Renal/GU Flashcards
1
Q
Hypernatremia
A
Na > 145
- usually due to free water loss than sodium gain
2
Q
Hypernatremia: PE/History
A
- presents with THIRST due to hypertonicity
- neuro sx: mental status changes, weakness, focal neuro deficits
- “doughy:” skin
3
Q
Hypernatremic causes “6 D’s”
A
- Diuresis
- Dehydration
- Diabetes insipidus
- Docs (iatrogenic)
- Diarrhea
- Disease ( sickle cell, kidney,)
4
Q
Tx: euvolemic hypernatremia
A
- use hypotonic fluids (e.g. D5W or .45% NaCl)
5
Q
Tx: hypovolemia hypernatremia
A
- D5W
- if vital signs unstable, use 0.9% NaCL before correcting free water deficit
6
Q
Tx: hypervolemia hypernatremia
A
Use diuretics and D5W to remove excess sodium
7
Q
Important key facts to keep in mind during correction of hypernatremia
A
- Chronic hypernatremia (> 36 - 48 hrs) should occur over 48- 72 hrs (<0.5mEq/L/hr to prevent cerebral edema
8
Q
Hyponatremia
A
Na < 135mEq/L
- almost due to increased ADH
9
Q
Hx/PE: hyponatremia
A
- may be asymptomatic or may present with confusion, lethargy, muscle cramps, hyporeflexia, and nausea
- can progress to seizures coma, or brainstem herniation
10
Q
Dx: high osmolality hypernatremia
A
> 295mEq/L
- due to hyperglycemia, hypertonic infusion (e.g mannitol)
11
Q
Dx: normal osmality hyponatremia
A
280-295mEq/L
- caused by hypertriglyceridemia, paraproteinemia (pseudohyponatremia)
12
Q
Dx: low osmolality hyponatremia
A
< 280 mEq/L
- majoriity of cases
13
Q
Tx: hypervolemia hyponatremia
A
- Water resitriction
- consider diuretics
- cortisol replacement w/ adrenal insufficiency
- thyroid replacement w/ hypothyroidism
14
Q
Tx: euvolemia hyponatremia
A
water restriction
15
Q
Tx: hypovolemia hyponatremia
A
replete volume w/ normal saline
16
Q
Complication of correcting hyponatremia too quickly?
A
Central pontine myelinosis
– hyponatremia > 7 hrs should be corrected more than 0.5mEq/L/hr
17
Q
Hyperkalemia
A
> 5mEq/L
18
Q
Spurious hyperkalemia
A
- hemolysis of blood sample
- delays in sample analysis
- extreme leukocytosis or thrombocytosis
19
Q
Hyperkalemia 2/2 to decreased excretion
A
- Renal insufficiency
- Drugs (e.g. spironolactone, triamterene, acodisos, calcineurin)
20
Q
Hyperkalemia 2/2 to cellular shifts
A
- Cell lysis
- Tissue injury (rhabdo)
- Insulin deficiency
Drugs (e.g. succinylcholine, digitalis, B-blockers)
21
Q
Hx/PE: hyperkalemia
A
- may be asymptomatic
- may present w/ nausea, vomiting, intestinal colic, areflexia, weakness
22
Q
Dx: hyperkalemia
A
- confirm w/ repeat blood draw esp in setting of extreme leukocytosia or thrombocytosis
23
Q
- ECG findings: hyperkalemia
A
tall peaked T waves, wide QRS,
PR prolongation
loss of P waves
24
Q
Tx: hyperkalemia
A
C BIG K DROP
- Give calcium gluconate for cardiac cell membrane stabilization
- Give bicarb and/or insulin + glucose to temp shift K into cells
- B-agonists (e.g. albuterol) to promote cellular reuptake of K
- Kayexalate to remove K from body
25
Contraindications to kayexylate (esp for tx of hyperkalemia)
- Ileus
- Bowel obstruction
- Ischemic gut
- Pancreatic transpants
26
Hypokalemia
< 3.5 mEq/L
27
Etiologies of hypokalemia
1. Transcellular shifts (e.g. insulin, B-agonists)
2. GI losses (e.g. diarrhea, laxatives, vomiting)
3. Renal losses (e.g diuretics, hypomagnesemia)
28
ECG findings: hypokalemia
T wave flattening, U waves (additional wave after T wave)
| ST segment depression leading ot AV block and cardiac arrest
29
Tx: hypokalemia
- treat underlying disorder
- Oral and/ IVpotassium repletion
- Don't excess 20mEq/hr
30
Carbonic anhydrase inhibitors: site of action
| e.g acetazolamide
proximal convoluted tubule
31
Carbonic anhydrase inhibitors (e.g acetazolamide): mechanism of action
inhibit carbonic anhydrase
- increase H+ reabsorption
- block Na+/H+ exchange
32
Carbonic anhydrase inhibitors (e.g acetazolamide): side effects
Hyperchloremic metabolic acidosis
| Sulfa allergy
33
Osmotic agents (e.g. mannitol, urea): site of action
entire tubule
34
Osmotic agents: (e.g. mannitol, urea): mechanism of action
increase tubular fluid osmolarit
35
osmotic agents (e.g mannitol, urea): side effects
pulmonary edema due to CHF and anuria
36
Furosemide
- loop diuretic
- inhibits Na/K/2Cl in thick ascending limb loop of Henle
- abolishes hypertonicity of medulla preventing concentration of urine
37
Furosemide: Clinical Use
edematous states (CHF cirrhosis, nephrotic syndrome, pulmonary edema)
- HTN
- Hypercalcemia
38
Furosemide: Side effecs
OH DANG
- Ototoxicity
- Hypokalemia
- Dehydration
- Allergy (sulfa)
- Nephritis (interstinal)
- Gout
39
Ethacrynic acid
- loop diuretic
- inhibits Na/K/2Cl in thick ascending limb loop of Henle
- abolishes hypertonicity in medulla
40
Ethacrynic acid: clinical use
