Nephrology - MTB Flashcards
(323 cards)
1
Q
Best initial test in nephrology
A
- Urinalysis
- BUN/ Cr
2
Q
Urinalysis measurements
A
- Protein
- WBC
- Red cells
- Specific gravity and pH
- Nitrites
3
Q
Severe proteinuria
A
- means glomerular damage
4
Q
Tamm-Horsfall protein
A
- tubules secrete slight amounts of protein
- less than 30 - 50 mg per 24 hrs
5
Q
If there is persistent proteinuria
A
- not related to prolonged standing (orthostatic proteinuria), a kidney biopsy should be performed
6
Q
Activities that increase urinary protein excretion
A
- Standing
- Physical activity
7
Q
Normal protein per 24 hrs
A
< 300 mg
8
Q
Assess proteinuria
A
- UA is the intial test
- Protein to creatinine ration is more accurate at determining the amount
9
Q
Protein to creatinine ratio
A
1 is equivalent to one gram of protein on a 24 hr
10
Q
Protein: creatinine ratio vs 24 hr urine
A
Protein: creatinine ratio can be superior in accuracy
11
Q
Microalbunemia
A
- tiny amount of protein that is too small to detect on UA
- long term microalbinuria leads to worsening renal function in a diabetic patient should be treatment
12
Q
Microalbunemia
A
- 30 - 300 mg/24 hrs
13
Q
Diabetic patient is evaluated with a UA that shows no protein. Microalbuminuria is detected (level btwn 30 and 300 mg per 24 hrs). Next best step?
A
ACE inhibitors or angiotension receptor blocker
- best initial therapy for any degree of proteinuria in a diabetic patient
14
Q
Is Bence-Jones protein in myeloma detectable on dipstick?
A
No. Use Immunoelectrophoresis
15
Q
White blood cells on UA
A
- detect inflamation, infection, and allergic interstitial nephritis
16
Q
Eosinophils
A
- indicate allergic or acute intersitial nephritiris
17
Q
Detecting eosinophils in the urine
A
Wright and Hansel stains
- allergic intersitial nephritis
-
18
Q
Hematuria
A
= / > 5 RBCs per high power field
- stones in bladder, ureter, or kidney
- hematologic disorders that cause bleeding (coagulopathy)
- infection (cystitis, pyelonephritis)
- cancer of bladder, ureters, or kidney
- tx ( cyclophosphamide gives hemorrhagic cysts)
- trauma
- glomerulonephritis
19
Q
Ig A nephropathy
A
common for mild recurrent hematuria
20
Q
Reason for false positive tests for hematuria
A
- Hemoglobin OR
- myoglobin
21
Q
Woman is admitted to the hospital with trauma and dark urine. The dipstick is markedly positive for blood. Best initial test to conform the etiology?
A
Microscopic exam of the urine
22
Q
Why is intravenous pyelogram is always wrong on boards?
A
- Slower and the contrast is renal toxic
23
Q
When is dysmorphic red cells?
A
Glomerulonephritis
24
Q
If the patient has hematuria without infection or prior trauma but
- Renal U/S or CT doesn’t show etiology
- Bladder shows mass for possible biopsy
Next step?
A
Cystoscopy
25
Most accurate test of the bladder
Cystoscopy
26
Red cell casts in UA
Glomerulonephritis
27
White cell casts in UA
Pyelonephritis
28
Eosinophils casts in UA
Acute (allergic) interstitial nephritis
29
Hyaline casts in UA
Dehydration concentrates the urine and the normal Tamm-Horsfall protein precipitaes or concentrates into a cast
30
Waxy casts in UA
Chronic renal disease
31
Granular "muddy-brown" casts on UA
Acute tubular necrosis
| - they are collections of dead tubular cells
32
Acute Kidney Injury
- formerly called acute renal failure
| - decrease in creatinine clearance resulting in a sudden rise in BUN and creatinine
33
Three different types of AKI
- Prerenal azotemia (decreased perfusion)
- Postrenal azotemia (obstruction)
- Intrinsic renal disease (ischemia and toxins)
34
Prerenal azotemia
- due to inadequate perfusion of the kidney when kidney is normal
- hypotension
- hypovolemia
- renal artery stenosis
35
NSAIDS on afferent arteriole
- constrict the afferent arteriole
36
ACE inhibitors on efferent arteriole
- cause efferent arteriole vasodilation
37
Postrenal azotemia
- obstruction of any cause damages the kidney by blocking filtration at the glomerulus
38
Causes of postrenal azotemia
- PROSTATE HYPERTROPHY or cancer
- STONE in the ureter
- Cervical CANCER
- Urethral CANCER
- Neurogenic (atonic) bladder
- Retroperitoneal FIBROSIS
39
Causes of retroperitoneal fibrosis
- Bleomycin
- Methylsergide
- Radiation
40
Most common cause of intrinsic renal disease
Acute tubular necrosis
| - from toxins and prolonged ischemia of the kidney
41
Other causes of intrinsic renal disease
- Acute (allergic) interstitial nephritis
- Rhabdomyolysis and hemoglobinuria
- Contrast agents, aminoglycosides, cisplatin,
- Crystals such as hyperuricemia, hypercalcemia
- Bence-Jones protein from myeloma
- Poststreptococcal infection
42
Clinical presentation of intrinsic renal disease
- Nausea and vomiting
- Tired/malaise
- Weak
- Short of breath and edema from fluid overload
43
Clinical presentation of severe intrinsic renal disease
- Arrhythmia from hyperkalemia and acidosis
| - Sharp, pleuritic chest pain from PERICARDITIS
44
Clinical presentation of postrenal azotemia
- Enlargement (distention) of the bladder
| - Massive diuresis after urinary catheter
45
Best initial test for acute kidney injury
- BUN : Cr
46
Prerenal azotemia
- BUN:CR > 20:1
| - Clear hx of hypoperfusion and hypotension
47
Postrenal azotemia
- BUN:Cr > 20:1
- Distended bladder or massive release of urine with catheter placement AND bilateral or unilateral HYDRONEPHROSIS on U/S
48
Intrinsic renal disease
- BUN: Cr < 10:1
49
When is kidney biopsy the answer for AKI?
