Renal Flashcards
1
Q
What criteria define Nephrotic syndrome?
A
>3.5g of protein/day Hypoalbuminemia --> edema Hyperlipidemia/ Hypercholesterolemia Hypogammaglobulinemia Hyper coagulable state --> lose ATIII
2
Q
What criteria define Nephritic syndrome?
A
Hypertension Increase BUN and creatinine (Azotemia) Oliguria (decreased urine volume) Hematuria RBC casts in urine
3
Q
What does focal mean?
What does diffuse mean?
A
< half of glomeruli affected
> half of glomeruli affected
4
Q
What does membranous mean?
A
Basement membrane is thickened
5
Q
What does proliferation mean?
A
There are increased number of cells
6
Q
Post-Streptococcal glomerulonephritis
a. Pathophysiology
b. Seen in:
c. Presentation
e. On light microscopy
f. On immunofluorescence
g. On electron microscopy
A
a. Type III hypersensitivity; immune complexes are deposited in glomerulus. Treating strep with Abx does NOT prevent post-strep GN
b. Children who had strep infection three weeks earlier
c. Peripheral and periorbital edema, cola-colored urine, HTN
e. Glomeruli enlarged and hyper cellular
f. starry sky granular appearance; lumpy bumpy due to IgG, IgM and c3 deposition along GBM and mesangium
g. Subeptihelial immune complex humps
7
Q
IgA nephropathy
a. Pathophysiology
b. Presentation
c. Associated with
d. On LM
e. On IF
A
a. Increased IgA
b. Hematuria, after URI
c. Henoch Schonlein purpura
d. Mesangial proliferation
e. IgA based IC deposits in mesangium
8
Q
Alport syndrome
a. Pathophysiology
b. Presentation
c. On EM
A
a. Mutation in type IV collagein –> thinning and splitting of glomerular BM; most commonly X linked
b. Eye problems, glomerulonephritis, sensorineural deafness
c. Basket weave appearance
9
Q
Goodpasture’s
a. Pathophysiology
b. Presentation
c. on LM and IF
A
a. Type II hypersensitivity with Abs to GBM and alveolar basement membrane
b. Hemoptysis, hematuria
c. Crescent moon shape –> crescents consist of fibrin and plasma proteins –> linear pattern
10
Q
What are three types of rapidly progressive glomerulonephritis (Crescentic)
A
Goodpastures
Wegeners (GPA)
Microscopic polyangiitis
11
Q
Diffuse Proliferative Glomerulonephritis
a. Pathophysiology
b. Presentation
c. on LM
d. on EM
A
a. Due to SLE or membranoproliferative glomerulonephritis
b. Sometimes presents as nephrotic and nephritic syndrome concurrently (heavy proteinuria)
c. Wire looping of capillaries - makes BM look really pronounced
d. Subendothelial IgG immune complexes with C3 deposition
12
Q
Most common cause of death in SLE
A
Diffuse proliferative glomerulonephritis
13
Q
Minimal Change Disease
a. Pathophysiology
b. Presentation
c. on LM
d. on EM
e. Treatment
A
a. idiopathic or triggered by infection/immunization; secondary to lymphoma
b. CHILDREN; proteinuria, edema, hyperlipidemia, hypoalbuminemia
c. NORMAL glomeruli
d. EFFACEMENT (fusion) of foot processes
e. Responds to steroids
14
Q
Focal Segmental Glomeruloscelsosis
a. Pathophysiology
b. Presentation
c. on LM
d. on IF
e. on EM
f. Treatment
A
a. Idiopathic or secondary to HIV!!!!, sickle cell, heroin abuse, obesity, interferon treatment, chronic kidney disease
b. Adults (african american and hispanics); nephrotic syndrome
c. segmental sclerosis and hyalinosis
d. nonspecific of foot process similar to minimal change disease
e. effacement of foot process similar to minimal change disease
f. Does not respond to steroids
15
Q
Membranous Nephropathy
a. Pathophysiology
b. Presentation
c. on LM
d. on IF
e. on EM
A
a. Idiopathic or secondary to drugs, HBV, HCV, SLE, tumors
b. Caucasian adults
c. Diffuse capillary and GBM THICKENING
d. granular from immune complex deposition
e. Spike and dome appearance with SUBEPITHELIAL DEPOSITS
16
Q
Membranoproliferative glomerulonephritis
a. Pathophysiology
b. Presenation
c. Type I
d. Type II
A
a. Nephritis syndrome that co present with nephrotic syndrome
b. Idiopathic or due to HBV/HCV infection, SLE or subacute bacterial endocarditis
c. Subendothelial immune complex deposits with granular IF = TRAM TRACK appearance on PAS stain from GBM splitting
d. Intramembranous IC deposits
17
Q
Diabetic nephropathy
a. Pathophysiology
b. On Biopsy…
A
a. Non-enzymatic glycosylationg of GBM –> increased permeability and thickening
b. Kimmelstiel Wilson lesions, mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis
18
Q
Linear pattern of IgG deposition on IF
A
Goodpasture syndrome (anti GBM Abs)
19
Q
Lumpy bumpy deposits of IgG, IgM, C3 in the mesangium
A
Post-strep glomerulonephritis
20
Q
Deposits of IgA in the mesangium
A
IgA Nephropathy (Berger disease)
21
Q