- diuresis in patients allergic to sulfa drugs
41
Ethacrynic acid: toxicity
- can cause hyperuricemia
| * * never use to treat gout
42
Hydrochlorothiazide
- thiazide diuretic
- inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of neuron
- decreases Ca excretion
43
Hypothiazide: clinical use
- HTN
- CHF
- idiopathic hypercalciuria
- nephrogenic insipidus
44
Hydrochlorothiazide: toxicity
Hyper GLUC
- hypokalemic metabolic alkalosis
- hyponatremia
- hyperglycemia
- hyperlipidemia
- hyperuricemmia
- hypercalcemia
45
K sparing diuretics
- spironolactone
- triamterene
- amiloride
46
K sparing diuretics: mechanism
- sprironolactone and epelerone are aldosterone receptor antagonists in the cortical collecting tubules
- triamterene and amiloride block Na channels in CCT
47
K sparing diuretics: clinical use
Hyperaldosteronism
K depletion
CHF
48
K sparing toxicity
Hyperkalemia (can lead to arrhythmias)
| Endocrine effects w/ spironolactone (e.g. gyncecomastia, antiandrogen effects)
49
ACE inhibitors
- captopril, enalapril, lisinopril
50
ACE inhibitors: mechanism
inhibit ACE --> decr. angiotensin II --> decr. GFR by preventing constriction of efferent arterioles
- levels of renin incr due to feedback inhibitor
51
ACE inhibitors: clinical use
```
HTN
CHF
proteinuria
diabetic renal disease
- prevent heart remodeling due to chronic hypertension
```
52
ACE inhibitor toxicity
CATCHH
- Cough
- Angioedema
- Teratogen (fetal renal malformations)
- Creatinine increase (decr. GFR)
- Hyperkalemia
- Hypotension
53
Renal Tubular Acidosis I
- found in distal tubules
- defect in H+ secretion
- hypokalemia
- pH > 5.3
54
Etiology of RTA
- hereditary
- cirrhosis
- autoimmune disorders (e.g. SLE, Sjorgen's syndrome, sickle cells disease)
- Drugs (lithium, amphotericinB
55
RTA I: Treatment
Replace bicarbonaate
56
RTA I: Complications
Nephrolithiasis
57
RTA II
defect in bicarb reabsorption
- low K
initially urine pH is 5.4 , then < 5.3 once serum becomes more acidotic
58
RTA II: Etiologies
```
Hereditary (Fanconi's syndrome or cystinosis)
Drugs (carbonic anhydrase inhibitor)
Multiple myeloma
Amyloidosis
Heavy metal poisoning
Vitamin D deficiency
```
59
RTA II: Treatment
Thiazide
| Volume depletion to increase absorption
60
Complications of RTA: II
Rickets, osteomalacia
61
RTA IV
- in distal tubules
- aldosterone deficiency
- high K
urine pH > 5.3
62
RTA IV: Etiologies
1st aldosterone deficiency
hyporeninemic hypoaldosteronims
(e.g. kidney disease, ACEis, NSAIDS(
Drugs (e.g amilorde
63
Treatment of RTA IV
- Furosemide
| - Mineralcorticoids +/- glucocorticoid replacement
64
Acid Base Disorder: pH < 7.4, pCO2 > 40 mmHG
respiratory acidosis
65
Causes of Respiratory Acidosis
Hypoventilation (retaining CO2)
- Airway obstruction
- Acute lung disease
- Chronic lung disease
- Opioids, narcotics
- Weakening of respiratory muscles
66
Acid Base Disorder: pH < 7.4, pCO2 < 40 mmHg
Metabolic acidosis
| **check anion gap (Na - [K + Cl])
67
Anion gap metabolic acidosis
MUDPILES
- Methanol
- Uremia
- Diabetic ketoacidosis
- Paraldehyde or pheniform
- Iron tablets or INH
- Lactic acidosis
- Ethylene glycol --> kidney stons
- Salicylates
68
Normal anion gap acidosis
```
HARDUP
Hyperalimentation
Acetazolamide use
Renal tubular acidosis
Diarrhea
Uretocolonic fistula
Pancreatic fistula
```
69
Acid Base Disorder: pH >7.4, pCO2 < 40 mm Hg
respiratory alkalosis
70
Causes of respiratory alkalosis
```
Hyperventilation (e.g. high altitude exposure)
Aspiration ingestion (early)
```
71
Acid base disorder: pCO2 > 40 mm Hg
Metabolic alkalosis with compensation (hypoventilation)
- Diuretic use
- Vomiting
- Antacid use
- Hyperaldosteronism
72
Acute Kidney Injury
- defined as abrupt decline in renal fxn
- retention of BUN and Cr
- decreased urine output ( < 500 cc/day)
73
Prerenal AKI
- cause by hypoperfusion
74
Common causes of prerenal AKI
- Hypovolemia
- Sepsis
- Drugs (ACEis, NSAIDS)
- Renal artery stenosis
- De
75
Intrinsic AKI
- injury within nephron unit
76
Common causes of instrinscicAKI
ischemic or nephrotoxic ATN
Allergic interstitial nephritis
Glomerulonephritis
77
Post renal AKI
- urinary outflow obstruciton
78
Common causes of post renal AKI
- prostatic disease
- pelvic tumors
- intratubular causing obstruction
79
Ddx scrotal swelling
- Hydrocele
- Varicocele
- Epididymitis
- Testicular torsion
80
Painless causes of scrotal swelling
- Hydrocele
| - Varicocele
81
Hydrocele
- remnant of processus vaginalis
| - usually asymptomatic, transilluminates
82
Varicocele
- dilation of pampiniform venous plexus ("bag of worms")
- asymptomatic or presents with vague scrotal pain
- affects left testicle more than right
- may disappear in supine position
- DOES NOT TRANSILLUMINATE
83
Hydrocele: Dx