Never
50
Tests for AKI of unclear etiology
1. Urinanalysis
2. Urine sodium
3. Fractional excretion of sodium
4. Urine osmolality
51
Best test for AKI of unclear etiology
Urinalysis
52
Increased urine osmolality
- when intravascular volume is low, normally ADH levels should rise
- healthy kidney will reabsorb more water to fill vascularture
- increased water reabsorption leads to an increase in urine osmlolality -- more concentrated urine
53
Isosothenuria (same osmolality to the blood ~ 300 mOsm/L) or Low urine osmolality
- During ATN, the urine cannot be concentrated because the tubules cells are damaged
54
Urine osmolality: Healthy person with fluid overload
Low urine osmolality or dilute urine
55
Urine osmolality: Health person with dehydration
High urine osmolality or concentrated urine
56
20 y/o African American man comes for a screening test for sickle cell. He is found to be heterozygous (trait or AS) for sickle. Best advice for him?
Avoid dehydration
| - sickle cell trait in renal concentrating ability or isosthenuria
57
Prerenal azotemia
- BUN:Cr > 20:1
- Urine Na < 20mEq/L
- Fractional excretion of sodium: < 1%
- Urine osmolality: > 500 mOsm/kg
58
Acute tubular necrosis
- BUN: Cr < 20: 1
- Urine Na > 20mEq/L
- Fractional excretion of sodium: >1%
- Urine osmolality: < 300mOsm/kg
59
Acute Tubular Necrosis
- an injury to the kidneys from ischemia and/or toxins resulting sloughing off of tubular cells into the urine
- Sodium and water reabsorptive mechanisms are lost with the tubular cells
- Proteinuria is not significant since protein, not tubule, spills into the urine
60
Urine specific gravity correlates to urine osmolality
- High UOsm = high specific gravity
61
Pt has acute renal failure and a toxin. What is the most likely diagnosis?
Acute Tubular Necrosis
62
Pt comes with fever and acute, left lower quadrant abdominal pain. Blood cx on admission grow E.coli and Candida albicans She is started on vancomycin, metronidazole, and gentamicin, and amphotericin. She has a CT scan that identifies diverticulitis. After 36 hrs, her creatinine rises dramatically. Most likely cause of her renal insufficiency?
Contrast media
| - rapid onset of injury
63
Timeline for nephrotoxic drugs
Drugs (e.g. vancomycin, gentamicin, and amphotericin)
are nephrotoxic
- usually takes 5 to 10 days to result in nephrotoxicity
64
74 y/o blind man is admited with obstructive uropathy and chest pain. He has a hx of hypertension and diabetes. His creatinine drops from 10mg/dL to 1.2 mg/dL 3 days ater catheter placement. The stress test show reversible ischemia. Most appropriate management?
Saline hydration is has the most proven benefit at prevent contrast-induced nephrotoxicity
65
Pt with mild renal insufficiency undergoes angiograpy and develops 2mg/dL rise in creatinine from ATN despite the use of saline hydration before and after the procedure. What do you expect to find on lab testing?
Urine sodium 5 (very low), FENA
66
Pt with extremely severe myeloma with a plasmacytoma is admitted for combination chemotherapy. Two days later, the creatinine rises. Most likely cause?
Hyperuricemia
- most likely from tumor lysis syndrome
- cisplatin (drug toxicities) would not produce RISE in CREATININE In 5-10 days
67
Prevention of tumor lysis syndrome
- Allopurinol, hydration, and rasburicase should be given prior to chemotherapy to prevent renal failure from tumor lysis sndrome
68
Pt who is suicidal ingests an unknown substance and develops renal failure 3 days later. Her calcium level is also low and the urinalysis shows an abnormality. What did she take?
Ethylene glycol
- AKI based on oxalic avid and oxalate precipitating within the kidney tubules cause ATN
- envelope shaped crystals
69
Drug-induced ATN
- nonoliguric renal injury caused by aminoglycosides, amphotericin, cisplatin, vancomycin, acyclovir, and cyclosporine
- slower onset: FIVE to TEN days
- dose dependent
70
What electrolyte deficiency predisposes someone to drug-induced aminoglycosides?
Low magnesium levels
| - may increase risk of aminoglycosides or cisplatin toxicity
71
Contrast media nephrotoxicity
- can cause immediate renal toxicity
- prevented with saline hydration
- n-acetylcysteine and sodiu bincarbonate proven beneficial
72
Rhabdomyolysis
- caused by TRAUMA, prolonged IMMOBILITY, snake bites, seizures, and CRUSH INJURIES
- best initial test to confirm UA
73
Hyperuricemia
- ATN
- usually from tumor lysis syndrome
- long standing hyperuricemia from gout can cause chronic renal failure
74
Best initial to confirm the diagnosis of rhabdomyolysis
UA
| - positive only on dipstick for large amounts of blood, but no cells will be seen on microscopic examination
75
Reasons for false positive urine dipstick
Urine dipstick can't tell the difference between:
- Hemoglobin
- Myoglobin
- Red blood cells
76
Bence Jones protein
- directly toxic to renal tubules
77
Rhabdomyolysis: lab findings
- ELEVATED CPK - lets you know "hematuria" is myoglobin
- HYPERKALEMIA due to release of K from damaged cells
- HYPERURICEMIA due to degradation of nucleic acid from damaged cells
- HYPOCALCEMIA due to increased calcium binding to damaged muscle
78
Rhabdomyolysis: treatment
- SALINE HYDRATION
- MANNITOL as an osmotic diuretic
- BICARBONATE which drives K back into cells and prevent precipitation of myoglobin
79
Do you treat hypocalcemia in rhabdomyolysis?
No, if patient is asymptomatic.
| - in recovery, the calcium will come back out of muscles
80
A man comes to ED after a triathlon, followed by status epilepticus. He takes simvastatin at triple the recommended dose. His muscles are tender and the urine is dark. IV fluids are started . What is the next step?
