Week 7 (Exam 3) Flashcards
(249 cards)
1
Q
Pathogenesis of Primary Membranous Glomerulo-Nephropathy
A
In-situ immune complex formations involving Phospholipase A2 Receptor on Podocytes
Involves in MAC and IgG4
Usually presents as Nephrotic Syndrome
2
Q
Acute Proliferative Glomerulonephritis presentation in children
A
Malaise, fever, nausea, oliguria and hematuria 1-2 weeks after recovery from sore throat
Dysmorphic red cells or abc casts, mild proteinuria, periorbital edema and mild-moderate HTN
3
Q
Whats the etiological difference between Cystitis Cystic and Cystitis Glandulars (CC and CG)?
A
Utothelium metaplasia into buds (nests of von Brunn), then invades the lamina propria. In CC it then differentiates into cystic deposits. In GC, it differentiates into intestinal columnar mucin-secreting glands
4
Q
Clinical presentation of Renal Cell Carcinoma
A
Classic Triad: Hematuria, Costovertebral pain, palpable flank mass
Clear cells are from Glycolgen and Lipid accumulation
5
Q
Main Renal Loss mechanisms of hypokalemia
A
Diuretics Increased Mineralocorticoid (aldosterone, ENaC) Hypomagnesemia Increased Distal Delivery of Na and H2O RTA type 1 or 2 Intrinsic renal defect
6
Q
Clinical presentation of WAGR
A
Genitourinary malformation: males have undescended testes and females have streak gonads or uterine malformations
7
Q
Sx of Hypokalemia
A
Cardiac Arrhythmias Skeletal Muscle (esp Diaphragm) weakness Rhabdomyolysis Metabolic Alkalosis Nephrogenic Diabetes Insipidus
8
Q
Pathophysiology of Gitelman Syndrome
A
AR mutations of NaCl co-Transporter (NCCT)
NaCl wasting, Hypovolemia, RAAS (increased collecting duct Na reabsorption, H and K secretion)
Increased Ca reabsorption
Hypomagnesemia from down regulating TRPM6 in DCT
9
Q
Calcium and cardiac AP
A
Increased Ca raises the threshold (makes it harder)
Lowered Ca lowers the threshold (makes it easier)
10
Q
glomerular pathology of chronic glomerulonephritis
A
normal, lipid in tubules
loss of foot processes, no deposits
11
Q
Glomerular Pathology of Membranous Glomerulo-Nephropathy
A
Diffuse Capillary Wall Thickening without increased cells
Spikes of Silver Staining Matrix from BM to urinary space
Supepithelial deposits of dense IgG and G3 with overlying obliterated foot processes
12
Q
How to replace a potassium deficit
A
Potassium Chloride: K increases by 0.1 for every 10 given
13
Q
Most common benign renal neoplasia
A
Renal papillary adenoma (benign), less than 1cm
14
Q
Rapidly Progressive Glomerulonephritis Type I
A
Anti-GBM Ab
Renal Limited, Goodpasture syndrome
15
Q
Patterns of tubular damage in Toxic injury
A
Continuous necrosis in PCT and PST
Patchy necrosis in Ascending LOH
16
Q
Criteria of Malignant HTN
A
180/120 BP
Papilledema, Retinal hemorrhages, encephalopathy, CV abnormalities, renal failure
Early sx are from increased intracranial pressure
17
Q
Pathophysiology of Minimal change disease
A
Unknown, loss of glomerular polyanion, podocyte injury
Its a nephrotic syndrome
Proteinuria and effacement of glomerular foot processes without Ab deposits. Responds well to steroids
Prensents as Edema and FPF on Bx
18
Q
Pathophysiology of Liddle Syndrome
A
Mutated ENaC channel in collecting duct
Prevents degradation of them from luminal surface of principle cells via ubiquitin (too many!)
Increases Na reabsorption and urine K and H hypokalemia and metabolic alkalosis)
19
Q
Clinical manifestations of Liddle Syndrome
A
Resistant Hypertension
Hypokalemia
Metabolic Acidosis (saline non-responsive)
20
Q
Glomerular Pathology of Post-infectious Glomerulonephritis
A
Endocapillary Proliferation, leukocyte infiltration
Granular IgG and C3 in GMB, maybe IgA
Supepithelial humps, sub endothelial deposits
21
Q
Amiloride
A
Blocks luminal Na Channels in collecting duct
Spironolactone blocks aldosterone receptor in collecting duct
22
Q
First line treatment for stage 2/moderate hyponatremia
A
Vaptan or Hypertonic NaCl
23
Q
Clinical Applications of Spironolactone
A
counteracts K loss induced by other diuretics in the treatment of HTN
off-label for reducing fibrosis post-MI heart failure
24
Q
Toxicities of HCTZ
A
Sulfonamide etc
25
Clinical manifestations of Chronic Kidney Disease
Starts silent, develops uremia
Persistently diminished GFR (below 60 3+ months)
Persistent albuminuria
Generally Irreversible
26
What happens with ethylene glycol damage to the kidney?