Lab and radiologic workups rarely indicated
| - obtain U/S if concern for inguinal hernia or testicular cancer
84
Epididymitis
- infection of epididymitis, usually for STDs, prostatitis and/or reflux
- affects > 30 y/o
- presents w/ epididymal tenderness
- enlarged testicles, fever, scrotal thickening, erythema, and pyuria
- pain may decrease with elvevation
85
Epididymitis: Dx
- UA, culture (pyuria)
- Culture often shows N. gonorrhoeae, E.coli, or Chlamydia
- Doppler ultrasound shows normal to increased flow to testes
86
Hydrocele: Tx
Typically none unless hernia is present beyond 12-18 mths age
- indicates patent processus vaginalis, which leads to increased risk for inguinal hernia
87
Varicocele: Dx
Ultrasound
88
Varicocele: Tx
- if symptomatic or if testes makes < 40% of total volume, maybe treated surgically w/ a varicocelectomy or ligation or through embolization via IR
89
EpididymitisL Tx
Abx (tetracyclines, fluoroquinolone)
NSAIDS
Scrotal support
90
Testicular torsion
- twisting of spermatic cord, leading to ischemia and possible testicular torsion
91
Testicular torsion:
Typically affects those < 30 y.o
- presents with intense, acute-onset scrotal pain that increases or remains the same w/ scrotal elevation
- pain accompanied by N/V and/or dizxiness
- loss of cremestaric reflex
92
Testicular torsion: dx
Doppler ultrasound shows DECREASED blood flow to testes
| - SURGICAL EMERGENCY
93
Testicular torsion: tx
attempt manual detorsion
- immediate surgery to salvage testis (testis is often unsalvageable after 6 hrs of ischemia)
- orchiopexy of both testes to prevent future torsion
94
BPH
- enlargement of prostate that is normal part of aginge
> 80% of men by 80
- can result in urinary retension, recurrent UTIs, bladder and renal calculi, hydronephrosis and kidney damange
95
BPH: Hx
Obstructive sx: hesitancy, weak stream, urinary retenton
Irritative sx: nocturi, daytime frequency, urge incontinence
- DRE shows uniformly enlarged with rubbery texture
96
BPH: Dx
DRE to screen for masses, if findings are suspicious
Obtain UA and urine culture to r/o infection and hematuria
Measure creatinine levels to r/o obstructive uropathy and renal insufficiency
97
BPH : Treatment
Alpha-blockers (e.g. terasozin) - relax smooth muscles in prostate and bladder neck
5-alpha reductase inhibitors (e.g. finasteride) - inhibit production of DHT
- TURP or open prostatectomy is appropriate for patients
98
Renal Cell Carcinoma
- adenocarcinoma from tubular epithelial cells ( 80-90% malignant tumors of kidney)
- tumors can spread along renal vein to IVC
- can metastasize to lung and bone
99
Risk factors for RCC
- Male gender
- Smoking
- Obesity
- Acquired cystic kidney disease in ESRD
- von Hippel Lindau disease
100
RCC: Hx
- presenting signs: hematuria, flank pain, and palpable mass
- left sided varicocele often seen due to blockage of gonadal vein into left renal vein then into IVC
- anemia is common but may see polycythemia
101
DDx for hematuria
```
I PEE RBCS
Infection (UTI)
Polycystic kidney disease
Exercise
External trauma
Renal glomerular disease
Benign prostatic hyperplasia
Cancer
Stones
```
102
RCC: Dx
Ultrasound and/or CT to characterie renal mass as complex cysts or solid tumor
103
RCC: Treatment
Surgical resection may be curative in localized disease
| Response rate from radiation or chemotherapy are only 15-30%
104
Sx of ARF
- fatigue, nausea and vomiting, anorexia, SOB, menal status changes
105
Signs of ARF
- increased BUN and Cr
- metabolic acidosis
- hyperkalemia
- tachypnea (due to acidosis and hypervolemia)
- hypervolemia (b/l rales on exam, JVD, and dilutional hyponatremia)
106
Three broad categories of renal failure
- Prerenal
- Renal/intrarenal
- Post renal
107
Prerenal failure
- inadequate perfusion to kidney (which is normal)
108
Common cause of prerenal failure
- HYPOTENSION - (SBP < 90 mm Hg) from sepsis, anaphylaxis, bleeding
- HYPOVOLEMIA - diuretics, burns, pancreatitis
- Renal artery stenosis
109
Dx for prerenal failure
- Urinanalysis
- Urine sodium
- Fractional excretion of Na
- Urine osmolality
110
Prerenal failure (in terms of Una and FeNa)
low Una < 20
| low FeNa < 1%
111
Sx of hypovolemia
- tachycardia, weak pulse, decreased fontanelle
112
Postrenal failure
- urine is blocked from excreting at some point beyond the kidneys (ureters, prostate, urethra)
113
Low urine osmolality in healthy persion (no renal issues)
- can be sign of hypervolemia (fluid overload0
114
Urine osmolality in patient with ATN
- inappropriate LOW urine osmolality
| * * patient cannot absorb water b/c of damaged tubule cells**
115
High urine osmolality in healthy person
Signs of dehydration
116
Why should pts with sickle cell trait avoid dehydration?