EKG
- to detect life threatening hyperkalemia
* * potassium replacement in a person with rhabdomyolysis would be fatal**
81
Rhabdomyolysis proven to benefit ATN
- No therapy proven to benefit ATN
| - diuretics increase urine output, but do not change overall outcome
82
Wrong answers for treatment of ATN
- Low-dose dopamine
- Diuretics
- Mannitol
- Steroids
83
Indications for dialysis
- Fluid overload
- Encephalopathy
- Pericarditis
- Metabolic acidosis
- Hyperkalemia
84
BUN:Cr indications for dilaysis
- No specific level of BUN:Cr
| - based on development of life threatening conditions
85
Hypocalcemia symtpoms
- Seizures
| - prolonged QT interval leading to arrhythmia
86
Patient develops from ATN from gentamicin. She is vigorously hydrated and treated with high doses of diuretic, low dose dopamine, and calcium acetate as a phosphate binder. Urine output increases but she still progresses to end-stage renal failure. She also becomes deaf. What causes her hearing loss?
Furosemide
| - causes ototoxicity by damaging the hair cells of the cochlea, resulting in sensorineural hearing loss
87
Hepatorenal syndrome
renal failure developing secondary to liver disease
| - kidneys are intrinsically neural
88
Hepatorenal syndrome: Hx and PE
- severe liver disease (CIRRHOSIS)
- new-onset renal failure w/ no other explanation
- VERY LOW URINE NA (less than 10 - 15 mEq/L)
- FENA < 1%
- ELEVATED BUN:Cr > 20:1
89
Hepatorenal syndrome: Treatment
- Midodrine
- Octreotide
- Albumin (albumin is less clear)
90
Atheroemboli: Etiology
- CHOLESTEROL PLAQUES found in aorta and/or coronary arteries can be "broken off" manipulated during catheter procedures
- CHOLESTEROL EMBOLI lodged in kidney causes AKI
- BLUE/PURPLISH SKIN LESIONS in fingers and toes, LIVEDO RETICULARIS and ocular lesions
91
Peripheral pulses in atheroemboli
- cholesterol plaques are too small to occlude vessels such as the radial or brachial artery
92
Atheroemboli: diagnostic tests
- Eosinophilia
- Low complement levels
- Eosinophiluria
- Elevated ESR
93
Most accurate diagnostic test for atheroemboli?
- Biopsy of one purplish skin lesions
- cholesterol crystals, but this result does not change management b/c there is no specific therapy to reverse atheroembolci disease
94
Acute (Allergic ) Interstitial Nephritis
- is a form acute renal failure that damages the tubules occurring on idiopathic issues
- antibodies and EOSINOPHILS ATTACK THE CELLS LINING THE TUBULES as a rxn to the drugs (70%), infxn, and autoimmune disorders
95
Most common cause of acute (allergic) interstitial nephritis
- PENICILLINS and cephalosporin
- SULFA DRUGS
- Phenytoin
- Rifampin
- Quinolones
- Allopurinol
- Proton Pump Inhibitors
96
Medications that cause AIN are that same as those cause:
- Drug allergy and rash
- Stevens-Johnson syndrome
- Toxic epidermal necrolysis
- Hemolysis
97
Acute (Allergic) Interstitial Nephritis: Clinical Presentation
- FEVER (80%)
- RASH (50%)
- Arthralgias
- Eosinophilia and EOSINOPHILURIA (80%)
98
Aside from drugs, other causes of AIN
Autoimmune diseases (e.g. SLE, Sjorgen, and sarcoidosis)
99
AIN Diagnostic Tests
- Elevated BUN: CR < 20:1
| - White and red cells in the urine
100
Most accurate test for acute (allergic) interstitial nephritis
- Hansel or Wright stain determines whether eosinophils are present
101
Acute interstitial nephritis: treatment
AIN usually resolves spontaneously w/ stopping the drug or controlling the infection
102
Analgesic Nephropathy
- ATN from direct toxicity to the tubules
- AIN
- MEMBRANOUS GLOMERULONEPHRITIS
- VASCULAR INSUFFICIENCY
- PAPILLARY NECROSIS
103
Vascular insufficiency induced analgesic nephropathy
- INHIBIT PROSTAGLANDINS
| - NSAIDS inhibit prostaglandins to constrict afferent arteriole and decrease renal perfusion
104
Papillary necrosis
- sloughing off of the renal papillae
| - caused by toxins such as NSAIDS, or sudden vascular insufficiency leadingot death of cells in the pappillaw
105
Papillary necrosis: Hx and PE
- patient loses 60 - 70% renal function before the creatinine even begins to rise
- Look for extra NSAID use with a hx of:
- SICKLE CELL DISEASE
- Diabetes
- Urinary obstruction
- Chronic pyelonephritis
106
Papillary necrosis: Clinical presentation
- sudden onset of flank pain, fever, and hematuria in a patient with one of the diseae perviously list
107
Best initial test for suspected papillary necrosis
Urinanalysis
| - grossly visible NECROTIC MATERIAL passed IN THE URINE
108
Most accurate test for papillary necrosis
CT scan
| - shows the abnormal internal structures of the kidney from the loss of the papillae
109
Papillary Necrosis: Treatment
No specific therapy
110
Pyelonephritis
- onset in a few days
- Sx: dysuria
- Urine cx: positive
111
CT findings of pyelonephritis
Diffusely swollen kidney
112
Pyelonephritis: Treatment
Antibiotics
| - such as ampicillin/gentamicin or fluoroquinolones
113
Papillary necrosis
- onset in a few hours
- necrotic material in urine
- negative urine culture
114
Papillary necrosis: treatment
No treatment
115
Tubular Disease: Overview
- Acute
- Toxins
- None nephrotic
- No biopsy usually
- No steroids
- Never additional immunosuppressive agents
116
Tubular Disease: Treatment
- Correcting HYPOPERFUSION and REMOVING TOXIN
117
Glomerular Diseases
- generally chronic
- not caused by toxins or hypoperfusion
- all of them can cause nephrotic syndrome
- biopsy indicated
- treated with steroids
- additional immunosuppresive medications
118