Virtually all PCT epithelial cells show swelling and vacuolization
27
Pathophysiology of IgA nephropathy
Unknown, recurrent hematuria or proteinuria
| Isolated (or can be nephritic)
28
Clinical manifestations of AKI
Rapid decline in GFR
Severe can have oliguria or anuria
Maybe from Glomerular, interstitial, vascular, or ATN
Can be reversible or become CDK
29
Triamterene
Similar to amiloride for edema and off-label for HTN, rapidly absorbed, 6-9 hours, eliminated as drug metabolized
30
Criteria for End Stage Renal Disease
GFR blow 5% normal
| End stage of uremia
31
Insulin and K
Drives K into the cell (decreases serum k)
| Alkalemia, ICF donates H+ to the ECF
32
Benign Nephrosclerosis
Pattern of hyaline sclerosis of renal arterioles, small a
| multi-focal ischemia of kidney parenchyma supplied by sclerotic vessels
33
Characterizations of Acute Proliferative Glomerulonephritis
Marked Hypercellularity
Leukocyte infiltration: exudative within glomerular tuft
Granular deposits of IgG, IgM, C3
34
Where do renal oncocytoma arise from?
Type A intercalated cells of cortical collecting ducts
(acid-base homeostasis)
Mahogany-brown and well-circumscribed with central stellate scar. Packed with Mitochondria
35
Goodpasture Ag
Peptide within noncollagenous regions of collagen IV
36
Acute pyelonephritis
```
Acute bacterial infection of the kidney
95% from the bladder with pre-existing defect
Vesicoureteral Reflux (back-flow up ureter)
```
37
Pathophysiology of Postinfectious Glomerulonephritis
Immune complex mediated, circulating or planted Ag
| Usually Nephritic Syndrome
38
Clinical Applications of Conivaptan
Treats euvolemic and hypervolemic hyponatremia
For Hospitalized, symptomatic pts unresponsive to fluid restriction
Watch out for too rapid of serum sodium correction
39
Cardiac Arrhythmias associated with Hypokalemia
Premature Atrial Contractions
Premature Ventricular Contractions
Tachycardia, Bradycardia, V Fib
40
Renal Angiomyolipoma
AD, Lesions of brain, skin, kidney, heart, lungs, eyes
| Strong association with Tuberous Sclerosis/TSC
41
Chlorothiazide
Similar to HCTZ but poor oral absorption
42
Uremia
Azotemia + constellation of findings of renal damage
43
3 main reasons for hypokalemia
```
Transcellular Shift (Insulin, b2 agonist, m. alkalosis)
Extrarenal Loss (GI: vomiting, diarrhea, Sweating)
Renal Loss
```
44
Toxicities of Desmopressin
Black Box Hyponatremia
45
Differentiate Central vs Nephrogenic Diabetes Insipidus
Central: lack of ADH (tx with ADH agonist / dDAVP)
Nephrogenic: Unresponsive to ADH (tx with water and thiazide unless its from lithium: give amiloride instead)
46
Vaptan MOA
block ADH receptors at the collecting duct
47
Etiology of RTA 2
Most common in children is Cystinosis
| Most common in adults with Fanconi is MM
48
Clinical applications of HCTZ
HTN, Not effective in patients with low GFR
| Calcium nephrolithiasis
49
Negative Urine Anion Gap
Appropriate distal nephron urinary acidification
50
Symptoms of Uremia
CV: HTN, Atherosclerosis, Stenosis, CGF
GI: Occult bleeding, N/v, Uremic Fetor
Neuro: Uremic Encephalopathy, Amyloidosis
Skin: Fluid retention, CaP deposits, Nail Atrophy
51
Respiratory acidosis and K
Increaes serum K
52
RTA type 1 most common secondary causes
Auto-immune disorders
53
RTA type 2 most common secondary causes
Fanconi's syndrome, MM, drugs
54
Medullary Sponge Kidney
Non-Hertiable, Benign
Medullary Cysts on Excretory Urography
Hematuria, UTI, Recurrent Renal Stones
55
3 groups of predisposing to Wilms Tumors patients
WAGR (wilms-aniridia-genital-retardation)
Denys-Drash Syndrome (gonadal and renal tumors)
Beckwith-Wiedemann syndrome (non-WT1, IGF 2)
56
Chronic Hypernatremia
Greater than 48 hours or unknown duration
57
Pathophysiology of Goodpasture
Anti-GBM COL4-A3 Ag
| Rapidly Progressive Glomerulonephritis
58
Diagnosis of RTA 2
Urine pH can be high or low
| Urine Anion gap is Negative
59
a-Intercalated cells transporters
H-ATPase
| H/K-ATPase
60
Nephritic Syndrome
Glomerular Disease dominated by acute onset hematuria, proteinuria, HTN, Oliguria with Azotemia
Usually immune mediated glomerular injury
61
What bladder cancer staging is optimistic vs very bad?