Anti-GBM antibodies, hematuria, hemoptysis
A
Goodpasture’s syndrome
22
Q
Nephritis, deafness, cataracts
A
Alport syndrome
23
Q
Crescent formation in the glomeruli
A
Rapidly progressive glomerulonephritis
24
Q
Wire loop appearance on LM
A
Lupus nephritis
25
Most common nephrotic syndrome in children
Minimal change disease
26
Most common nephrotic syndrome in adults
Focal segmental glomerulonephritis
27
Kimmelstiel-Wilson lesions (nodular glomerulosclerosis)
Diabetic nephropathy
28
EM shows effacement of epithelial foot processes
Minimal change disease
29
Nephrotic syndrome associated with Hepatitis B
Membranoproliferative glomerulonephritis
30
Nephrotic syndrome associated with HIV
Focal Segmental Glomerulosclerosis (FSGS)
31
EM: sub endothelial humps and tram-track appearance
Membranoproliferative glomerulonephritis
32
LM: segmental sclerosis and hyalinosis
FSGS
33
Purpura on back or arms/legs, abdominal pain, IgA nephropathy
Henoch Schonlein Purpura
34
EM: spiking of GBM due sub epithelial deposits
Membranous nephropathy (Spike and dome)
35
Nodular hyaline deposits in the glomeruli
Kimmelstiel-Wilson nodules
36
Glomerulonephritis plus pulmonary vasculititis
GPA
| Goodpasture
37
RBC casts
Indicate glomerular damage
Glomerulonephritis, malignant HTN
Appear yellowish-brown, cylindrical with ragged edges
38
WBC casts
Indicate acute pyelonephritis
| Means damage is ALL the way up in kidney
39
Bacterial casts
Pyelonephritis
40
Epithelial cell cast
ATN, toxic ingestions
| Difficult to distinguish from WBC casts
41
Waxy casts
Chronic renal failure
| Low urine flow situations
42
Hyaline casts
Most common cast type
Solidified Tam horsefall proteins
Not necessarily pathology
Tend to see them in concentrated urine, dehydration
43
Fatty cast
Nephrotic syndrome
44
Granular cast
From breakdown of cellular casts or aggregates of plasma proteins (albumin, light chains)
Chronic renal disease
ATN (muddy brown cast)
45
Where is common location of kidney stone?
Ureterovesicular junction
46
Radiopaque
| Envelope or dumbbell shaped
Calcium kidney stones
47
Risk factors for calcium oxalate stones
Ethylene glycol or Vitamin C abuse, malabsorption
48
Treatment for calcium stones
Hydration, Thiazides, Citrate
49
Hypercalciuria and normocalcemia
Most common kidney stone presentation; calcium stones
50
Radiopaque, coffin lid stones
Struvite (ammonium, Mg, phosphate stones)
51
Cause of Struvite stones
Infection with urease + bugs
52
Urease + bugs
```
Proteus mirabilis
Staph saphrophyticus
Klebsiella
Pseudomonas
They all hydrolyze urea to ammonia --> causes urine alkalinization
```
53
Treatment for struvite stones
Eradication of infection, surgical removal of stone
54
Form staghorn calculi (outlines the renal pelvis - looks like a big stag's horn)
Struvite stones
55
RadioLUCENT
| Precipitates at Decreased pH
Uric acid stone
56
Uric acid stone
Radiolucent - can't see on plain film but can see on US and CT
Strong association with hyperuricemia (gout); seen in diseases with increased cell turnover like leukemia
57
Treatment of uric acid stones
Allopurinol, alkalinization of urine
58
Risk factors for uric acid stones
Decreased urine volume, arid climates, acidic pH
59
Cystine stones
Seen in patients with Cystinuria (children)
Staghorn calculi
Treated with alkalinization of urine
Hereditary condition where cystine-reabsorbing transporter loses function --> causing cystinuria
60
Paraneoplastic syndromes associated with renal cell carcinoma
Ectopic erythropoietin --> polycythemia
ACTH --> Cushing syndrome
PTHrP --> hypercalcemia
Prolactin --> hypogonadism, galactorrhea
61
Complications of Renal cell carcinoma
Invades inferior vena cava -> spreads hematogenously
| Associated with von Hippel Lindau syndrome
62
Most common renal malignancy of children aged 2-4
Wilms tumor
63
Presentation of Wilms tumor
Hematuria
| Large flank mass
64
Pathogenesis of Wilms tumor
Deletion of WT1 or WT2 on chromosome 11 (tumor suppressor gene)
65
Beckwith-Wiedemann syndrome
Wilms tumor
Aniridia
Genitourinary malformation
mental Retardation
66
Most common tumor of urinary tract
Transitional cell carcinoma (in renal calcyes, renal pelvis, ureters, bladder)
67
Risk factors for transitional cell carcinoma
Smoking
Aniline dye exposure
Cyclophosphamide
68
Cause of diffuse cortical necrosis
Vasospasm
DIC
Occurs in very sick patients
69
Most common causes of ATN
```
Ischemia
Nephrotoxic drugs (aminoglycosides, cephalosporins, polymyxins, radio contrast dye)
```
70
Key finding in ATN
Granular muddy brown casts
71
What is renal papillary necrosis?