Most accurate diagnostic test for glomerular disease
- Steroids
119
Main difference between glomerulonephritis and nephrotic syndrome
Degree or AMOUNT of proteinuria
120
Diagnostic tests for glomerulonephritis
- UA with HEMATURIA
- "DYSMORPHIC" red cells
- RED CELL CASTS
- Urine sodium and FENA are low
- PROTEINURIA
121
Goodpasture Syndrome
- presents with LUNG AND KIDNEY involvement
- no UPPER RESPIRATORY TRACT INVOLVEMENT
- no skin, joint, GI, eye, or neurological involvement
122
Best initial test for Goodpasture Syndrome
- Antiglomerular basement membrane antibodies
123
Most ACCURATE test for Goodpasture Syndrome
- Lung or kidney biopsy with "LINEAR DEPOSITS"
| - anemia is often present from chronic blood loss from hemoptysis
124
Goodpasture Syndrome: Treatment
- Plasmapheresis and steroids
125
IgA Nephropathy
- most common cause of acute glomerulonephritis in US
- look for Asian patient w/ recurrent epsiodes of gross hematuria 1 - 2 days after upper respiratory tract infxn
- poststreptococcal glomerulonephritis follows pharyngitis by 1 -2 weeks
126
Most accurate test for IgA nephropathy
Kidney biopsy
| ** IgA levels are increased in 50%**
127
Proteinuria and progression of disease
More proteinuria = worse progression
128
IgA Nephropathy
- no treatment proven to reverse the disease
| - severe proteinuria is treated with ACE inhibitors and steroids
129
Postinfectious Glomerulonephritis
- most common organism leading to infectious glomerulonephritis is Streptococcus
- follows throat infectiou or skin infection (impetigo) by 1 to 3 weeks
130
Postinfectious Glomerulonephritis: Clinical Presentation
Patients present with:
- dark (cola-colored) urine
- periorbital edema
- hypertension
- oliguria
131
Postinfectious Glomerulonephritis: Diagnostic Tests
UA with proteinuria, red cells, red cell casts
| - low complement
132
Pt had infection 2 weeks ago and is c/o dark urine, facial edema, and oliguria. Next step?
ASO titers and anti-DNAse antibod
133
Most accurate test for postinfectious glomerulonephritis
Kidney biopsy
134
Postinfectious glomerulonephritis: Treatment
Supportive treatment such as:
- antibiotics
- diuretics to control fluid overload
135
Alport Syndrome
congenital defect of type I collagen that results in glomerular disease combined with:
- sensorineural hearing loss
- visual disturbance from loss of the collagen fibers that hold lens of eye in place
136
Alport Syndrome: Treatment
No specific therapy to reverse defect
137
Polyarteritis Nodosa
systemic vasculitis of small and medium sized arteries that commonly affect kiney
- SPARES THE LUNG
- ASSOCIATED WITH HEPATITIS B
138
Why do patients with PAN have neuropathy?
Damage to small blood vessels around nerves starve them into neuropathy
139
Polyarteritis Nodosa: Clinical Presentation
Nonspecific symptoms of: fever, malaise, weight loss, mya;gias, and arthralgia
GI: abdominal pain, pain worsened by eating due to mesenteric ischemia
Neurologic: "mononeuritis multiplex" when damage occurs around large peripheral nerve (brachial, radial, ulnar)
Skin: purpura (large), petechiae (small), digital gangrene, livedo reticularis
140
Young patient has a stroke or MI.
Think vasculitis
| - PAN
141
Polyarteritis Nodosa: Diagnostic Tests
Blood tests will show:
- anemia and leukocytosis
- elevated ESR and C-protein
- ANCA NEGATIVE
- ANA and rheumatoid
Angiography
142
Best diagnostic for polyarteritis nodosa
ANGIOGRAPHY of the renal, mesenteric, or hepatic artery showing aneurysmal dilation in association with new-onset w/ HTN
143
Most accurate test for polyarteritis nodosa
Biopsy
144
POlyarteritis Nodosa: Treatment
Prednisone
Cyclophosphamide
- treat Hep B when found
145
Lupus Nephritis
- SLE can give any degree of renal involvement
can present with normal or mild proteinuria
- severe disease presents with membranous glomerulonephritis
146
Most accurate test for lupus nephritis
Biopsy
- will show glomerulosclerosis which has no active inflammatory component
- helps determine therapy based on stage
147
Lupus Nephritis: Treatment
Glucocorticoids combined with either cyclophosphamide or mycophenolate
148
Which conditions give LARGE kidneys on sonogram or CT scan?
- Amyloid
- HIV
- Nephropathy
- Polycystic kidneys
149
Amyloidosis
Abnormal protein produced in association with:
- myeloma
- chronic inflammatory diseases
- rheumatoid arthritis
- inflammatory bowel disease
- chronic infections
150
Most accurate test for amyloidosis
Biopsy
| - show green birefringerence with Congo red staining
151
Amyloidosis: Treatment
Melphalan and prednisone
152
Nephrotic Syndrome
- measure of the severity of proteinuria in association with glomerular disease
- Massive proteinuria leads to:
- edema
- hyperlipidemia
- thrombosis: urinary anticoagulants protein C, protein S, and antithrombin
153
Nephrotic Syndrome: Etiology
Diabetes and HTN are most common causes of nephrotic syndrome
154
Nephrotic Syndrome associated with cancer (solid organ)
Membranous
155
Nephrotic syndrome associated with children
Minimal change disease
156
Nephrotic syndrome associated with drug use and AIDS
Focal segmental
157
Nephrotic syndrome associated with SLE
All types of nephrotic syndrome
158
Major difference between nephritic syndrome and nephrotic syndrome
Amount of proteinuria
159
Nephrotic syndrome: clinical presentation
Generalized edema
160
Why are infections more common with nephrotic syndrome?
Increased urinary loss of immunoglobulins and complement
161
Why are patients more clot prone with nephrotic syndrome?