Ta, Tis, T1 are low stage. Isn't cured, but not deadly
| T2 - T4, highly muscle invasive, is very bad
62
Visceral Epithelial Cell (podocyte) Injury
Abs causing foot process effacement (fusion).
| Associated with Detachment of epithelial cells and protein leakage through defective GBM and filtration slits
63
Diagnosis of RTA 1
Unable to acidify urine pH below 5.5
Hypokalemia (urinary k wasting)
UAG is Positive
64
Advanced Renal Hyaline Arteriolosclerosis
Often found in diabetes
Thickened, tortuous afferent arteriole
Amorphous (thickened) vascular wall
65
Pathophysiology of Chronic Glomerulonephritis
Variable, usually presents as chronic renal failure
66
Metolazone
Long acting thiazide diuretic like HCTZ
67
Clinical manifestations of Gitelman Syndrome
Hypokalemia
Metabolic acidosis (non-saline responsive)
Low to normal blood pressure
HYPOCALCIURIA (opposite bartter), like w/ Thiazides
Hypomagnesemia
68
Normal Osmolality Gap
10
69
Where does urothelial carcinoma of the kidney originate
Urothelium of the Renal Pelvis
| Presents with Hematuria, may block urinary outflow and lead to palpable hydronephrosis and flank pain
70
Clinical Applications of Conivaptan
Treats euvolemic and hypervolemic hyponatremia
For Hospitalized, symptomatic pts unresponsive to fluid restriction
Watch out for too rapid of serum sodium correction
71
Black box warnings of amiloride
hyperkalemia
72
Vaptan MOA
Prevents ADH-mediated insertion of the aquaporin water channels into luminal membrane of principal cells in collecting duct (prevents water reabsorption)
73
Rapidly Progressive Glomerulonephritis Type III
Pauci-Immune. NO anti-GBM Abs!
ANCA-Associated, Idiopathic
Granulomatosis with Polyangiitis, Microscopic Polyangiitis
74
Toxicities of Furosemide
Sulfonamide
Ototoxicity
Hyper-Glycemia, -uremia
Hypo-kalemia, -natremia, -calcemia, -magnesemia, etc
75
Papillary necrosis pattern of analgesic nephropathy
Red-brown necrotic papillae sloughed into calyces
76
Adult Polycystic Kidney Disease
AD PKD (polycystin) 1 / 2, always bilateral
Large multi cystic kidney, liver cysts, berry aneurysms
Hematuria, flank pain, UTI, renal stones, HTN
77
Where do sodium channel blockers work?
Cortical Collecting Duct
78
Glomerular Pathology of Goodpasture
Extracapillary Proliferation with crescents, necrosis
Linear IgG and C3, Fibrin in crescents
No Deposits, GBM disruptions, fibrin
79
How to Identify Acute Kidney Injury
Rapid Decline in GFR
Severe forms can have oliguria and Anuria
Maybe from glomerular, interstitial, vascular, tubular injury
Can be reversible or progress to CKD
80
Where do loop diuretics work?
Thin Ascending Loop
81
PKD 1 vs PKD 2
PKD1: 16p13.3, Polycstin-1, Cell-Cell/Cell-Matrix interaction
PKD2: 4q13-p23, Polycsytin-2, Ca2+ channel
82
RTA Type 4
Hyperkalemic RTA
Decreased Aldosterone Secretion or Aldosterone Resistance
Leads to decreased net H and K secretion in collecting duct
83
Crescentic Glomerulonephritis
Collapsed, compacted, glomerular tufts
Crescent shaped mass of proliferating visceral and parietal epithelial. Wrinkling of GBM, fragmenting and disruption
Rapid Obliteration of urinary space
Infiltrates of Macrophages and Leukocytes
84
Major pathological finding of Papillary urothelial neoplasms of low malignant potential
Thickened epithelium covering papillary projections
| minimal cellular atypia
85
Exchange Resins
```
Sodium Polystyrene Sulfonate / Kayexalate (exchanges Na_ ions for K mostly in the colon)
Zirconium Cycloslicate (exchanges Na and H ions for K throughout intestines)
Patiromer (exchanges Ca+ for K primarily in colon)
```
86
How to treat Hyperkalemia via K removal
Loop Diuretics or Thiazide
Exchange Resins
Hemodialysis
87
Etiology of malacoplakia
Defective phagosome function and related to chronic infection (E coli, usually)
88
Where does Renal Cell Carcinoma arise from?