Sloughing of necrotic renal papillae that causes gross hematuria and proteinuria
72
What triggers renal papillary necrosis? Associations?
Recent infection or immune stimulus
| Associated with sickle cell disease, acute pyelonephritis, NSAIDs, diabetes mellitus
73
Three categories of acute renal failure
Prerenal - not enough blood
Intrinsic
Postrenal - outflow obstruction causing back up
74
Causes of prerenal failure
Hypovolemia
Shock
Hypotension
Renal vasoconstriction with NSAIDS
75
a. BUN/creatinine ratio in pre-renal azotemia
b. FENa
c. urine Na
d. urine osmolality
a. >20
b. < 1%
c. <20
d. 500
76
Causes of intrinsic renal failure
```
Acute interstitial necrosis
Glomerulonephritis
ATN
DIC
Acute pyelonephritis
```
77
a. BUN/creatinine ratio in intrinsic renal failure
b. FENa
c. Urine Na
d. Urine osmolality
a. < 15
b. > 2%
c. > 40
d. < 350
78
Causes of post-renal disease
Stones, BPH, neoplasia, congenital anomalies
| ONLY happens with bilateral obstruction
79
Post-renal azotemia
a. BUN/creatinine
b. FENa
c. Urine Na
d. Urine osmolality
a. Varies
b. > 1% mild, >2% severe
c. >40
d. < 350
80
Consequences of renal failure
| MADHUNGER
```
Metabolic Acidosis
Dyslipidemia
Hyperkalemia (retain K without normal kidney function)
Uremia (Nausea, anorexia, asterixis)
Na/H20 retention
Growth retardation
Erythropoietin failure (anemia)
Renal osteodystrophy
```
81
What is renal osteodystrophy?
Failure of vitamin D hydroxylation, hypocalcemia, hyperphosphatemia --> secondary hyperparathyroidism
Causes subperiosteal thinning of bones
82
ADPKD
Adults
Bilateral enlarged kidneys
Flank pain, hematuria, HTN, urinary infection, renal failure
83
ARPKD
Kids
84
Fever, Rash, Eosinophilia, Azotemia
Drug Induced Interstitial Nephritis
85
Changes in metabolic panel of renal failure
Elevated potassium
Decreased calcium
Elevated BUN and Cr
86
Thyroid like appearance of kidney
Chronic pyelonephritis
87
Associated with Hodgkin lymphoma
Minimal Change Disease
| effacement of foot processes from cytokines
88
Selective proteinuria (loss of albumin but not immunoglobulin)
Minimal Change Disease
89
HIV, heroin use, Sickle cell
FSGS
90
Nephrotic syndromes
```
Minimal Change Disease
Focal Segmental Glomerulosclerosis
Membranous nephropathy
Membrano-Proliferative Glomerulonephritis
Diabetic Nephropathy
Amyloidosis
```
91
Nephritic syndromes
```
Post-Strep Glomerulonephritis
IgA Nephropathy
Rapidly Progressive Glomerulonephritis (Goodpastures, Wegeners, Microscopic polyangiitis)
Alport Syndrome
Diffuse Proliferative Glomerulonephritis
```
92
Positive sodium cyanide nitroprusside test with kidney stones
Cystinuria - Cyanide converts cystine to cysteine and a purple color is created when nitroprusside binds cysteine
93
POTTER Sequence
```
Pulmonary hypoplasia
Oligohydramnios
Twisted face (flattened)
Twisted skin
Extremity defects
Renal failure (in utero)
Babies who can't PEE in utero, develop Potter sequence
```
94
Causes of POTTER sequence
ARPKD
Obstructive uropathy (posterior urethral valves)
Bilateral renal agenesis
95
Which artery traps horseshoe kidney?
| What is it associated with?
Inferior Mesenteric Artery
| Turner's syndrome
96
Where does ureter lie compared to uterine artery?
Ureter is UNDER Uterine artery
| Water under the bridge
97
How much of body water is extracellular fluid?
1/3 of TBW
| 20% of body weight (1/3 of 60%)
98
How much of TBW is intracellular fluid?
40% (2/3 of TBW)
99
How much of Extracellular fluid is Interstitial fluid?
75% of ECF
100
How much of Extracellular fluid is Plasma?
25% of ECF
101
What are the units of clearance?
Volume/unit time
102
What is the equation for clearance?
UV/P
U = urine concentration of substance
V = urine flow rate (mL/min)
P = plasma concentration
103
What is the excretion rate equation?
Urine concentration of substance (mg/mL) X urine flow rate (mL/min) = mg/min
104
What is measured to calculate GFR?
Inulin is best but not practical
| Creatinine - only a small amount is secreted
105
What is normal GFR?
90-135ml/min (100ml/min)
106
What is renal plasma flow?
Blood going to glomeruli AND blood going to tubules
Estimated with PAH (filtered AND secreted in tubule)
U(PAH) x V/P(PAH
107
What is filtration fraction? What is the equation?
The position blood going to the kidney that is filtered through the glomerulus
FF = GFR/RPF (clearance of creatinine/clearance of PAH)
Normally 20%
108
How do NSAIDS affect GFR?