- Sickle cell patients have defect in concentrating urine due to defect in renal concentrating ability
117
Lab testing for prerenal failure
BUN:Cr > 20
UNa < 20mEq/L
FeNa < 1%
UOsm > 500 mOsm/kg
118
Acute Tubular Necrosis
- injury to kidneys from ischemia and/or toxins resulting in sloughing of tubulr cells in urne
119
Discuss IV contrast and renal failure
- IV contrast can precipitate renal failure esp in diabetics and pts w. renal sdsase
- if must do so, give saline hydration
- may use acetylcysteine before and day of administration
120
Causes of toxin-induced ATN
- Aminoglycoside abx
- Amphotericin
- Cisplatin
- Vancomycin
- Acyclovir
- Cyclosporine
* ** occurs within 5 - 10 days
121
Causes of ATN
- Toxins (e.g. aminoglycosides)
- Contrast media
- Hemoglobin and myoglobin (rhabdomyolysis)
- Hyperuricemia
- Ethylene glycol
- Bence-Jones protein
- NSAIDS
122
Ethylene glycol induced ATN
- caused by precipitation of calcium oxalate in renal cortex
- appears as envelope-shaped crystals
- associated with hypocalcemia
123
Rhabdomyolysis
- caused by trauma
- prolonged immobility
- snake bites, seizures
- crush injuries
124
Best test to diagnosis rhabdomyolysis
URINANALYSIS
125
Lab values associated with rhabdomyolysis
- Urine test positive for myoglobin
- Creatinine phosphokinase (CPK) are elevated
- Hyperkalemia occurs with release K from damaged cells
- Hypocalcemia due to calcium binding to muscle
- Hyperuricemia due to damaged cells releasing nucleaic acids
126
Treatment of rhabdomyolysis
- saline hydration
- mannitol (as osmotic diuretic)
- bicarbonate (to drive potassium back into cells and prevent precipitation from tubtules
127
Prevention of tumor lysis syndrome
Before chemotherapy, give:
- allopurinol
- hydration
- rasburicase
128
Treatment of ATN
- - no therapy proven to benefit ATN
- patients should be managed w/ hydration and correction of electrolyte abnormalities
* *DIURETICS HAVE NO ADDED BENEFIT**
129
Indications for dialysis
AEIOU
- Acidosis
- Electrolyte abnormalities
- Intoxicants
- Overload (volume)
- Uricemia
130
How does furosemide cause ototoxicity?
Furosemide damages hair cells of cochlea resulting in sensoneurial hearing loss
- caused by how fast it is injected
131
Hepatorenal syndrome
renal failure developed secondary to liver disease
| - kidneys are intrinsically normal
132
Sx of hepatorenal syndrome
- severe liver disease (cirrhosis)
- new-onset renal failure w/ no other explanation
- very low urine sodium (< 1%
- elevated BUN:Cr (> 20:1)
133
Tx of hepatorenal syndrome
Midodrine
Octeotride
Albumin
134
Atheroemboli
- cholesterol plaques in aorta or near coronary arteries that are fragile enough that they can be "broken off" when vessels are manipuated during catheter procedures
135
How can atheroemboli cause AKI?