Renal Tubular Epithelium (adenocarcinoma)
| Happens a lot with smoking
89
Multicystic renal dysplasia
non-heritable absence of ureter, cauasing obstruction
Irregular kidneys with cysts of various size
Bilateral= renal failure, surgically cured if unilateral
90
Rapidly Progressive Glomerulonephritis
Nephritic syndrome with rapid decline in GFR
| Implies Glomerular Injury
91
Chlorthalidone
Similar to HCTZ but half life of 40-60 hours
| Prolonged/stable response with proven benefits
92
Why are urinary diverticulae commonly acquired?
Persistent urethral obstruction (like prostatic enlargement)
93
#1 neoplastic SIADH cause
Oat cell carcinoma
94
Classic phases of AKI/ARF
Initiation: 36 hours, oliguria
Maintenance: HyperKalemia
Recovery: HypoKalemia from urine loss, infection
95
Loop Diuretics MOA
Blocks NaK2Cl cotransporter in TAL
96
Glomerular pathology of chronic glomerulonephritis
Hyalinized glomeruli, replacement of virtually all
| Granular or negative on fluorescence microscopy
97
Glomerular pathology of Dense-Deposit Disease aka MPGN II
Mesangial proliferative or membranoproliferazive patterns of proliferation, GBM thickening, splitting
C3, no C1q or C4
Dense deposits
98
Bartter Syndrome Type 3 Mutation
All are AR
| CLC-Kb
99
Most common tumor of men
Testicular Germ Cell Tumors
100
IV K replacement
K Chloride, K Acetate (usually just for severe)
| 10 - 20 mEq/hour
101
Simple (renal) cysts
Non-heritable, benign
Single or several cysts, normal-sized kidneys
Microscopic hematuria
102
Clear cell carcinoma
Most common renal cell carcinoma
Non-papillary, sporadic 95%
When familial, chromosome 3 short arm deletions/translocations (VHL ts gene)
103
Treatment of Liddle Syndrome
Amiloride or Triamterene (blocks sodium channel)
| Low salt diet
104
Clinical Manifestations of Bartter syndrome
Hypokalemia
Metabolic Alkalosis (saline non-responsive)
Low to normal BP
Hypercalciuria and Nephrocalcinosis
105
RTA Type 2
Proximal RTA
| Decreased HCO3- reabsorption in PCT. Lost in urine, low in serum. Eventually stabilizes
106
K Homeostasis cells in the distal nephron
Principle cells for secretion
| a-intercalated cells for reabsorption
107
Basement membrane is moth-eaten, or frayed
Alport Syndrome
108
Vaptan MOA
Prevents ADH-mediated insertion of the aquaporin water channels into luminal membrane of principal cells in collecting duct (prevents water reabsorption)
109
Primary vs Secondary Nephrotic Syndrome
Primary: Renal Only, primary kidney disease is most common in children
Secondary: Systemic, more common in adults (DM, SLE)
110
Amiloride
Blocks luminal Na Channels in collecting duct (ENaC)
| Spironolactone blocks aldosterone receptor in collecting duct
111
Normal HCO3-
24
112
Adult-onset Nephronophthisis
AD
Corticomedullary cysts, shrunken kidneys
Salt wasting, polyuria
113
Tolvaptan
Selective AVP V2 receptor antagonist administered Orally
Hotta use it less than 30 days for hyponatremia (hepatotoxic)
It can also slow progression of adult PKD
114
Osmotic Demyelination Syndrome
Happens in Pontine and Extrapontine Neurons
Delayed 2 - 6 days
Can develop Locked in syndrome
115
Three major causes of decreased renal K secretion Hyperkalemia
```
Low Aldosterone Secretion
Aldosterone Resistance (K sparing Diuretics)
AKI or CKD (low GFR)
```
116
Best method for assessing renal K+ excretion
24 hour urine potassium
117
Licorice
Has glycyrrhizic acid, potentiates aldosterone effects in kidney and dose-dependently increases systolic BP
118
Bartter Syndrome Type 4 Mutation
All are AR
| Barttin Mutation
119
3 circulating Auto-Abs in DMI
Anti-Insulin, -GAD, -ICA512
120
Xanthogranulomatous Pyelonephritis association
Proteus sp.