They constrict afferent arterioles
| Decrease RBF and GFR --> no change in FF
109
How does Angiotensin II affect kidney?
Constricts efferent arteriole --> congestion of blood in glomerulus --> Renal blood flow decreases but GFR increases --> filtration fraction increases
110
Effect of ACE inhibitors on kidney
Dilate efferent arteriole --> decrease GFR and increase RPF
111
Constriction of afferent arterioles effects
GFR decrease
RBF decrease
FF no change
112
Constriction of efferent arteriole effects
GFR increase
RBF decrease
FF increase
113
Dilation of afferent arteriole effects
GFR increase
RBF increase
FF no change
114
Dilation of efferent arteriole effects
GFR decrease
RBF increase
FF decrease
115
Increase in serum protein effects on GFR, RBF, FF
GFR decrease
RBF no change
FF decrease
116
Ureter stone obstruction
```
GFR decrease (back up of urine causes increased hydrostatic pressure in the tubules --> favors blood staying in capillaries)
RBF no change
FF decrease
```
117
ACE inhibitors effect on GFR, RBF, FF
GFR decrease
RBF increase
FF decrease
-This is why serum creatinine goes up initially when patients are started on ACE inhibitors
118
NSAIDS effect on GFR, RBF, FF
GFR decrease
RBF decrease
FF no change
119
What is the filtered load equation?
GFR x the plasma concentration of the substance
120
What is the excretion rate equation?
urine concentration x urine flow rate (U x V)
121
What is threshold for glucosuria?
Plasma glucose of 200mg/dL
122
When are all glucose transporters fully saturated?
Plasma glucose of 375mg/dL
123
What is Hartnup disease?
Deficiency in transporter for neutral amino acids like Tryptophan in proximal renal tubules --> aminoaciduria and decrease absorption from gut --> no tryptophan for conversion to niacin (B3) --> pellagra (diarrhea, dementia, dermatitis)
124
How do you treat Hartnup disease?
High protein diet
| Nicotinic acid
125
Where are glucose and amino acids reabsorbed?
ALL in the proximal tubule
126
What kind of absorption takes place in proximal tubule?
Isotonic absorption
127
What does carbonic anhydrase do?
Converts CO2 and H2O into H+ and Bicarb --> bicarb is reabsorbed into the interstitium (blood)
128
Which part of the nephron is impermeable to water?
The thick ascending loop of Henle
129
Which part of the nephron is impermeable to Na?
Thick descending loop of Henle - passively absorbs water (it is a concentrating segment --> makes urine hypertonic)
130
Where is the Na/K/Cl transporter?
Thick ascending loop of Henle
131
```
Which class of drugs inhibits the Na/2Cl/K symporter in the thick ascending loop of Henle?
What kind of water excretion do these drugs cause?
```
Loop diuretic
| Isotonic water excretion
132
How and where are Ca and Mg reabsorbed in the nephron?
In the thick ascending limb they are absorbed paracellularly through positive lumen potential generated by K+ back leak
133
What is happening in early distal convuluted tubule?
Reabsorbs Na/Cl
Makes urine most dilute (hypotonic)
PTH increases reabsorption of Calcium through Ca/Na exchanger
134
What actions are taking place in collecting tubule?
Reabsorbs Na in exchange for secreting K/H (action of Aldosterone)
Water is reabsorbed - ADH
135
What two types of cells compose the collecting duct and the last segment of the distal tubule? What do they do?
Principal cells - Reabsorb Na, H20 and secrete K
| Intercalated cells - Secrete Hydrogen, bicarb and reabsorb K
136
What determines how much water is reabsorbed in collecting tubule?
ADH - acts on V2 receptors on principal cells and tells them to inset Aquaporin water channels
137
What class of diuretics directly affects the principal cells?
K sparing diuretics
Spironolactone/Epleronone = aldosterone antagonists
Inhibit epithelial Na channels - Triamterene, Amiloride
138
What effect does aldosterone have on principal cells and intercalated cells of collecting duct?
Principal cells - Reabsorption of Na and secretion of K
| Intercalated cells - Stimulates secretion of H+ ions
139
Site of secretion of organic anions and cations
Proximal tubule
140
Site of isotonic fluid reabsorption
Proximal tubule
141
Site responsible for diluting urine
Thick ascending limb
142
Mechanism of Acetazolamide
Carbonic anhydrase inhibitor --> inhibits formation of H+ and bicarb from CO2/H2O --> causes limited NaHCO3 diuresis and decreased total body bicarbonate stores
143
Uses for Acetazolamide
Glaucoma - (bc Bicarb draws water into the eye to make aqueous humor)
Urinary alkalinization
Metabolic alkalosis
Altitude sickness - (partial pressure of O is lower so you have to breathe faster and deeper --> blow off CO2 --> respiratory alkalosis)
Pseudotumor cerebri
144
S/E of Acetazolamide
Metabolic acidosis
NH3 toxicity
Sulfa allergy!!!
145
What are the sulfa drugs?
Acetazolamide
| Furosemide, Bumetanide, Torsemide
146
What is mechanism of Mannitol
Osmotic diuretic that prevents reabsorption of free H20 --> increases urine flow --> decreases intracranial/intraocular pressure
147
What is the use of Mannitol?
