurrent bacterial prostatitis, what is the recommended treatment and duration?
fluoroquinolone or TMP-SMX
| 12 weeks
332
Treatment for xanthogranulomatous pyelonephritis
nephrectomy
333
Initial treatment for emphysematous pyelonephritis
Percutaneous drainage
Elective nephrectomy on follow-up
334
Treatment of asymptomatic bacteriuria is given only in (4)
* Pregnant women
* Persons undergoing urologic surgery
* Neutropenic patients
* Renal transplant recipients
335
Accepted threshold for bacteriuria to meet the definition of CAUTI
≥10^3 CFU/mL of urine
336
Risk factors for candiduria (3)
* ICU patients
* Those taking broad-spectrum antimicrobial drugs
* Those with underlying diabetes mellitus
337
Therapy for candiduria is recommended for patients who (5)
* Have symptomatic cystitis or pyelonephritis
* Neutropenia
* Undergoing urologic manipulation
* Clinically unstable
* Low-birth-weight infants
(At high risk for disseminated disease)
338
First-line regimen for Candida infections of the urinary tract
Fluconazole – (200–400 mg/d for 7–14 days)
339
Three prophylactic strategies for recurrent UTI in women
Continuous therapy (6 months)
Postcoital therapy
Patient-initiated therapy
340
Most common cause of bacterial cystitis
Escherichia coli
341
An unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder, associated with lower urinary tract symptoms of more than 6 weeks’ duration, in the absence of infection or other identifiable causes
INTERSTITIAL CYSTITIS/BLADDER PAIN SYNDROME
342
Ulcer in the bladder
Hunner lesion
343
How many % of interstitial cystitis/bladder pain syndrome has Hunner lesion?
≤10%
344
Most common site of interstitial cystitis/bladder pain syndrome
Suprapubic (80% of women) – most severe pain
345
In 95% of patients, bladder filling exacerbates the pain and/or bladder emptying relieves it
interstitial cystitis/bladder pain syndrome
346
Functional somatic syndromes that can accompany IC/BPS (3):
a. Gynecologic chronic pelvic pain
b. Irritable bowel syndrome
c. Fibromyalgia
347
Oral medications for interstitial cystitis/bladder pain syndrome:
a. NSAIDs
b. Amitriptyline
c. Pentosan polysulfate
348
Treatment of hunner lesion in interstitial cystitis/bladder pain syndrome:
Fulguration (solutions containing lidocaine, hyaluronic acid, or dimethyl sulfoxide can be instilled into the bladder)
349
Normal points of narrowing are common sites of urinary tract obstruction (4)
* Ureteropelvic junction
* Ureterovesical junction
* Bladder neck
* Urethral meatus
350
Most common cause of utinary tract obstruction in childhood
Congenital malformations
* Narrowing of the ureteropelvic junction
* Abnormal insertion of the ureter into the bladder
351
Most common cause of bilateral hydronephrosis in boys
Posterior urethral valves
352
Most common causes of urinary tract obstruction in adults (3)
* Pelvic tumors
* Calculi
* Urethral stricture
353
Symptom that most commonly leads to medical attention in urinary tract obstruction
Flank pain
354
Flank pain that occurs only with micturition is pathognomonic of
vesicoureteral reflux
355
Partial bilateral UTO often results in (3)
1. Acquired distal renal tubular acidosis
2. Hyperkalemia
3. Renal salt wasting
356
Struvite is made of what mineral/compound?
Magnesium ammonium phosphate
357
Used for the diagnosis of vesicoureteral reflux and bladder neck and urethral obstructions
Voiding cystourethrography
358
T or F. Even in obstruction without infection, immediate surgical intervention must be done to avoid complications
False. When infection is not present, surgery is often delayed until acid-base, fluid, and electrolyte status is restored
359
Functional obstruction secondary to neurogenic bladder may be decreased with the combination of (2)
frequent voiding and cholinergic drugs
360
Duration of obstruction wherein kidney function recovery is unlikely
After 8 weeks of obstruction
361
Imaging performed after a prolonged period of decompression and to predict the reversibility of renal dysfunction
Renal radionuclide scan
362
Total body water is composed of ____ intracellular, and ____ extracellular
2/3
| 1/3
363
Extracellular fluid is composed of ___ plasma, and ___ interstitial edema
¼
| 3/4
364
Fluid is returned from the interstitial space into the vascular system through the
Lymphatic system
365
A parameter that represents the filling of the arterial tree and that effectively perfuses the tissues
Effective arterial blood volume
366
Decrease effective arterial blood volume will _____ renin release
Increase
Decreased effective arterial blood volume -> diminished renal blood flow -> translated by the renal juxtaglomerular cells (specialized myoepithelial cells surrounding the afferent arteriole) into a signal -> increased renin release
367
Specialized myoepithelial cells surrounding the afferent arteriole that detects diminished renal blood flow
juxtaglomerular cells
368
Angiotensinogen is synthesized in the
Liver
369
Angiotensin II has generalized vasoconstrictor properties, particularly on the
renal efferent arterioles
370
Aldosterone acts on the _____ by _____
Collecting tubule
Enhances sodium reabsorption and potassium excretion
371
RAAS effect on Na and water
Retention
372
Arginine vasopressin is secreted by
posterior pituitary gland
373
Arginine vasopressin secretion occurs in response to
increased intracellular osmolar concentration
374
AVP stimulates what receptors
V2 receptors
375
Site of action of AVP in the kidney
distal tubules and collecting ducts
376
Action of AVP on the kidney
increases the reabsorption of free water
377
Potent peptide vasoconstrictor released by endothelial cells
Endothelin-1
Elevated in patients with severe heart failure
378
Stimulates release of ANP
Atrial distention
379
ANP and BNP are stored in these sites respectively
Atrial myocytes
| Ventricular myocytes
380
Stimulates release of BNP
When ventricular diastolic pressure rises
381
Effects of ANP and BNP on Na and water
Excretion of sodium and water
Augmenting glomerular filtration rate
Inhibiting sodium reabsorption in the proximal tubule
Inhibiting release of renin and aldosterone
382
Primary alteration in the nephrotic syndrome causing edema
diminished colloid oncotic pressure
383
Causes of edema in hepatic cirrhosis (4)
1. Hepatic venous outflow obstruction leading to increase splanchnic blood volume
2. Hepatic lymph formation
3. Hypoalbuminemia
4. Peripheral artery vasodilation
384
Multiple peripheral arteriovenous fistulae result in reduced effective systemic perfusion and effective arterial blood volume and leading enhancing edema formation in this condition
Beriberi heart disease
385
Edema develops or becomes intensified when famished subjects are first provided with an adequate die
Refeeding edema