121
What would you order to assess the volume status of a hypotonic hyponatremic patient?
Random Urine Sodium Level
Urine Osmolarity
(serum Uric Acid if considering SIADH: high in urine)
122
Thiazide MOA
Block NaCl cotransporter in DCT
| Mg is reabsorbed in primarily in TALH/distal nephron
123
Immune complexes in Subepithelial Humps
Acute Glomerulonephritis
124
How to treat Transcellular Shift Hyperkalemia
Insulin and Dextrose
B2 Agonist (albuterol)
Bicarb (likely not effective)
125
Risk of too rapid of sodium correction in chronic hyponatremia case
Osmotic Demyelination Syndrome (ODS) from brain swelling and rapid shrinking
126
Actue vs Chronic Hyponatremia criteria
Acute: Less than 48 hours
Chronic: Longer than 48 hours or unknown
127
Beckwith Widemann Syndrome clinical presentation
Hemihypertrophy, macroglossia
128
Major pathogenesis of Transcellular Shift Hyperkalemia
```
Pseudohyperkalemia
Metabolic Acidosis
Insulin deficiency, hyperglycemia, hyperolsmolarity
Increased Tissue Catabolism
Meds, Exercise, Blood Transfusion
```
129
Microscopy findings in Diffulse Proliferative Lupus Nephritis
Glomerulus really biggened, looks stuffed into Bowmans
| Resultant decrease in urinary space
130
Anion Gap above 20
Suspect Alcohol ingestion
131
Sarcoma botryoides
Embryonal Rhabdomyosarcoma, Cambium layer of tumor cells right below the epithelium results in nevoid appearance
132
Most common malignancy associated with ectopic ADH production
Small Cell Lung Cancer
133
Focal Segmental Glomerulosclerosis Collapsing Variant
in HIV and mores in Black patients
134
Where do thiazide diuretics work?
DCT
135
Pediatric Polycystic Kidney Disease
AR
Enlarged, cystic kidneys at birth
Hepatic Fibrosis
136
Hereditary Segmental Glomerulosclerosis
Mutations in cell adhesion coding genes NPHS1 and 2
Those coding for Nephrin, Podocin, a-actinin 4 (AD)
TRPC6 (transient receptor potential calcium channel 6)
APOL-1 on Chr 22 in Black patients (related to resistance to trypanosomal infection)
137
Ethacrynic acid
Non-sulfonamide loop diuretic reserved for those with sulfa allergy
138
Bence-Jones proteins and the kidney
Causes or is indicative of a tubulointerstitial nephritis
139
Thin basement membrane lesion
Benign clinical course, like Alport syndrome involves mutations in genes coding for GBM type IV collagen
In spectrum of diseases that includes hereditary nephritis
Asymptomatic Hematuria, most are heterozygous
140
Eplerenone
More selective aldosterone antagonist than spironolactone
| Approved for post-MI heart failure and alone for HTN
141
Toxicities of Desmopressin
Black Box Hyponatremia
142
Most common causes of End Stage Renal Disease
DM (primarily glomerular)
| HTN (primarily vascular / arteriolar / tubulointerstitial)
143
Ddx of NAGMA
```
DURHAAM:
DIARRHEA
Ureteral Diversion
RENAL TUBULAR ACIDOSIS
Hyperalimentation
Acetazolamide
Addison's disease
Misc
```
144
Mutations of invasive and bad bladder cancer vs superficial and non-invasive
TP53 (chr 17p) and RB is invasive
| Chr 9 monosomy or deletions are usually fine
145
Oral K
K chloride, K phosphate, K bicarb (precursors citrate, gluconate)
146
Common Etiologies of RTA 1
Glue Sniffing and Sjogrens
| Can manifest with nephrolithiasis or nephrocalcinosis
147
Malignant arteriolosclerosis
Injury associated with malignant / accelerated HTN
Ischemic kidneys, elevated renin
"flea-Bitten" appearance of renal hemorrhages
148
Polar Scarring of the kidney
Often from VUR with Chronic Pyelonephritis
149
Painless Hematuria
```
Think Urothelial (transitional cell) Carcinoma!
Theres usually multiple tumors at initial diagnosis
```
150
glomerular pathology of focal segmental glomerulosclerosis
focal and segmental sclerosis and hyalinosis
| "increasingly, a category of disease"
151
Mesangial Immune Deposits
IgA nephropathy
152
Normal Anion Gap
12
153
How would you identify a tubulointerstitial nephritis?