Drug overdose
Elevated intracranial/intraocular pressure - with acute glaucoma
Shock
148
S/E of Mannitol
Pulmonary edema
Dehydration - from losing free water
C/I in anuria, HF
149
Furosemide, Bumetanide, Torsemide mechanism
```
Loop diuretic; inhibits Na/K/2Cl transporter in thick ascending limb; prevent concentration of urine
LOSE CALCIUM (loops lose calcium, thiazides retain calcium)
```
150
Ethacrynic acid
Loop diuretic that is NOT a sulfonamide
| Can be used in patients with Sulfa allergy
151
Use of loop diuretics
```
Patients with serious edema
CHF
Pulmonary edema
Nephrotic syndrome
Cirrhosis
```
152
S/E of loop diuretics
```
Ototoxicity
HYPOkalemia
Dehydration
Nephrotoxicity
Gout - interfere with uric acid secretion
Allergy (SULFA)
```
153
Chlorthalidone, HCTZ mechanism
```
Inhibit Na/Cl reabsorption in early DCT --> decrease diluting capacity of nephron
Retain Calcium (decrease Ca excretion)
```
154
Uses for Thiazide diuretics
HTN
HF
Idiopathic hypercalciuria (normal serocalcemia but dumps a lot in urine --> calcium stones)
Nephrogenic diabetes insipidus
155
S/E of Thiazides
```
Hyper LIPIDEMIA
hyper GLYCEMIA
hyper CALCEMIA
hyper URICEMIA
Sulfa allergy
```
156
Uses for K sparing diuretics
Hyperaldosteronism
K depletion
HF (improve mortality)
157
S/E of K sparing diuretics
```
Hyperkalemia --> arrhythmia
Endocrine effects (gynecomastia, anti-androgen)
```
158
Mechanism of Tiamterene, Amiloride
Block Na channels in the cortical collecting tubule --> spare K
159
What are kidney endocrine functions?
Make EPO in response to hypoxia
1alpha hydroxylase converts vitamin D into active form (1,25 OH2 D3) when stimulated by PTH
Renin is secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge (B1)
160
When is PTH secreted?
| What are it's actions?
PTH is secreted in response to low calcium, increased phosphate or low vitamin D
It activates vitamin D, increases Calcium reabsorption and decreases phosphate reabsorption
161
When is ANP secreted?
| What are it's actions?
Secreted in response to increased atrial pressure
| Causes increased GFR and increases Na filtration with NO compensatory REABSORPTION of Na --> Na, volume loss
162
How does Lithium cause Diabetes Insipidus?
ADH causes aquaporins to be put into luminal cell to reabsorb water --> lithium interferes with this process
163
Signs of hyponatremia
```
Confusion, altered mental status
Seizures
Stupor
Coma
(messes with resting potential or neurons)
```
164
Signs of hypercalcemia
Stones
Bones
Groans (abdominal)
Psychiatric overtones (confusion, delirium)
165
Hypocalcemia signs
Tetani (Trousseau sign = Tighten BP cuff, Chvostek sign = cheek)
166
Hypomagnesemia signs
Tetani
167
Hypermagnesemia signs
Depressed reflexes
168
Hypokalemia
Prolongs QT interval --V tach and Torsades
| Flattened T waves
169
Hyperkalemia
V tach
| PEAKED T waves
170
What kinds of things shift K outside of cells --> hyperkalemia?
```
Low insulin
Beta blockers
Acidosis - cells trying to correct acidosis by moving H+ ions out of blood (exchange H for K)
Digoxin
Cellular lysis (leukemia)
```
171
What kinds of things shift K inside to cells?
Insulin
Beta agonist
Alkalosis
Cell formation
172
Three emergency treatments for hypokalemia?
Beta agonist (Albuterol)
IV Insulin
IV Bicarb
173
Treatment for central DI
Desmopressin
174
Treatment for nephrogenic DI
HCTZ
Indomethacin
Amiloride
175
Treatment for Lithium-Induced Nephrogenic DI
Amiloride
176
Causes of hypernatremia
```
Diuretics
Dehydration
Diabetes Insipidus
Docs (iatrogenic)
Diarrhea
Disease of Kidney
```
177
Causes of respiratory acidosis
```
Hypoventilating
Airway obstruction
Air trapping
Lung disease (interstitial especially)
Weak respiratory muscles
Opioids
```
178
Causes of metabolic acidosis
Adding acid to blood of losing excessive Bicarbonate
| Can be classified by high or low metabolic anion gap
179
Increased anion gap metabolic acidosis (MUDPILES)
```
(ADDING ACID TO BLOOD)
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets/Isoniazid
Lactic acidosis (shock, not perfusing)
Ethylene glycol
Salicylates (LATE)
```
180
Normal anion gap metabolic acidosis (HARD-ASS)
```
(FROM LOSING BICARBONATE)
Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
```
181
Causes of respiratory alkalosis
```
Hyperventilating --> blowing off CO2
Psychogenic
High altitude
Acute hypoxemia (PE)
Aspirin toxicity (EARLY) --ASA directly stimulates respiratory center in brain and causes hyperventilation and later you MIGHT see metabolic acidosis
```
182
Causes of metabolic alkalosis
Losing Hydrogen ions
Excessive vomiting
Diuretics
Hyperaldosteronism (Hypokalemia, hypertension, metabolic alkalosis)
183
Renal Tubular Acidosis
1. Type 1 RTA - distal; alpha intercalated cells can't secrete hydrogen --> metabolic acidosis ---> hypokalemia, urine pH > 5.5, increased bone turnover
2. Type 2 RTA - proximal; defect in PCT Bicarbonate reabsorption
3. Type 4 RTA - from hyperaldosteronism --> causes hyperkalemia --> decreased ammonia synthesis in PCT --> decreased NH4 excretion, urine pH < 5.5; Caused by decreased aldosterone production, aldosterone resistance
184
What is winter's formula?