Emboli lodge in kidney
136
PE signs of atheroemboli
- Purplish skin lesions in fingers and toes
- Livedo reticularis
- normal peripheral pulses (artheroemboli too small to occlude radial or brachial artery)
137
Diagnostic tests for atheroemboli
- Eosinophilia
- Low complement levels
- Eosinophiluria
- Elevated ESR
138
Most accurate test for atheroemboli
Biopsy of purplish skin lesions
139
Acute (Allergic) Interstitial Nephritis
- form of ARF that damages tubules on idiopathic basis
| - antibodies and eosinophis attack tubule linings as reaction to drugs
140
Common meds associated with AIN
- Penicillins
- Sulfa drugs (e.g. thiazides and furosemide)
- Phenytoin
- Rifampin
- Quinolones
- PPIs
- Allopurinol
141
Important note about AIN
- Same meds that cause AIN are the same that cause:
- Drug allergy and rash
- Steven-Johnson syndrome
- Toxic epidermal necrolysis
- Hemolysis
142
Common presentation of AIN
- Fever
- Rash
- Arthralgias
- Eosinophilia and eosinophiluria
143
Diagnostic tests for AIN
- Elevated BUN and Cr with ratio < 20
- White and red cells in urine
- Hansel or Wright stain which determines whether eosinophils are present
* * UA can't detect eosinophils
144
Treatment of AIN
Usually resolves spontaneously with stopping the drug or controlling the infection
- Severe is managed with dialysis
- If Cr continues to rise after drug has been stopped, give glucosteroids
145
Analgesic nephropathy presents with?
- ATN from direct toxicity
- AIN
- Membranous glomerulonephritis
- NSAID use
- Papillary necrosis
146
How do NSAIDs cause analgesic nepropathy?
Vascular insufficiency inhibit prostaglandins
- prostaglandins dilate afferent arteriole
- NSAIDS constrict afferent arteriole and decrease renal perfusion
- important in elderly or pts with renal insufficiency
147
Papillary necrosis
- sloughing of renal pappilae
- caused by NSAIDS or sudden vascular insufficiency leading to cell death in papillae
- pts usually have baseline renal damage
- usually see 60 - 70% renal fxn loss before Cr begin to rise
148
History of patients with papillary necrosis
```
- - Look for NSAID use with hx of:
Sickle cell dz OR
Diabetes
Urinary obstruction
Chronic pyelonephritis
```
149
Papillary necrosis: classic presentation
Sudden onset of flank pain
Fever
Hematuria
150
Diagnostic tests for papillary necrosis
- CT scan
- UA that shows red and white cells -- may show necrotic kidney tissue
- Urine cx wlll be normal
151
Best test for papillary necrosis
CT SCAN
| - can show abnormal internal structures of kidney due to loss of papillaw
152
Pyelonephritis
- onset: few days
- symptoms: dysuria
- Positive urine cx
- Swollen kidney on CT
153
Tx of pyelonephritis
Abx such as ampicillin/gentamicin or fluoroquinolones
154
Papillary necrosis
- onset: few hrs
- sx: necrotic material in urine
- Negative urine cs
- Bumpy contour of interior where papillae were loss
155
Tx of papillary necrosis
None
156
Tubular Disease
- usually acute
- caused by toxins (drugs, myoglobin, Hgb)
- none cause nephrotic syndrome
- not treated with steroids
- add'l immunosuppressants are not used
- correct hypoperfusion and remove toxin
157
Glomerular Diseases
- chronic
- not from toxins/drugs
- can cause nephrotic syndrome
- biopsy sample
- often treated with steroids
158
Glomerulonephritis
- UA w/ hematuria
- Dysmorphic red cells (deformed as they squeeze through glomerulus)
- Red cell casts
- Urine sodium and FeNa are low
- Proteinuria
159
Goodpasture Syndrome
- present wit lung and kidney involvement
- NO UPPER RESPIRATORY INVOLVEMENT
- no systemic vasculitis
- no skin, joint, GI, or neuro involvement
160
Diagnostic Test of Goodpasture Syndrome
- antiglomerular basement membrane antibodies
- linear deposits
- most accurate test is kidney or lung biopsy
- anemia is often present due to hemoptysis
161
Tx of Goodpasture's Syndrome
- Plasmapheresis and steroids
| * * cyclophosphamide can be helpful
162
IgA Nephropathy (Berger disease)
- most common cause of glomerulonephritis in US
| - usually Asian pt with recurrent episodes of gross hematuria 1-2 days after URI
163
Diagnosis of IgA Nephropathy
- Kidney biopsy
| - may see increase in IgA levels by 50%
164
IgA Nephropathy
- no treatment proven to reverse disease
- 40 - 50% slowly progress to ESRD
- severe proteinuria treated wtih ACEi's and steroids
165
Postinfectious glomerulonephritis
- commonly caused by Streptococcus but can be caused by any organism
- occurs 1-3 WEEKS after throat infection
166
Postinfectious glomerulonephritis
- Dark (coca cola) urine
- Edema that is periorbital
- Hypertensin
- Oliguria
167
Dx of postinfectious glomerulonephritis
- UA with proteinuria, red cells, and recd cells cases
- ASO titers and anti-DNAse Ab tters
- Biopsy is most accurate but blood tests are sufficiently accurate
168
Tx of postinfectious glomerulonephritis
- antibiotics
| - diuretics to control fluid overload
169
Alport Syndrome