Inability to concentrate urine: polyuria (acute or chronic)
154
Metabolic alkalosis and K
Decreases serum K
155
Diagnosis and treatment of Pyroglutamic (5-oxoproline) acidosis
Urinary Organic Acid Screen
| Tx: discontinue acetaminophen, IVF, N-Acetylcysteine
156
Eosiniphilic Cystitis
Infiltration of submucosal eosinophils, can also represent nonspecific subacute inflammation etc
157
Pathophysiology of focal segmental glomeruloscerosis
Primary: Podocyte injury by unknown mechanisms
Secondary: ex. by prior glomerulonephtriytis, HTN, HIV...
Usually presents as nephrotic syndrome
158
Most common causes of Hypokalemic Transcelluar Shift
Insulin
b2 Agonist
Metabolic Alkalosis
159
Nephritic vs nephrotic presentations
Nephritic has greater hematuria
| Nephrotic has greater Proteinuria
160
Etiology of RTA 4
Deficiency of circulating Aldosterone (DM, drugs)
Aldosterone Resistance in collecting ducts
Both cause impaired Na reabsorption by principle cells
Hyperkalemia
Worsens Acidosis by preventing ammoniagenesis
161
Clinical applications for desmopressin
Central Diabetes Insipidus
| Primary Nocturnal Enuresis
162
Glomerular pathology of IgA nephropathy
Focal mesangial proliferative glomerulonephritis, mesangial widening
IgA +/- IgG, IgM, and C3 in mesangium
Mesangial and paramesangial dense deposits
163
Bartter Syndrome Type 2 Mutation
All are AR
| ROMK
164
How to treat Hyperkalemia with Peaked T waves
Calcium glutinate (stabilizes cardiac membrane)
165
Microscopy of malacoplakia
Foamy macrophages, multinuclear giant cells, some granulomas
| Laminated mineralized concretions, Michaelis-Gutmann bodies, in the macrophages
166
Licorice
Has glycyrrhizic acid, potentiates aldosterone effects in kidney and dose-dependently increases systolic BP
167
Patterns of tubular damage in Ischemic injury
Patchy necrosis of PCT, PST, Ascending LOH
168
Nephrotic Syndrome (there's 5 of them)
Glomerular Disease w/ severe proteinuria, hypoalbuminemia, edema, hyperlipidemia
Includes Membranous Nephropathy + Minimal Change Disease + Focal Segmental Glomerulosclerosis + Membranoproliferative Glomerulonephritis + Dense Deposit Disease (MPGN II)
Basically Leaky GBM (esp to albumin), RBCs don't enter urine
169
Clinical presentation of malacoplakia
Bladder inflammation with 3-4 cm soft yellow, plaques
170
K sparing diuretics
```
Na channel blockers (triamterene, amiloride)
Aldosterone Antagonists (spironolactone)
```
171
Metabolic Alkalosis ddx
```
Hypokalemia
Vomiting or NG tube
Diuretics
Volume Depletion
Mineralocorticoid Excess
```
172
Normal Arterial pH
Normal: 7.35 - 7.45
173
Prominent U wave
Hypokalemia
174
PAS Type IV Collagen Stain findings in Diabetic Glomerulosclerosis
Diffuse Capillary Basement Membrane Thickening
Diffuse Mesangial matrix increase
Acellular PAS+ nodules
175
Barium Toxicity
Blocks K+ channel and prevents efflux from cells
| Causes hypokalemia
176
5% albumin
Expands the plasma volume compartment
177
Labs of Azotemia
Elevated BUN, Decreased GFR
178
Sx of GC and CC
Chronic irritation, frequency, dysuria, urgency, hematuria
179
Anatomical sites of kidney stone lodging
UPJ and UVJ (not thought to be at the ureteral crossing of the iliac vessels as much)
180
Subendothelial Immune Deposits
Lupus Nephritis
| Membranoproliferative Glomerulonephritis
181
Bartter Syndrome Type 1 Mutation
All are AR
| NKCC2
182
Hypokalemia Criteria
Serum K below 3.5
183
Histology of Papillary Renal Cell Carcinoma
Papillae and foamy macrophages in stalk
184
How does metabolic acidosis work in hyperkalemia
K enters the cells so H exits them
| Decreased ammoniagenesis and ammonium chloride excretion in the kidneys
185
Acute Hypernatremia
Less than 48 hours
186
RTA Type 1
Distal RTA: unable to acidify urine
| Decreased net H+ ion secretion in DCT, collecting duct
187
Glomerular pathology of Membranoproliferazive glomerulonephritis Type 1
Mesangial proliferative or membranoproliferazive patterns of proliferation, GBM thickening, splitting
IgG++ C3, C1q++ C4
Subendothelial Deposits
188
Loop Diuretics MOA