Loss of antithrombin, protein C, and protein S
162
Best initial test for suspected nephrotic syndrome?
Urinalysis
| - wil show Maltese crosses, which are lipid deposits from sloughed off tubular cells
163
Urine albumin/creatinine ration
- measure of the average protein produced over 24 hrs
| - ratio of 2:1 means 2 grams of protein excreted over 24 hrs
164
Most accurate test to detect nephrotic syndrome
Renal biopsy
165
Nephrotic Syndrome: definition
Hyperproteinuria (> 3.5 g per 24 hrs)
Hypoproteinemia
Hyperlipidemia
Edema
166
Best initial therapy for nephrotic syndrome
Glucocorticoids
| - if no response after several weeks, immunosuppresive meds such as cyclophosphamide
167
How are ACE inhibitors and ARBs used in nephrotic syndrome?
Try to control proteinuria
168
How is edema managed in nephrotic syndrome
Salt restriction and diuretics
169
How is hyperlipidema managed in nephrotic syndrome
Statis
170
End Stage Renal Disease
- kidney failure so sever as to need dialysis
| - no defined as a particular BUN or creatiinine
171
Most common cause of end stage renal disease
Diabetes
| Hypertension
172
ESRD: Clinical Presentation
Uremia in the presence of:
- metabolic acidosis
- fluid overload
- encephalopathy
- hyperkalemia
- pericarditis
173
Manifestations of Renal Failure
- Anemia
- Hypocalcemia and osteomalacia
- Bleeding
- Pruritis
- Hypoerphosphatemi
- Hypermagnemias
- Atherosclerosis
- Endocrinopathy
174
Renal Failure: Anemia
- loss of erythropoietin leads to monochromic anemia
| - treat with erythropoietin and Fe supplements
175
Renal Failure: hypocalcemia
- less active 25- hydroxy-vitamin D into the much more active 1,25 dihydroxy vitamin D
- without 1,25 dihydroxy form of vitamin D, body will not absorb enough Ca from gut
- treat with vitamin D and calcium
176
Renal Failure: osteodystrophy
Low calcium leads to secondary hyperparathyroidism
| - high parathyroid levels remove Ca from bones, making them soft and week
177
Bleeding 2/2 bleeding
Platelets do not work normally in uremic enviroment
| - treat with DDVAP increases platelet function; use only when bleeding
178
Infection 2/2 renal failure
Neutrophils do not work because they cannot degranulate
179
Pruritis 2/2 renal failure
Urea accumulating in skin causes itching
| - treat with dialysis and UV light
180
Hyperphosphatemia 2/2 renal failure
Phosphate normally excreted throgh kidneys. High parathyroid levels release phosophate from bones, but body is unable to excrete
- treat with oral binders
181
Hypermagnesmemia 2/2 renal failure
- loss of excretory ability
| - treat with high Mg foods, laxatives, and antacids
182
Accelerated atherosclerosis and hypertension 2/2 renal failure
Immune system keeps artery clear of lipid acculiaton
WBCs dont work in uriemic environment - common cause of death in dialysis patients
- treat with dialysis
183
Endocrinopathy 2/2 renal failure
Women are anovulatory and men have low testosterone
| - treat with dialysis, estrogen (women ) and testosterone (men ) replacement
184
Erectile dysfunction 2/2 renal failure
Insulin level tend to go up because insulin is excreted renally Insulin resistance also increases. Glucose leels are therefore up and down
185
Treatment of hyperphosphatemia
Oral phosphate binders
- prevent reabsorption of phosphate from bowe
- treat hypocalemia eill b/c it is hyperparathyroidsm that causes increase phosphate release from bone
186
When treating hypocalcemia why should you give oral phosphate binders?
If you use Vitamin D alone without oral phosphate binder then bowel will absorb increase GI absorption of phosphate
187
Why do you never use aluminum phosphate binders?
Aluminum causes dementia
188
Thrombotic Thrombocytic Purpura
platelet disorder in which microthrombi block small vessels leading to end organ ischemia .
RBCs are fragmented by microthrombi leading to microangiopathic hemolytic anemia
189
TTP associated conditions
HIV
Cancer
Drugs (cyclosporine, ticlopidine and clopidogrel)
190
TTP presentation
Clinical syndrome with 5 symptoms (3 of 5)
- low platelet
- microangiopathic hemolytic anemia
- neuro changes (seizures, stroke, delirium)
- impaired renal function
- fever
191
How is TTP hemolysis visible on smear?
Schistocytes
| Helmet cells
192
Hemolytic Uremic Syndrome
- common in children
- associated with E.coli 0157:H7 and Shigella
- intravascular hemolysis (schistocytes)
- renal failure
- thrombocytopenia
193
TTP Treatment
Plasmaphoresis
* * if not a choice, choose fresh frozen plasma
* * NEVER CHOOSE PLASMA INFUSION
194
HUS: Treatment
Often resolves spontaneously
195
Simple renal cysts
- echo free
- smooth thin walls
- sharp demarcation
- good transmission to the back
196
Complex renal cysts
- mixed echogenecity
- thick, irregular walls
- lower density on back wall with demarcation
- transmission shows debris in cyst
197
Polycystic Kidney Disease
presents with:
- pain
- hematuria
- stones
- infection
- hypertension
198
What is the most common cause of death from PCKD?