Pco2 = 1.5 (HCO3) + 8 +/- 2
| Not that important for Step1
185
pH 7.4
HCO3 23
pCO2 40
Normal
186
pH 7.5
HCO3 35
pCO2 42
Metabolic alkalosis
187
pH 7.33
HCO3 13
pCO2 28
Metabolic acidosis with respiratory compensation
188
pH 7.42
HCO3 32
pCO2 64
Mixed respiratory acidosis/metabolic alkalosis
189
pH 7.2
HCO3 18
pCO2 40
Metabolic acidosis
190
pH 7.20
HCO3 24
CO2 54
Respiratory acidosis
191
pH 7.52
HCO3 22
CO2 22
Respiratory alkalosis
192
pH 7.66
HCO3 36
pCO2 30
Mixed alkalosis
193
pH 7.47
HCO3 14
PCO2 22
Respiratory alkalosis with metabolic compensation
194
pH 7.46
HCO3 35
PCO2 53
Metabolic alkalosis with respiratory compensation
195
pH 7.39
HCO3 12
PCO2 22
Mixed metabolic acidosis/respiratory alkalosis
196
pH 7.34
HCO3 31
pCO2 62
Respiratory acidosis with metabolic compensation
197
pH 7.10
HCO3 15
pCO2 50
Mixed acidosis
198
a. What is the pronephros?
b. What is the mesonephros?
c. What is the metanephros?
a. The embryonic kidney up until week 4 and then it degenerates
b. Functions as interim kidney for 1st trimester; later contributes to male genital system
c. Permanent; appears in 5th week of gestation; nephrogenesis continues through 32-36 weeks of gestation
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Which embryologic kidney is permanent?
Metanephros
200
Parts of metanephros?
a. Ureteric bud - derived from caudal end of mesonephric duct; gives rise to ureter, pelvises, calyces, collecting ducts --> entire collecting system
b. Metanephric mesenchyme - ureteric bud interacts with this tissue to induce differentiation and formation of glomerulus through to distal convoluted tubule
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What can cause several congenital malformations of the kidney during embryogenesis?
If the ureteric bud and metanephric mesenchyme interaction is abnormal
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What is the last part of the kidney to canalize? Why is this significant?
The ureteropelvic junction; it is the MOST common site of obstruction (hydrophrosis) in fetus
203
Cause of multi cystic dysplastic kidney
Abnormal interaction between ureteric bud and metanephric mesenchyme
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Cause of duplex collecting system
Bifurcation of ureteric bud before it enters the metanephric blastema creates Y shaped bifid ureter or can occur when two ureteric buds reach and interact with metanephric blastema
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Associations with duplex collecting system
Vesicoureteral reflux
Ureteral obstruction
Increased risk for UTIs
206
Why if left kidney taken during donor transplantation?
Left renal vein is longer
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Which vessels are at risk of damage during gynecologic procedures?
If there is ligation of uterine vessels in the cardinal ligament there is a possibility of damaging ureter --> ureteral obstruction or leak
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What makes up the glomerular filtration barrier?
Fenestrated capillary endothelium (size barrier)
Fused basement membrane with heparin sulfate (negative charge barrier)
Epithelial layer consisting of podocyte foot processes
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Which part of the glomerular filtration barrier is lost in nephrotic syndrome?
The charge barrier is lost --> albuminuria, hypoproteinemia, generalized edema, hyperlipidemia
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Equation for RBF
RBF = RPF/(1-Hct)
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What is the normal filtration fraction?
20%
212
Estimate of GFR?
| Estimate of Renal plasma flow?
```
GFR = creatinine clearance
RPF = PAH clearance (Filtered and secreted = 100% excretion)
```
213
How does constriction of ureter change GFR, RPF and FF?
Causes decreased GFR, no change in RPF and decreased FF
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Where is glucose reabsorbed?
100% reabsorbed in proximal tubule by Na/glucose co-transport
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What happens to glucose regulation in kidney during pregnancy?
It may decrease the ability of PCT to reabsorb glucose and amino acids --> glucosuria and aminoaciduria
216
What is Hartnup disease?
Deficiency of neutral amino acid transporter in proximal renal tubular cells and enterocytes --> neutral aminoaciduria and decreased absorption form the gut --> decreased tryptophan for conversion to niacin --> pellagra (diabetes, dementia, dermatitis)
217
How do you treat Hartnup disease?