- congenital defect of collagen that results in glomerular disease combined with:
- senorineural hearing loss
- visual disturbance from loss of the collagen fibers that hold the lens of the eye in place
170
Tx of Alport Syndrome
- No specific therapy to reverse defect of type IV collagen
171
Polyarteritis Nodosa
- systemic vasculitis of small/medium sized arteries that affect kidney
- affects nearly every organ except lung
-
172
Polyarteritis Nodosa associated with which diseases
- Hepatitis B
| - PAN should be tested for Hep B
173
Presentation of Polyarteritis Nodisa
- glomerulonephritis
| - nonspecific sx of fever, malaise, weight loss, myalgias, and arthralgia developing over months and weeks
174
GI sx associated with PAN
Abdominal pain, bleeding
| Pain worsened by eating
175
Neuro symptoms associated with PAN
vasculitis damages surrounding peripheral nerves (peroneal, ulnar, radial, and brachial nerve)
- mononeuritis multiplex
- stroke in young person
176
Skin symptoms associated with PAN
- Can cause purpura and petechia
| - can give ulcers, digital gangrene, and livedo reticularis
177
Diagnostic tests associated with PAn
- anemia and leukocytosis
- Elevated ESR and C-reactive protein
- ANCA _ NEGATIVE
- angiography showing aneurysms of renal, mesenteric, or hepatic arter
178
Most accurate test for PAN
Biopsy of symptomatic site such as skin, nerves, or muscles
179
Tx for PAN
Prednisone and cyclophosphamide
| - treat hepatitis when found
180
Lupus nephritis
- SLE can show mild, ansymptomatic proteinuria
| - severe disease presents with membranous glomerulonephritis
181
Most accurate test for lupus nephritis
Biopsy
| - more important to guide therapy for lupus nephritis
182
Tx for lupus nephritis
Severe nephropathy is treated with glucocorticoids combined with cyclophosphamide or mycophenolate
183
Amyloidosis
abnormal protein produced in association w/
- myeloma
- chronic inflammatory disease
- rheumatoid arthritis
184
Renal amyloidosis
primary (plasma cell dyscrasia)
| secondary (infectious or inflammatory) are most common
185
Renal amyloidosis (Hx and PE)
- patients may have multiple myelomaa or chronic inflammatory disease (e.g. rheumatoid arthritis)
186
Renal amyloidosis (Labs/ Histo)
Nodular glomerulosclerosis
- EM reveals amyloid fibrils
- apple green birefringence with Congo red stain
187
Tx of renal amyloidosis
Prednisone and melphalan
| - bone marrow transplant may used for multiple myeloma
188
Membranoproliferative nephropathy
- can also be nephritic
| - Type I : associated with HCV, cryoglobulinemia, SLE, and subacute bacterial endocarditis
189
Membranoproliferative nephropathy: Hx and PE
idiopathic form is present at 8-30 years of age
| - slow progression to renal failure
190
Membranoproliferative nephropathy: Labs and Histo
TRAM TRACK - double layered basement membrane
- Type I: subENDOthelial depositis and mesangial depositis
- all 3 types have low serum C3
- Type II occurs by way of nephritic factor
- IgG leads to constant activation of extrinsic clotting pathway
191
Membranoproliferative nephropathy: Tx
Corticosteroids and cytotoxic agens may help
192
Minimal change disease
- most comon cause of nephrotic syndrome in children
| - idopathic etiology: secondary causes include NSAIDS and hematologic malignancies (e.g. Hodgkins disease)
193
Minimal change disease: Hx and PE
tendency towards infections and thrombotic events
| - sudden onset of edema
194
Minimal change disease: Labs and Histo
light micropscopy appears normal
| - EM shows fusion of epithelial foot processes with lipid containing renal cortices
195
Minimal change disease: Tx
Steroids
| - excellent prognosis
196
Focal Segmental Glomerulosclerosis
-idiopathic, IV drug use, HIV, obesity
197
FSGS: History and PE
typical patient is young African American male with uncontrolled hypertension
198
FSGS: Labs and Histo
microscopic hematuria;
| biopsy shows sclerosis in capillary tufts
199
FSGS: Tx
Prednisone, cytotoxic therapy, ACEis/ ARBs to decrease proteinuria
200
Membranous nephropathy:
most common nephropathy in Caucasian adults
| - secondary causes are solid tumor malignancies, esp in pts > 60 and immune complex disease
201
Membranous nephropathy: History and PE
associated with HBV, syphillis, malaria, and gold
202
Membranous nephropathy: Labs and History
"Spike and dome" appearance due to granular deposits of IgG and C3 at basement membrane
203
Membranous nephropathy: Tx
Prednisone and cytotoxic therapy for severe disease
204
Diabetic nephropathy
has 2 characteristic forms:
| diffuse hyalinization and nodular glomerulosclerosis (Kimmlstiel-Wilson lesions)
205
Diabetic nephropathy: History and PE
Patients generally have long-standing, poorly controlled DM with evidence of retinopathy or neuropathy
- increased GFR is pathological mechanism
206
Diabetic nephropathy: Labs and Histo
Thickened GM
| - increased mesangial matrix --> nodular sclerosis
207