Renal failure
| - from recurrent episodes of pyelonephritis and nephrolithiasis
199
Conditions associated with PCKD
- liver cysts (most common site outside of kidney)
- ovarian cysts
- mitral valve prolapse
- diverticulosis
- berry aneurysms
200
Hypernatremia
due to loss of free water
- sweating, burns, fever
- pneumonia: insensible losses from hyperventilation
- diarrhea
- diuretic
201
Diabetes insipidus
- leads to high volume water losss from insufficient or ineffective ADH
202
Central diabetes insipidus
- can be caused by CNS disorders (stroke, tumor, trauma, hypoxia, infection) can damage ADH production in hypothalamus or storage in posterior pituitary
- low ADH
203
Nephrogenic diabetes insipidus
- loss of ADH effect on collecting duct of the kidney
- can be caused by lithium or demecycline, CKD, hypokalemia, or hypercalcemia
- elevated ADH
204
Pt has high volume nocturia
Think about presence of diabetes insipidus
205
Diabetes insipidus: presentation
DI w/ hypernatremia presents with neurological symptoms such as:
- confusion
- disorientation
- lethargy
- seizures
206
Complications of diabetes insipidus
If uncorrected, severe hypernatremia causes coma and irreversible brain damage
207
Polyuria
- high urine volume
208
Hypernatremia: diagnostic test
```
hyperosmolality
fluid losses from skin, kidney, or stool lead to:
- decreased urine volume
- increased urine osmolality
- decreased urine sodium
```
209
Diabetes Insipidus: Diagnostic Test
- high urine volume in DI
| - decreased urine osmolality in DI
210
Best initial test for diabetes insipidus
Water deprivation then observation of urine output and urine osmolality
- In DI, high volume urine and low urine osmolality
211
Central diabetes insipidus response to ADH
Sharp decrease in urine volume, increase in osmolality
212
Nephrogenic diabetes insipidus response to ADH
No change in urine volume or osmolality with ADH administration
213
Positive water deprivation
means urine volume stays high despite withholding water
214
Diabetes inspidus: Treatment
1. Fluid loss: correct underlying water loss
2. CDI: replace ADH
3. NDI
- correct potassium and calcium
- stop lithium and demeclocycline
- give thiazide or NSAIDs despite these interventions
215
Complications of hypernatremia
Cerebral edema -- if sodium levels brought down too rapidly from shift of fluids from vascular space into cells of brain
- presents with worsening confusion and seizures
216
Hyponatremia
- characterized according to overall VOLUME STATUS of the body
217
Hypervolumia hyponatremia: causes
- CHF
- Nephrotic syndrome
- Cirrhosis
218
Intravascular volume depletion in regards to ADH levels
Increased ADH levels
| - pressure receptors in atria and carotid sense decrease in volume and stimulate ADH production and release
219
Hypovolemia hypernatremia: causes
- Sweating
| - Pneumonia: due to secondary losses from hyperventilation
220
Addison disease
- loss of adrenal function also causes hyponatremia b/c of loss of aldosterone
- less aldosterone, less sodium
221
Euvolemia hyponatremia: causes
- Pseudohyponatremia (hyperglycemia)
- Psychogenic polydipsia
- Hypothyroidism
- Syndrome of inappropriate ADH
222
Hyperglycemia induced hyponatremia
- very high glucose levels lead to a decrease in soidum levels
- hyperglycemia acts an osmotic draw on fluid inside the cells
223
Na correction with hyperglycemia
For every 100 mg/dL of glucose above normal, there is a 1.6 mEq/L decrease in Na
224
Psychogenic polydipsia
massive ingestion of free water above 12 to 24 liters/day will overwhelm kidney's ability to excrete water
- minimum urine 50 mOsm/kg
- can produce 12 - 24 liters of urine a day, depending whether or not you can get urine osmolality down to 50 or 100 mOsm/kg
225
Pt is hyponatremic with a hx of bipolar disorder. Likely diagnosis?
Psychogenic polydipsia
226
Hypothyroidism induced hyponatremia
- thyroid hormone is needed to excrete water. If thyroid hormone level is low, free water excretion is decreased
227
SIADH induced hyponatremia
Any LUNG or BRAIN DISEASE can cause SIADH for unclear reasons
- certain drugs: SSRIs, sulfonyureia, vincristine, cyclophosphamide
228
Cancers associated with SIADH
Small cell cancer of the lung produce ectopic ADH
229
Hyponatremia presentation
Presents entirely with CNS symptoms
- confusion
- lethargy
- disorientation
- seizures
- coma
230
Hyponatremia: Diagnostic Test
SIADH - urine is appropriately concentrated (high urine osmolality)
- urine sodium is high in SIADH
- uric acid level and BUN are low in SIADH
231
Most accurate test for SIADH
high ADH level
232
Mild hyponatremia: treatment
restrict fluids
233
Moderate hyponatremia: treatment
Saline and loop diuretic
| * pt may present with minimal confusion
234
Severe hyponatremia: treatment
* patient presents with lethargy, seizures, coma
| - treat with hypertonic saline, conivaptan, tolvaptan
235
ADH antagonists
Tolvaptan and conivaptan
| - treated for severe, symptomatic SIADH
236
Chronic SIADH
- can be from underlying disorder that cannot be corrected (e.g. metastatic cancer)
237
Chronic SIADH: treatment
Demeclocycline
| - blocks the action of ADH at the collecting of the kidney tubule
238
Hyponatremia complications
Central pontine myelinolysis
| - must be corrected "slowly" as under 0.5 - 1.0 mEq/hr or 12 to 24 mEq per day
239
Pseudohyperkalemia
Falsely elevated potassium levels due to:
- hemolysis
- repeated fist clenching with tourniquet
- thrombocytosis or leukocutosis will leak out of cells in the lab specimen
240
Hyperkalemia due to decreased excretion
- Renal failure
- Aldosterone decrease
- ACE inhibitors/ ARBS
- type IV renal tubular acidosis
- spironolactone and eplerenone (aldosterone inhibitors)
- triamterene and amiloride (K sparing diuretics)
- Addison disease
241
Hyperkalemia due to K release from ittuse
- Tissue destruction (hemolysis, rhabdomyolysis, tumor lysis syndrome)
- Decreased insulin (insulin drive K into cells)
- Acidosis: cells take in H+ and release K in exchange
- Beta blockers and digoxin: drugs inhibit Na/K ATPase
- Heparin increases K levels, presumable through increased tissue release
242
Hyperkalemia: presentation
K disorders interfere with muscle contraction and cariac conductance
- weakness
- paralysis when severe
- ileus (paralyzes gut muscles)
- cardiac rhythm disorders
243
Best initial test for hyperkalemia
EKG
244
Hyperkalemia: EKG findings
Peaked T waves
Wide QRS
PR interval prolongation
245
Treatment for life threatening hyperkalemia
1. Calcium chloride or calcum gluconate
2. Insulin and glucose to drive potassium back into cells
3. Bicarbonate: drive potassium into cells but should be used most when acidosis causes hyper
246
Removing potassium fro body
Kayexalate (sodium polystyrene sulfonate) removes potassium from body through bowel
-
247
Other methods to lower potassium
- Inhaled beta agonists
- Loop diuretics
- Dialysis
248
When there is hyperkaelmia and an abnormal EKG, what is the most appropriate next step?
