Morning Report: o g epo

Transcription

Morning Report: o g epo
Morning
o
g Report:
epo
60 y.o. man with pink urine
10/27/10
Edward
Ed
dG
Gometz
t
Shana Ratner
Diane Altkorn
MKSAP
•
•
A 52-year-old man is evaluated for a 3-month history of perineal
and suprapubic pain. He has experienced urinary frequency and
dysuria for 4 to 6 weeks. The patient reports fatigue, insomnia,
and low mood for the past 6 months. He has hypertension.
Current medications are hydrochlorothiazide and
acetaminophen as needed for pain.
On physical examination, temperature is normal, blood pressure
is 138/80 mm Hg, and pulse rate is 78/min. BMI is 29.
Abdominal examination is normal with mild suprapubic
tenderness. The prostate is not enlarged; it is mildly tender
without nodularity. Testicular examination is normal.
MKSAP
• On laboratory study, urinalysis is normal, and urine
culture is negative. Prostate-specific antigen level is
0 8 ng/mL (0
0.8
(0.8
8 µg/L)
µg/L).
• Which of the following is the most appropriate
p
treatment for this patient?
• A Levofloxacin
• B Naproxen
• C Oxybutynin
• D Saw palmetto
• E Terazosin
T
i
MKSAP
• On laboratory study, urinalysis is normal, and urine
culture is negative. Prostate-specific antigen level is
0 8 ng/mL (0
0.8
(0.8
8 µg/L)
µg/L).
• Which of the following is the most appropriate
p
treatment for this patient?
• A Levofloxacin
• B Naproxen
• C Oxybutynin
• D Saw palmetto
• E Terazosin
T
i
MKSAP Answer
•
•
•
Chronic prostatis/chronic pelvic pain syndrome manifestations:
– GU/pelvic pain
– Voiding
g symptoms
y p
– Urine culture negative
– Presence or absence of leukocytes in the urine has little clinical
utility
– There are no lab or diagnostic findings
Among pharmacologic therapies, efficacy data is strongest for use of
alpha blockers in treating chronic prostatitis and chronic pelvic pain
syndrome
d
There is no evidence for a bacterial cause.
– It is common practice to prescribe 4-6 weeks of antibiotics, but
there is lack of clinical trial evidence
The Case
60 y/o man hx CKD, HTN p/w 2 day hx of
urine that looks like “pink
p
lemonade”
HPI
• Urinaryy
– Mild dysuria (stinging pain) started today
– Increased frequency and urgency for past week
– Right sided lower back and flank pain intermittent
for past 5 days
– Noticed urine was reddish for p
past 2 days
y
• ROS
– 30lb weight loss over 12 months (unintentional)
– No recent fevers, but occasional night
sweats/chills for weeks
– Occasional postprandial abd pain and nausea.
Denies vomiting, diarrhea
History
Past Medical History
•
•
•
•
•
Chronic Kidney Disease, stage IV
Hypertension
Uveitis
Spinal Surgery (1995)
•
Family Hx
•
•
•
•
•
•
•
Both parents deceased,
deceased had
hypertension
Social Hx
w
w
Allergies
Married, retired, 3 children
40 pyh tob, significant alcohol
abuse (quit 1 year ago), no IVDU
NKDA
Home Medications
•
Amlodipine/ Benazepril 5mg5mg
20mg daily
Carvedilol 25 mg BID
Minoxidil 2.5mg
gq
qAM
Minoxidil 5 mg qPM
Thiamine 100mg daily
Folate 1mg
g daily
y
Colace 100 mg daily
Tums 1 to 2 tabs with meals
Physical Exam
y Vitals: T 361 P 82 BP 130/69 R 18 O2 Sat 96% RA
y Gen: A&OX3, in NAD y HEENT: PERRLA, EOMI, poor dentition, clear oral pharynx, no ,
,p
,
p y ,
y
y
y
y
y
y
y
pallor, no scleral icterus, mildly injected sclera
Neck: No lymphadenopathy, no neck mases
CVS: RRR, nl S1 & S2, no m/r/g, no JVD
Extremities: Warm, pulses 2+ bilaterally, no edema
Lungs: Non‐labored respirations, CTA bilaterally
Abd: Soft, hypoactive bowel sounds, non‐distended, slight right yp
g
g
flank tenderness, palpable liver below costal angle
Neuro: CN intact, UE & LE strength 5/5, sensation intact
Skin: no rashes or lesions
Initial Labs
(10.5‐12.0)
11.7
134
109
35
208
7.6
33.3
MCV 82.2
N 56 L 30 M 14 E 2 12.3
1.7
124
3.5
15
2.7
3.2
(2.3‐2.7)
AG 10
7.4
Urinalysis: leuk est +, nitrite -, Prot 3+,
Bl d 3+
Blood
Ionized Ca++: 7.26 (NR:4.6-5.4)
Lipase: 60
3.5
03
0.3
31
26
84
Initial Labs
(10.5‐12.0)
11.7
134
109
35
208
7.6
33.3
MCV 82.2
N 56 L 30 M 14 E 2 12.3
1.7
124
3.5
15
2.7
3.2
(2.3‐2.7)
AG 10
7.4
Urinalysis: leuk est +, nitrite -, Prot 3+,
Bl d 3+
Blood
Ionized Ca++: 7.26 (NR:4.6-5.4)
Lipase: 60
3.5
03
0.3
31
26
84
Differential
• Initial differential
• Initial management
• What next?