Blocks NaK2Cl cotransporter in TAL
189
Clinical presentation of interstitial cystitis (Hunner ulcer)
Chronic, persistent, painful, 30-40 yo women
| Intermittent suprapubic pain, urinar frequency, urgency, hematuria, dysuria, Culture Negative
190
Most common defect associated with acute pyelonephritis
Defective Vesicoureteral Junction (children with UTIs)
| Bladder Outlet Obstruction (prostatic hypertrophy)
191
3% and 5% NaCl
Expands the ECF while shrinking the ICF
192
ADAMTS13
Protease regulating vWF
| Mutations founding TTP (prominent neuro sx)
193
Acute Post-Infectious Glomerulonephritis
Nephritic syndrome
Usually after Strep infection in children and young adults
Deposition of immune complexes, mainly sub epithelial
Neutrophils and glomerular cell proliferation. Good Px
194
Criterion for Hypernatremia
Serum Sodium above 145
195
Acute proliferative glomerulonephritis
Immune complex injury from exogenous Ag
Presents in adults with edema, elevated BUN, etc
Historical antecedent infection by b-hemolytic strep-specific nephritogenic strains of Lancefield Group A
196
Pathophysiology of membranoproliferazive glomerulonephritis (MPGN) type 1
Nephrotic when primary, nephritic when secondary
| Immune complex mediated
197
What is usually the cause of bacterial urethritis
Gonorrhea, Chlamydia, HPV
198
Cardiac changes in hyperkalemia
V Fib
Bradycardia form AV block
Asystole
199
Bumetanide
Sulfonamide like furosemide but more predictable oral absorption
200
Spironolactone MOA
Competitive antagonist aldosterone receptors
Partial agonist at androgen receptors
K+ sparing diuretic
201
K losing diuretics
Thiazides (NaCl cotransporter blockers)
Loop Diuretics (Na K 2Cl Cotransporter blockers)
Carbonic Anhydrase inhibitors
Osmotic diuretics (nonreabsorbable solutes)
202
Why does Metabolic Alkalosis happen with Hypokalemia
K moves from inside to outside cell to maintain [K+]
| Leads to H+ going inside from outside cell for electric reasons
203
Presentation of Alport Syndrome
Hematuria progressing to chronic renal failure
Nerve deafness and eye disorder (cataracts, etc)
X-Linked 85% of the time
204
Papillary necrosis pattern of DM
Pale Grayish necrosis
| Limited to papillae
205
Alport Syndrome
Form of Hereditary Nephritis (homozygous)
Mutated genes encoding GBM type IV collagen
Manifests as Hematuria and slow progressing proteinuria and declining renal function
Glomeruli are normal until late in disease course
206
HAGMA ddx
GOLD MARK
| Glycols, Oxoproline (acetaminophen), L- and D- Lactic Acidosis, Methanol, Aspirin, Renal Failure, Ketoacidosis
207
Renal Tubular Defects that can lead to RTA
Impaired H ion Secretion
| Impaired HCO3- Reabsorption
208
HCTZ MOA
Blockade of NaCl cotransporter
| K-Losing
209
Pathophysiology of Heymann Glomerulonephritis
Immune complex deposition on foot processes
210
Rapidly progressive Glomerulonephritis Type II
Immune Complex
Idiopathic, Post-Infectious Glomerulonephritis
Lupus nephritis, Henoch-Schonlein, IgA Nephropathy
211
Clinical presentation of Denys Drash
Gonadal Tumors
212
Pathophysiology of Bartter Syndrome
Transporter mutations at Thick Ascending Loop
NaCl loss, volume depletion, 2nd hyperaldosteronism
Cl- loss in macula dense causes PGE2 increase: renin (more aldosterone, hypokalemia, met alkalosis)
"Net result is like Loop Diuretics"
213
Frequent misdiagnosis of Polypoid cystitis
Papillary carcinoma. Look for this in in-dwelling catheters as this irritates the bladder mucosa
214
Diagnostics of Liddle Syndrome
Genetic testing, Low Aldosterone levels and renin levels
215
Two eponymic diseases associated with IgA Nephropathy
```
Berger Disease (renal, not systemic)
Henoch-Schönlein Purpura
```
216
Normal PCO2
40
217
Acquired Renal Cystic Disease
Non-heritable, dialysis-dependent
Cystic degeneration in end-stage kidney disease
Hemorrhage, erythrocytosis, neoplasia
218
Clinical applications of Furosemide
Management of edema
Decreases preload, EC volume, Rapid dyspnea
Treatment of HTN (works with low GFR, unlike thiazides)
219
Where is NH4 produced?