High protein diet and nicotinic acid
218
Where does Angiotensin II exert it's effects?
The proximal tubules (Na/H exchanger) --> causes Na, H20 and bicarb reabsorption
219
Where does Parathyroid hormone exert effects in nephron?
1. Inhibits Na/PO4 co-transport in PCT --> causes PO4 excretion
2. Causes increased Ca/Na exchange in early distal convoluted tubule --> increased Ca reabsorption
220
Where does ADH act?
Acts at V2 receptor (Gs receptor) --> insertion of aquaporin H20 channels on apical side --> increased H20 reabsorption
221
Where does Aldosterone act?
a. Acts on mineralcorticoid receptor --> mRNA --> protein synthsis
b. In Principal cells it causes apical K+ conductance, increased activity of Na/K pump, Increased ENaC channels --> lumen negativity --> K+ loss
c. In alpha-intercalated cells --> increased H+ ATPase activity --> HCO3/Cl exchanger activity
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Generalized reabsorptive defect in PCT
| What does it cause?
Fanconi syndrome
Increased excretion of all amino acids, glucose, HCO3, PCO4
May result in metabolic acidosis
223
Reabsorptive defect in thick ascending loop of Henle
| Results in what?
Bartter syndrome
| Affects Na/K/2Cl co-transporter --> results in hypokalemia and metabolic alkalosis with hypercalciuria
224
Reabsorptive defect of NaCl in DCT
| Results?
```
Gitelman syndrome (less severe than Bartter)
Causes hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria
```
225
Gain of function mutation --> increased Na reabsorption in collecting tubules
Liddle syndrome
226
Hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone (not deficiency of 11B hydroxysteroid dehydrogenase)
Liddle syndrome (autosomal dominant)
227
Treatment of Liddle syndrome
Amiloride (blocks Na channels in collecting tubule)
228
11B-hydroxysteroid dehydrogenase deficiency
Syndrome of apparent mineralcorticoid excess --> cortisol doesn't get converted to cortisone and excess cortisol acts on mineralocorticoid receptors to cause hypertension, hypokalemia, metabolic alkalosis
229
Acquired 11B-hydroxysteroid dehydrogenase deficiency
From licorice (glycyrrhetic acid)
230
Where does ACE come from?
Lungs and kidney
231
What causes increased production of renin?
1. Decreased BP sensed by JG cells
2. Decreased Na delivery sensed by macula densa
3. Increased sympathetic tone (B1 receptors) (Gs)
232
Where does Angiotensinogen come from?
Liver
233
Effects of AT II
| How does it avoid reflex bradycardia?
Acts at angiotensin II receptor on vascular smooth muscle to cause vasoconstriction and increased BP
It affects baroreceptor function and limits reflex bradycardia which would normally accompany pressor effects
234
What does ADH primarily regulate?
Osmolarity (but also responds to low volume state)
235
What dose Aldosterone primarily regulate?
ECF volume and Na content (but also responds to low volume states)
236
What makes up the Juxtaglomerular apparatus?
```
Mesangial cells
JG cells (modified smooth muscle of afferent arteriole)
Macula densa (NaCl sensor, part of DCT)
```
237
Function of JG cells?
Secrete renin in response to decreased renal BP and increased sympathetic tone
238
Function of macula densa?
Sense decreased NaCl delivery to DCT --> cause adenosine release --> vasoconstriction
239
How do beta blockers decrease BP through the kidney?
They inhibit B1 receptors of the JGA and cause decreased renin release
240
Kidney endocrine functions (4)
1. EPO is released by interstitial cells in peritubular capillary bed in response to hypoxia
2. PCT cells convert 25-OH vitamin D to 1,25-OH2 Vitamin D via 1alpha hydroxylase
3. JG cells secrete renin in response to decreased renal arterial pressure and increased sympathetic tone
4. Paracrine secretion of prostaglandins vasodilator the afferent arterioles to increase RBF
241
What K+ shift does Digitalis cause?