Urine microscopy
Imaging?
•
Renal Ultrasound: Renal calculus. Hydroureter and
hydronephrosis.
•
CT Abd/ Pelvis: Right ureteral stent in anatomic position,
resolving hydronephrosis, evidence of hydroureter with renal
calculus present on right side. Moderately enlarged prostate
without bladder distension. No other abnormalities noted.
Types of kidney stones
Types of Kidney Stones
•
Calcium ((Oxalate or Phophate)
p
)
– Most common type of kidney stone (80-85%)
– Can occur in hyper and hypo calcemia
– Inability
I bilit tto process oxalate
l t rich
i h ffoods
d effectively
ff ti l
•
Struvite
– Less common type
yp of kidney
y stone ((10-15%))
– Infectious (most commonly Proteus mirabilis, also Klebsiella
•
Uric acid
– Much less common type of kidney stone (~5-10%)
– Seen with conditions that promote hyperuricosuria (low pH)
•
Cystine
– Rare type of kidney stone (most often linked to genetic defect)
Clinic management of kidney
stones
Confirm Diagnosis
•
KUB can help assess stone burden, size, and location;
•
Intravenous Urography (gold standard)
•
Renal U/S can also be adequate to assess a stone but also look for
hydronephrosis/ hydroureter
•
CT is rarely used for stone assessment alone and usually locates a
stone as an incidental finding
Assess severity
•
Stone size, location, and patient symptoms all are implicated in
determining whether you have an urological emergency vs.
conservative management.
Clinic management of kidney
stones
Medical Expulsive Therapy
•Analgesia
•Stone retrieval strategies
•Extracorporeal shock wave lithotrypsy
•“Ureteral-relaxing”
g medications
- Nifedipine
- Tamsulosin
- Prednisone
Back to the case
• Patient with nephrolithiasis
134
109
12.3
35
124
3.5
15
2.7
1.7
3.2
Spectrum of Hypercalcemia
Spectrum of hypercalcemia indicated by serum total
and ionized calcium levels.
Differential for
Hypercalcemia??
Hypercalcemia Manifestations
Renal “stones”
Nephrolithiasis
Nephrogenic diabetes insipidus
Dehydration
Nephrocalcinosis
Skeleton “bones”
Bone pain
Arthritis
Osteoporosis
Osteitis fibrosa cystica in hyperparathyroidism
(subperiosteal resorption, bone cysts)
Gastrointestinal “abdominal moans”
Nausea,, vomiting
g
Anorexia, weight loss
Constipation
Abdominal pain
Pancreatitis
Peptic
p ulcer disease
Neuromuscular “psychic
groans”
Impaired concentration and memory
Confusion, stupor, coma
Lethargy and fatigue
M
Muscle
l weakness
k
Corneal calcification (band keratopathy)
Cardiovascular
Hypertension
Shortened QT interval on electrocardiogram
g
Cardiac arrhythmias
Vascular calcification
Other
Itching
Keratitis, conjunctivitis
Differential for Hypercalcemia
Parathyroid hormone-related
Medications
Primary hyperparathyroidism*
Sporadic familial
Sporadic,
familial, associated with multiple
endocrine neoplasia I or II
Tertiary hyperparathyroidism
Associated with chronic renal failure or vitamin D
deficiency
y
Thiazide diuretics (usually mild)*
Lithium
Milk-alkali syndrome (from calcium
antacids)
Vitamin A intoxication (including analogs
used to treat acne)
Other endocrine disorders
Vitamin D-related
Vitamin D intoxication
Usually 25-hydroxyvitamin D2 in over-the-counter
supplements
l
t
Granulomatous disease sarcoidosis, berylliosis,
tuberculosis
Hodgkin's lymphoma
Hyperthyroidism
Adrenal insufficiency
Acromegaly
Pheochromocytoma
Genetic disorders
Familial hypocalciuric hypercalcemia:
mutated calcium-sensing receptor
Malignancy
Other
Humoral hypercalcemia of malignancy* (mediated by
PTHrP)
Solid tumors, especially lung, head, and neck
squamous cancers, renal cell tumors
Local osteolysis* (mediated by cytokines) multiple
myeloma, breast cancer
Immobilization, with high bone turnover
(e.g., Paget's disease, bedridden
child)
Recovery phase of rhabdomyolysis
Work Up?