From Glutamine metabolism in PCT
220
Ddx of increased Serum Osmolality Gap
```
Methanol
Ethanol
Diethylene glycol (diuretic mannitol)
Isopropyl alcohol (rubbing alcohol)
Ethylene Glycol
```
221
Insulin and K
Drives K into the cell
| Alkalemia, ICF donates H+ to the ECF
222
Principle Cell Transporters
Na channel: creates net luminal negative charge
| Indirectly favors tubular H secretion
223
Wire loops on light microscopy
Renal Glomerular capillary basement membrane with sub endothelial dense deposits (also in mesangium)
Found in SLE
224
Metabolic acidosis and K
Increases serum K
225
0.45% NaCl
Expands ICF and ECF, but mostly the ECF
226
Hyperkalemia criteria
Serum K over 5.0 or 5.5
227
Pathophysiology of Dense Deposit Disease (MPGN type II)
Auto-Ab, alternative complement pathway via C3NeF (nephritic factor) binding C3 convertase
"unique permeation of glomerular basement membranes by electron dense material"
Usually presents as Hematuria and chronic renal failure
228
RTA type 2 most common secondary causes
Fanconi's syndrome, MM, drugs
229
Histology of Interstitial cystitis (Hunner ulcer)
Mast cells, lymphocytes
| Inflammation and fibrosis of the bladder wall, fissures
230
Oral K
K chloride, K phosphate, K bicarb (precursors citrate, gluconate)
231
Three sources of Pseudohyperkalemia
Transcellular shift:
RBC hemolysis (during venipuncture)
Serum Blood samples (clotted blood samples)
Leukocytosis
232
K losing diuretics
Thiazides (NaCl cotransporter blockers)
Loop Diuretics (Na K 2Cl Cotransporter blockers)
Carbonic Anhydrase inhibitors
Osmotic diuretics (nonreabsorbable solutes)
233
Emergency management of hyperkalemia
```
IV calcium (antagonize cardiac effects)
Redistribute K into cells (insulin, glucose, bicarb, b2)
K elimination (K-losing diuretic, mineralocorticoid, etc)
Monitor Intake
```
234
Sickle Cell Nephropathy
generally hematuria and hyposthenuria
Patchy papillary necrosis
Sometimes proteinuria, rarely nephrotic
235
Post-renal azotemia
Seen when urine flow is obstructed distal to calyces and renal pelvis
236
Eplerenone
More selective aldosterone antagonist than spironolactone
| Approved for post-MI heart failure and alone for HTN
237
Familial Juvenile Nephronophthisis
AR MCKD1 and 2 mutations
Corticomedullary Cysts, Shrunken Kidney
Salt Wasting, Polyuria, Polydipsia, Growth Retardation
238
Epimembranous Immune Deposits
Membranous Nephropathy
| Heymann Glomerulonephritis
239
Osmotic pressure of glucose (or any non-dissociating solute) at 1mmol/L
19.3 mmHg
240
Positive Urine Anion Gap
Inappropriate Distal Nephron Urinary Acidification
241
Differentiate Central vs Nephrogenic Diabetes Insipidus
Central: lack of ADH (tx with ADH agonist / dDAVP)
Nephrogenic: Unresponsive to ADH (tx with water and thiazide unless its from lithium: give amiloride instead)
242
Wilms tumor Histopathology
Often have precursor Nephrogenic Rests
triphasic (favorable): Blastemal, epithelial, stroll
anaplastic (unfavorable): Diffuse (always bad) or Focal
243
Follicular Cystitis
Aggregation of lymphocytes in lymphoid follicles in the mucosa and underlying wall. Usually associated with Chronic Infection
244
Triamterene
Similar to amiloride for edema and off-label for HTN, rapidly absorbed, 6-9 hours, eliminated as drug metabolites
245
Pre-renal azotemia
From Hypoperfusion of the kidneys in the absence of primary renal parenchymal damage
Ex. Hemorrhage, shock, CHF, volume depletion
246
Thiazide MOA
Block NaCl cotransporter in DCT
| Mg is reabsorbed in primarily in TALH/distal nephron
247
Delta Delta Gap
Used in patients with HAGMA to determine if there is a coexistent NAGMA or Metabolic Alkalosis
248
Typical vs Atypical HUS
Typical: from E Coli O157:H7 or Shigella
Atypical: Inherited complement mut, endothelial injury (chemo / immunosuppression), other
249
Black box warnings of amiloride
hyperkalemia