Diabetic nephropathy:
Tight control of sugar
| - ACEis
208
Nephrotic syndrome
- > 3.5 g/dam
- generalized edema
- hypoalbunemia
- hyperlipidemia
- hypercoagulable state
- increased atherosclerosis
209
Nephritic Syndrome Findings
```
"PHAROAH"
P-roteinuria
H- ematuria
A - zotemia
R -BC casts
O - liguria
H - ypertension
```
210
Immune Complex nephritic syndromes
- Postinfectious glomerulosclerosis
| - IgA Nephropathy
211
Post-infectious glomerulonephritis
- classically associaed with recent Group A B- hemolytic streptococcal infection, but can be seen in any infection (usually 2-6 weeks prior)
212
Postinfectious glomerulonephritis: Hx and PE
- oliguria
- edema
- hypertension
- coca-cola urine
213
Postinfectous glomerulonephritis: Labs and Histo
Low serum C3 that normalizes 6-8 weeks after presentation
| - increased ASO titer, lumpy-bumpy immunoflourescence
214
Postinfectous glomerulonephritis: Tx
supportive with diuretics to prevent fluid overload
| - most patients have complete recovery
215
IgA nephropathy
- most common type: typically follows upper respiratory or GI infections
- commonly seen in young males, may be seen in Henoch Schonlein purpura
216
IgA nephropathy: Hx and PE
episodic gross hematuria or persistent microscopic hematuria
217
IgA nephropathy: Labs and Histo
Normal C3
218
IgA nephropathy: Treatment
Glucocorticoids for select patients
ACEis in patients with proteinuria
Some 20% of cases progress to ESRD
219
Pauci-immune nephritic disease
- Wegener's granulomatosis
- Goodpasture's syndrome
- Alport Syndrome
220
Wegener's granulomatosis
- granulomatous infection of the respiratory tract and kidney with necrotizing vasculitis
221
Wegener's granulomatosis: Hx and PE
- Fever, weight loss, hematuria,
- Hearing disturbances
- Repiratory and sinus symptoms
- Cavitary pulmonary lesions bleed and lead to hemoptysis
222
Wegener's granulomatoisis: labs and histo
ANCA positive
| Renal biopy shows segmental necrotizing glomerulonephritis with few immunoglobulin deposits on immunoflourescence
223
Wegener's granulomatosis: Tx
High dose corticosteroids and cytotoxic agents
| Patients tend to have frequent relapses
224
Goodpasture's syndrome
rapidly progressing glomerulonephritis with pulmonary hemorrhage
-peak incidence is in males in their mid 20s
225
Goodpasture's syndrome: hx and pe
hemoptysis, dyspnea, possible respiratory failure
| No upper respiratory tract involvement
226
Goodpasture's syndrome: labs and histo
Linear anti-GBM deposits on immunofluorescence
Iron deficiency anemia
Hemosiderein filled macrophages in sputum
Pulmonary infiltrates on CXR
227
Goodpasture's syndrome: Tx
Plasma exchange therapy
Pulsed steroids
May progress to ESRD
228
Alport's Syndrome
- hereditary glomerulonephritis
| - presents in boys 5-20 years of age
229
Alport's syndrome: Hx and PE
asymptomatic hematuria
| associated with sensoneurial hearring loss and eye disorders
230
Alport's syndrome: Labs and histo
GBM splitting on EM
231
Alport's syndrome: tx
Progresses to renal failure
| anti-GBM nephritis may recur after transplant
232
Drug induced interstitial nephritis
```
Bactrum
Sulfonamides
PCNs
Rifampin
Phenytoin
```
233
Drug induced interstitial nephritis
Arthralgia
| Diffuse maculopapular rash
234
Drug induced interstial nephritis
Eosinophils on UA
| WBC casts
235
Sx of uremia
- Pericardial rub
- Asterixis
- hHypertension
- Decreased urinary output
- Increased respiratory rate
236
Hyaline casts in urine sediment
normal finding
- increased amt suggests volume depletion
- assoc w/ prerenal AKI
237
Red cell casts, dysmorphic red cells in urine sediment
Glomerulonephritis
| - sign of intrinsic AKI
238
White cells, eosinophils in urine sediment
Allergic interstitial nephritis
- atherembolic disease
- sign of intrinsic AKI
239
Granular casts, renal tubular cells, "muddy brown casts" in urine sediment
ATN
| - sign of intrinsic AKI
240
White cells, white cell casts in urine sediment
Pyelonephritis
| - sign of postrenal AKI
241
Hypercalcemia
> 10.2 mg/DL
- most common causes are hyperparathyroidism and malignancy
- use mneumonic CHIMPANZEE
242
Causes of hypercalcemia
CHIMPANZEE
- Calcium supplementation
- Hyperparathyroidism/Hyperthyoridism
- Iatrogenic (e.g. thiazides, parental nutrition)/ Immobility (esp in ICU setting)
- Milk-alkali syndrome
- Paget's disease
- Adrenal insufficiency/Acromegaly
- Neoplasm
- Zollinger-Ellison (e.g. MEN I)
- Excess Vitamin A
- Escess Vitamin D
- Sarcoidosis adn other granulomatous disease
243
Hypercalcemia: PE and Hx
```
Asymptomatic but may present with:
Bones (osteopenia, fractures)
Stones (kidney stones)
Groans (anorexia, constipation)
Psychiatric overtones (weakness, fatigue, altered mental status)
```
244
Hypercalcemia: Diagnosis
- Order Ca
- Order Albumin, phosphate, PTH, PTHrP, Vit D, and ECG
-
245
Hypercalcemia finding on ECG
short QT interval
246
Hypercalcemia: Tx
IV hydration followed by furosemide to increase calcium excretion