• PTH: 7 (NR: 15-75)
Work-Up
• CT Abd/ Pelvis: as reported before, no evidence of
malignancy
li
• Chest X-Ray:
X Ray: Prominent hilar lynphadenopathy,
large pulmonary arteries, bibasilar scarring, no acute
abnormalities
•
•
•
•
•
•
PTHrH: Negative
Alk Phos: 84 (NR: 30-120)
Protein Electrophoresis: Negative for Myeloma
Calcitriol (1,25 Dihydroxy Vit D): Elevated
TSH 2.6
TSH:
2 6 (NR
(NR: 0
0.3-4.0)
3 4 0)
PSA: 1.6
CT Chest
Granuloma vs. Lymphoma
•
•
•
•
Clinical and serological evidence for both diagnosis.
ACE level: <5 (NR: 8-52)
– ACE level known to be unhelpful in diagnosing sarcoid when
patient
ti t is
i taking
t ki an ACE-I
ACE I (our
(
ptt taking
t ki Benazepril)
B
il)
c-ANCA: Negative (eval for Wegener's granulomatosis)
PPD: Negative
What next?
• Consult pulmonology for bronchoscopy
Bronch results
Sarcoidosis - Epidemiology
• Affects both genders, but more prominent in women.
• The lifetime risk of sarcoidosis for U
U.S.
S whites is
estimated at 0.85 percent compared with 2.4 percent
in U.S. blacks. Sarcoidosis is most prevalent in
S d
Swedes,
D
Danes, and
dU
U.S.
S bl
blacks.
k
• The condition usuallyy p
presents in adults yyounger
g than
40 years, most frequently between 20 and 29 years
of age. Sometimes incidentally found in older people
g y asymptomatic.
y p
if theyy are largely
Sarcoidosis - Causes
•
Causes include genetic inheritance, infectious transmission, and
shared exposure to environmental agents
agents.
•
Infectious organisms such as viruses, mycobacteria, Borrelia
burgdorferi and Propionibacterium acnes have been implicated
burgdorferi,
as potential causes of sarcoidosis.
•
Environmental exposure to beryllium
beryllium, aluminum
aluminum, and zirconium
can result in a granulomatous response similar to that of
sarcoidosis.
•
Current theory suggests that disease develops in genetically
predetermined hosts who are exposed to certain environmental
agents that trigger an exaggerated inflammatory immune
response leading to granuloma formation
formation.
Sarcoidosis - Organs
Sarcoid - Therpies
• Systemic Corticosteroids
• Inhaled Corticosteroids
• Cytotoxic
C t t i Agents
A
t (methotrexate
( th t
t and
d azathioprine)
thi i )
• Immunomodulators
• Surgical
g
Intervention
Hospital course
•Urology
Urology consulted and placed stents for severe hydronephrosis
•IV fluids were immediately started to bring down the Ca++
•Creatinine remained stable
•Stone
Stone passed and found to be composed of calcium oxalate
•After 1 day, hematuria had started to clear, and flank pain had resolved.
Urine culture taken and patient was treated empirically with
Ciprofloxacin.
Ciprofloxacin
•Patient’s calcium level was 10.4 (~6.3 ionized) on discharge home.
•Patient was scheduled to follow up with pulmonology clinic as an
outpatient.
Take home points
• Makeup of kidney stones
• Outpatient management of kidney
stones
• Initial management and differential for
hypercalcemia
• Overview
O
i
off sarcoidosis
id i
References
• Carroll MF, Schade DS. A practical approach to
hypercalcemia. Am Fam Physician. 2003 May
1;67(9):1959-66.
; ( )
• Wu JJ, Schiff KR. Sarcoidosis. Am Fam Physician.
2004 Jul 15;70(2):312-22.
• http://www.kidneyatlas.org/book4/adk4-08.pdf
http://www kidneyatlas org/book4/adk4 08 pdf
• www.herringlab.com
• Up
p To Date
• Merck Manual Online
• Wikipedia

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