Shifts K+ out of cells causing hyperkalemia (blocks Na/K ATPase)
242
Things causing Hyperkalemia (6)
```
Digitalis
Hyperosmolarity
Lysis of cells (crush injury, rhabdomyolysis, cancer)
Acidosis
Beta blocker
High blood sugar (insulin deficiency)
```
243
Things causing Hypokalemia (4)
Hypo-osmolarity
Alkalosis
Beta adrenergic agonist (increased Na/K ATPase)
Insulin (increased Na/K ATPase; shifts K into cells)
244
Electrolyte disturbance causing tetany, seizures, QT prolongation
HYPOcalcemia
245
Electrolyte disturbance causing stones, bones, groans, thrones, psych overtones
HYPERcalcemia
246
Electrolyte disturbance causing nausea, malaise, stupor, coma seizures
HYPOnatremia
247
Electrolyte disturbance causing U waves on EKG, flattened T waves, arrhythmias, muscle spasm
HYPOkalemia
248
Electrolyte disturbance causing wide QRS and peaked T waves on EKG, arrhythmias, muscle weakness
HYPERkalemia
249
Electrolyte disturbance causing torsade de pointes, tetany, hypokalemia
HYPOmagnesium
250
Causes of respiratory acidosis
Hypoventilation (caused by airway obstruction, acute or chronic lung disease, opioids or sedatives, weakened respiratory muscles)
251
a. Another name for Methanol
| b. Another name for Ethylene glycol
a. Formic acid
| b. Oxalic acid
252
Cause of Normal anion gap metabolic acidosis (HARDASS)
```
Hyperalimentation
Addison disease - hypoaldosteronism
Renal tubular acidosis
Diarrhea - losing bicarbonate
Acetazolamide - not reabsorbing bicarbonate
Spironolactone
Saline infusion
```
253
Flank pain, hematuria, oliguria with high anion gap metabolic acidosis
Ethylene glycol poisoning
254
Cause of distal (type 1) renal tubular acidosis
Defect in ability of alpha intercalated cells to secrete H+ --> can't generate HCO3 --> metabolic acidosis
255
Symptoms of distal (type 1) renal tubular acidosis
Urine pH > 5.5
Hypokalemia
Increased risk for calcium phosphate kidney stones (from increased urine pH and bone turnover)
Normal anion gap metabolic acidosis
256
Cause of Proximal (type 2) renal tubular acidosis
Defect in PCT HCO3 reabsorption --> increased excretion of HCO3 in urine
257
Causes of proximal renal tubular acidosis
Fanconi syndrome
| Carbonic anhydrase inhibitors (Acetazolamide)
258
Cause of hyperkalemic (type 4) renal tubular acidosis
Hypoaldosteronism --> hyperkalemia --> decreased NH3 synthesis in PCT --> decreased NH4 excretion
259
Urine pH in hyperkalemic (type 4) renal tubular acidosis
260
Hematuria but no casts
Bladder cancer or kidney stones
261
Pyuria and no casts
Acute cystitis
262
What do presence of casts signify?
Hematuria/pyuria is of glomerular or renal tubular origin
263
Increased anti-DNase B titers, decreased complement levels
Acute post-strep glomerulonephritis
264
What do crescents consist of in Rapidly progressive glomerulonephritis?
Fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, macrophages
265
Treatment of rapidly progressive glomerulonephritis
Emergent plasmapheresis
266
MPO-ANCA
p-ANCA --> Microscopic polyangiitis
267
Basket weave appearance on EM
Alport syndrome (mutation in type IV collagen --> thinning and splitting of glomerular basement membrane)
268
Stones that precipitate at
a. increased pH
b. decreased pH
a. Calcium phosphate, Ammonium magnesium phosphate (Struvite)
b. Calcium oxalate, Uric acid, Cystine
269
Causes of calcium oxalate stones
Ethylene glycol (antifreeze) ingestion
Vitamin C abuse
Hypocitraturia
Malabsorption (Crohn's)
270
Treatment for calcium oxalate/phosphate stones
Increased citrate
Thiazide diuretics
Hydration
271
Bugs causing struvite stones
Proteus mirabilis
Staph saprophyticus
Klebsiella
(all urease +)
272
How does renal cell carcinoma spread?
Invades renal vein then IVC --> spreads hematogenously and metastasizes to lung and bone
273
Gene deletion associated with Renal cell carcinoma
Gene deletion on chromosome 3 (sporadic or inherited in von Hippel-Lindau)
274
Paraneoplastic syndromes associated with renal cell carcinoma
Ectopic EPO, ACTH, PTHrP
275
Renal oncocytoma histology
Large eosinophilic cells with abundant mitochondria without perinuclear clearing
276
Painless hematuria without casts
Bladder cancer
277
Associations of transitional cell carcinoma of bladder (P SAC)
Phenacetin, Smoking, Aniline dyes, Cyclphosphamide
278
Risk factors for squamous cell carcinoma of bladder
Schistosoma haematobium
Chronic cystitis
Smoking
Chronic nephrolithiasis
279
Lab findings of acute bacterial cystitis
+ leukocyte esterase
| + nitrites (for gram negative organisms)
280
Urethritis with sterile pyuria and negative urine cultures
Neisseria gonorrhoeae or Chlamydia trachomatis
281
Striated parenchymal enhancement of kidney on CT
Acute pyelonephritis
282
Thyroidization of kidney
Chronic pyelonephritis
283
Drugs causing acute interstitial nephritis
```
Diuretics
Penicillins
Proton pump inhibitors
Sulonamides
Rifampin
NSAIDS - (months after for this one)
```
284
Causes of acute tubular necrosis
Ischemic injury or nephrotoxic injury by drugs/crush injury/hemoglobinuria
285
SAAD with papillary necrosis
Sickle cell
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus
286
How do the following affect serum Calcium?
a. Hyperphosphateima
b. Decreased Vitamin D
a. Decreased serum Calcium by causing tissue calcifications
| b. Decreased intestinal Ca absorption
287
Associations of ADPKD
Berry aneurysms
Mitral valve prolapse
Benign hepatic cysts
288
Associated with congenital hepatic fibrosis
ARPKD
289
Shrunken kidneys on ultrasound
| Inability to concentrate urine
Medullary cystic disease
290
What are the types of renal cysts?
| Which ones need to be removed?
Simple - very common, clear on US, typically asymptomatic and found incidentally
Complex - septated, enhanced or have solid components on imaging; require follow up or removal due to risk of RCC