- AVOID THIAZIDES which can increase absorption of Ca
247
Discuss digitalis and hypokalemia
- digitialis and K fight for same site on Na/K pump so hypokalemia sensitizes patient to digitalis
248
Monosymptomatic enuresis
urinary incontinence in children > 5
249
Management of monosymptomatic enuresis
FIRST LINE: BEHAVIOR MODIFICATION
- avoid sugary drinks
- void regularly during day and immediately before bedtime
- drink ample fluid in morning & early afternoon
Pharm therapy
1st line: desmopression
2nd line: TCA
250
1st line pharm therapy in monosymptomatic enuresis
Desmopression
251
Best test for suspected BPH
Abdominal U/S to check for obstruction
252
Calcium oxalate/calcium phosphate
- most common type of renal stone
| - MCCs: idiopathic hypercalcuria and hyperparathyroidsm
253
Tx of calcium oxalate/calcium phosphate
Hydration, Dietary sodium and protein restriction, Thiazide diuretics
- DO NOT DECREASE CA INTAKE
- alkaline urine
- radiopaque
254
Struvite renal stones
```
associated w/ urease producing organisms (e.g Proteus)
form STAGHORN CALCULI
alkaline urine
radiopaque
- alkaline urine
```
255
Tx of struvite renal stones
Hydration
treat UT if present
surgical removal of staghorn stone
256
Uric acid stones
```
associated with gout, xanthine oxidase deficiency and high purine turnover rate (e.g. chemotherapy)
acidic urine (pH < 5.5)
RADIOLUCENT on plain film but detectable on CT
```
257
Tx of uric acid stones
Hydration
| Alkalinize urine w/ citrate with is converted to HCO in liver
258
Cystine renal stone
due to defect in renal transport of certain amino acids (COLA - cysteine, ornithine, lysine, and argine)
259
Dx of cystine renal stone
- HEXAGONAL CRYSTALS
| - POSITIVE CYANIDE NITROPRUSSIDE TEST
260
Tx of cystine renal stone
Hydration
Dietary sodium restriction
Alkalinization of urine
Penicillamine
261
Nephrolithiasis: Hx and PE
acute onset of severe, colicky flank pain that may radiate to testes or vulva
- associated w/ nausea and vomtng
- patient unable toget comfortable and shifts position frequently
262
Best test for nephrolithiasis
Non contrast CT for diagnosis of kidney stones
263
U/A for kidney stones
Microhematuria and altered urine PH
264
Best diagnostic modality for suspected kidney stones in children and pregnant women
Ultrasound
265
Tx for renal stones
Hydration and analgesia are intiail streatment
Stones < 5mm can pass spontaneously
Stones > 5mm but < 3cm can be treatmed with ESWL
266
AD Polycystic kidney disease
- usually asymptomatic until > 30 years
| - associated with increased risk of cerebral aneurtyrm esp in patients w/ positive family hx
267
Polycystic kidney disease: History and PE
- Pain and hematuria are most common symmptoms
| - Large palpable kidneys
268
Dx of Polycystic kidney disease
CT scan
| -wlll show multiple bilateral cysts through renal parenchy
269
Tx of polycystic kidney disease
prevent complications and decrease rate of progression of ESRD
- early mgmt of UTIs
- BP control (ACEis and ARBs)
270
Hydronephrosis
dilation of renal calcyces
| - usually secondary to obstruction of urinary tract
271
Hx and PE: Hydronephrosis
- may be asymptomatic
- may present w/ flank/back pain
- decreased urine output
- abdominal pain and UTiS
272
Dx of Hydronephrotis
- ULTRASOUND (first line) to detect dilitation of renal calyces or ureter
- can use CT scan
273
Tx of hydronephrosis
surgically tx anatomic obstruction
274
Complications of untreated hydronephrosis
- Urinary obstruction leading to HTN, acute or chronic renal failure
Sepsis
275
Vesiculoureteral reflux
- retrograde projection of urine from bladdder to ureteres and kidney
- may be due to posterior urethral valves, urethral or meatal stenosi
276
Hx and PE: of vesiculouretal reflux
patient present with recurrent UTIs, typically in childhood
277
Dx: of vesiculourethral reflux
Voiding cystogram (VCUG) to detect abnormalities at ureteral insert sites and identify grade of reflx
278
Tx of vesiculourethral reflux
- Treat infxns aggressively. Mild reflux with prophylactiv abx (amoxicillin < 2 mths or bactrim or nitrofurantoin)
- Surgery (urereteral reimplantation) reserved for children with high grade reflux
279
Complication of vesiculourethral reflux
- Progressive renal scarring and ESRD
280
Cryptochordism
- failure of 1 or both testes to descent into scrotum
| - LOW BIRTH WEIGHT IS A RISK FACTOR
281
History and PE: cryptochordism
Bilateral cryptochordism associated w prematurity, oligospermia, congenital malformation syndromes (Prader-Willi, Noonan) and infertility)
- associated w increased risk of testicular malignancy
282
Dx: cryptochordism
testes can't be manipuated into scrotal sac with gentle pressure
- may be palpable anywhere along inguinal canal or in abdomen
283
Tx: cryptochordism
Orchiopexy by 6-12 months of age (most testes will spontaneously descend by 3 months)
- treat w/ orchiectomy to avoid testicular cancer