Calcium chloride or calcium gluconate
249
Hypokalemia
- due to decreased intake
- shift in to cells
- renal loss
- hypomagnesmia
- renal tubular acidosis
250
Hypokalemia 2/2 shift into cells
- Alkalosis (H+ ions come out cell in exchange for K)
- Increased insulin
- Beta adrenergic stimulation (accelerates Na/K ATPase)
251
Hypokalemia 2/2 renal loss
- Loop diuretics
- Increased aldosterone
- Primary hyperaldosteronism (Conn syndrome)
- Volume depletion raises aldosterone
- Cushing syndrome
- Bartter syndrome (genetic disease causing salt loss in Loop of Henle)
- Licorice
252
Hypokalemia 2/2 hypomagnesmia
There are Mg-dependent K channels. When magnesium is low, they open and spill potassium in the urine
253
Hypokalemia 2/2 GI loss
- seen in vomiting, diarrhea, and laxative abuse
254
Hypokalemia presentation
Leads to issue with muscular contraction and cardiac conduction
- Weakness
- Paralysis
- Loss of reflexes
255
Hypokalemia EKG findings
U waves are the most characteristics
- ventricular ectopy (PVCs)
- flattened T waves
- ST depression
256
Hypokalemia: treatment
No maximum rate of oral K replacement
| - however with rapid IV potassium replacement, it can cause arrhythmia
257
PT is admitted with vomiting and diarrhea from gastroenteritis. His volume status is corrected with IV fluids and the diarrhea resolves. His pH is 7.40 and his serum bicarbonate has normalized. Despite oral and IV replacement, his potassium level fails to rise. What should you do?
Check magnesium level
| - hypomagnesmia can be lead to increased urinary loss of K
258
A woman with ESRD and G6PD deficiency skips dialysis for a few weeks and then is crushed in a MVA. She taking dapsone and has recently eating a few fava beans. What is the most urgent step?
EKG
| if abnormal, give patent Ca chloride
259
Renal Tubular Acidosis
metabolic acidosis with a normal anion cap (6 - 12)
260
Two most important causes of metabolic acidosis with normal anion gap
- RTA
| - Diarrhea
261
Why is the anion gap normal in RTA and diarrhea
Chloride level rises 2/2 they are also refer to hyperchloremic metabolic acidosis
262
Anion gap metabolic acidosis
due to ingested substances:
- ethylene glycol or methanol
- organic acids (e.g. lactate) that are anion and drive down chloride level
263
Distal RTA (Type I)
- distal tubule is responsible for generating new bicarbonate under the influence of aldosterone
- increased formation of kidney stones from calcium oxalate 2/2 alkaline urine
- calcifies the kidney parenchyma
264
Drugs that cause distal RTA (Type I)
- Amphotericin
| - Autoimmune disease (e.g. SLE or Sjorgen syndrome can damage distal tubule)
265
Best initial test for Distal RTA
Urinalysis
| - looking for an abnormally high pH > 5.5
266
Most accurate test for Distal RTA
- infuse acid into the blood with ammonium chloride
267
Treatment of Distal RTA
Replace bicarbonate which will be absorbed at the proximal tubule
268
Proximal RTA (Type II)
- decreased ability for kidney to reabsorb most of filtered bicarbonate
- eventually bicarbonate is lost in urine until the body is so depleted of bicarbonate that the distal tubule can absorb the rest
- the urine pH will become low (at or below 5.5)
- chronic metabolic acidosis can leach calcium to cause osteomalacia
269
Proximal RTA (Type II): Causes
- Amyloidosis
- Myeloma
- Fancomi syndrome
- Acetazolamide
- Heavy metal
270
Most accurate test for proximal RTA (Type II)
Testing urine pH after giving bicarbonate
271
Urine pH during proximal RTA (Type II)
First it is basic (above 5.5) until most bicarbonate is lost from body, then is low (below 5.5)
272
Status of potassium in both proximal and distal RTA
Hypokalemia
| - potassium is lost in the urine
273
Proximal RTA (Type II)
Thiazide diuretics cause volume depletion. Volume depletion will enhance bicarbonate reabsorption.
274
Hyporeninemia, hypoaldosteronism (Type IV RTA)
- occurs most often in diabetes
- decreased amount or effect of aldosterone at the kidney tubule
- leads to loss of Na and retention and K and H_
275
Best testing for Type IV RTA
Finding a persistently high urine sodium despite a sodium depleted diet
276
Treatment for Type IV RTA
Fludrocortisone
| - steroid with the highest mineralcorticoid or "aldosteronelike" effect
277
Urine anion gap (UAG)
way to distinguish between diarrhea and RTA
| Na - Cl
278
Why is chloride high in acidotic conditions
Acid excreted by kidney is buffered by NH4Cl
| - more acid excreted, the greater amount of chloride found in urine
279
Why is the UAG (Na - Cl) positive in RTA
RTA is defect in acid excretion into urine, so the amount of chloride in urine is diminished
280
Why is UAG (Na - Cl) negative in RTA
diarrhea associated w/ metabolic acidosis thus kidney tries to compensate by increasing acid excretion
- acid is excreted with chloride
- more acid in urine means more chloride in urine
281
Causes of metabolic acidosis
```
MUDPILES
Methanol
Uremia
Diabetes ketoacidosis
Paraaldehyde
Isoniazid or Iron
Lactate
Ethylene glycol
Salicylates
```
282
Metabolic acidosis 2/2 lactate
- caused by hypotension or hypoperfusion
- tested with blood lactate levels
- treat by correcting hypoperfusion
283
Metabolic acidosis 2/2 ketoacidosis
- caused by DKA and starvation
- tested by measuring acetone levels
- treat with insulin and fluids
284
Metabolic acidosis 2/2 oxalic acid
- caused by ethylene glycol overdose
- tested by seeing crystals in UA
- treat with fomepizole and dialysis
285
Metabolic acidosis 2/2 formic acid
- caused by methanol overdose
- tested by seeing inflamed retina
- treated with fomepizole and dialysis
286
Metabolic acidosis 2/2 uremia
- caused by renal failure
- test by evaluating BUN and Cr
- treated with dialysis
287
Metabolic acidosis 2/2 salicylates
- caused by aspirin overdose
- test for aspirin levels
- treat by alkanizing urine
288
ABG in metabolic acidosis
- decreased pH below 7.4
- decreased pCO2 indicating respiratory alkalosis as compensation
- decreased bicarbonate
289
Metabolic alkalosis
- elevated serum bicarbonate level
- compensated with respiratory acidosis
- relative HYPOventilation that will increased pCO2 to compensate for metabolic alkalosis
290
Metabolic alkalosis: etiology
- GI loss: vomiting or nasogastric suction
- Increased aldosterone: primary hyperaldosteronism, Cushing syndrome
- Diuretics
- Milk-alkali syndrome: high volume liquid antacids
- Hypokalemia: H+ move into cells so K can be released
291
Metabolic alkalosis on ABG
- increased pH > 7.4
- increased pCO2 indicating respiratory acidosis as compensation
- increased biarbonte
292
Minute ventilation
respiratory rate x tidal volume
293
Respiratory alkalosis
- decreased pCO2
- increased minute ventilation
- metabolic acidosis as compensation
294
Causes of respiratory alkalosis
- Anemia
- Anxiety
- Pain
- Fever
- Interstitial lung disease
- Pulmonary emboli
295
Respiratory acidosis
- increased pCo2
- decreased minute ventilation
- metabolic alkalosis as compensation
296
Respiratory acidosis: causes
- COPD / emphysema
- Drowning
- Opiate overdose
- Alpha 1 antitryspin deficiency
- Kyphoscoliosis
- Sleep apnea / morbid obesity
297
Most common cause of kidney stones (nephrolithiasis)
Calcium oxalate
| - which forms more frequently in an alkaline urine
298
Most common risk factor for kidney stones
Overexcretion of calcium in the urine
299
A 46 y/o M comes to the ER with excruciating pain in his left flank radiating to the groin. He has some blood in his urine. What is the most appropriate next step in the management of this patient?
Katerolac
- NSAID
- more important to provide relief than specific diagnostic testing
300
What is the most accurate diagnostic test for nephrolithiasis?
CT scan
301
Why does Crohn disease cause kidney stones?
Increased oxalate absorption
302
Best initial therapy for acute renal colic
- Analgesic and hydration
- CT and sonography to detect obstruction
- Stones < 5 mm pass spontaneously
- Stones 5 - 7 mm get nifedipine and tamsulosin to help them pass
303
Kidney stone etiology is determined with
- Stone analysis
- Serum calcium, NA, uric acid, PTH, Mg, and phosphate levels
- 24 hr urine for volume, Ca, oxalate, citrate, cysteine
304
Uric acid stones
- not detectable on X-ray but seen on CT
305
Cysteine stones
- managed with surgical removal, alkalinizing the urine
306
Woman with her 1st episode of renal colic is found to have a 1.8 cm stone in the L renal pelvis. She has no obstruction and her renal function is normal (normal BUN and Cr) What is the most appropriate next step in teh management of this patient?
Lithotripsy
307
UTIs leave patients prone to which type of kidney stones?
Struvite stones (Mg/Al/ P)
308
Long term management of nephrolithiasis
50% of those with kidneys stones will have reoccurence within 5 years
309
Man with a Ca oxalate stone is managed with lithotripsy and the stone is destroyed and passes. His urinary calcium level is increased. Besides increasing hydration, which will most likely benefit this patient?
Hydrochlorothiazide
| - removes calcium from urine
310
Metabolic acidosis and stone formation
Metabolic acidosis removes Ca from bones and increases stone formation
- acidosis decreases citrate levels
- citrate binds calcium making it unavailable for stone formation
311
Urinary Stress incontinence
- older woman w/ painless urinary leakage with coughing, laughing, or lifting heavy objects
312
Best test for urinary stress incontinence
have patient stand and cough
| - observe for leakage
313
Urinary stress incontinence: treatment
1. Kegel exercises
2. Local estrogen cream
3. Surgical tightening of urethra
314
Urinary urge incontinence
- sudden pain in the bladder followed immediately by overwhelming urge to urinate
315
Best test for urinary urge incontinence
pressure measurement in half full bladder
| manometry
316
Urinary urge incontinence: treatment
1. Bladder training exercises
2. Local anticholinergic therapy
- oxybutinin
- tolterodine
- solifenacin
- dariferancin
3. Surgical tightening of urethra
317
Hypertension
- systolic pressure > 140 mm Hg
- diastolic pressure > 90 mm Hg
- diabetic patient or someone with CRD > 130/80 mm Hg
318
Most common disease in the US
hypertension
319
Most common risk factor for the most common cause of death
Myocardial infarction
320
Causes of hypertension
- Renal artery stenosis
- Glomerulonephritis
- Coarctation of the aorta
- Acromegaly
- Sleep apnea
- Pheochromocytoma
- Hyperaldosteronism
- Cushing syndrome
- Congenital adrenal hyperplasia
321
Hypertension: symptomatic presentation
- CAD
- Cerebrovascular disease
- CHF
- Visual disturbance
- Renal insufficiency
- Peripheral arteru disease
322
Renal artery stenosis: presentation
- HTN
- bruit is auscultated at the flank
- continuous throughout systole and diastole
323
Coaractation of the aorta
- HTN
| - upper extremities > lower extremities
