Transcript Phil. J. Internal Medicine, 46:165-173

LeeChuy, Katherine
Lee, Sidney Abert
Lerma, Daniel Joseph
Legaspi, Roberto Jose
Li, Henry Winston
Li, Kingbherly
Lichauco, Rafael
Lim, Imee Loren
Lim, Jason Morven
Lim, John Harold
Lim, Mary
Lim, Phoebe Ruth
Lim, Syndel Raina
Lipana, Kirk Andrew
Liu, Johanna
Llamas, Camilla Alay
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Name: T. R.
Age: 60
Sex: M
Status: Married
Nationality: Filipino
Date of Birth: 12/10/1949
Place of Birth: Leyte
Religion: Roman Catholic
Eduacational attainment: High School Graduate
Occupation: retired; Grass cutter of Military Shrines Service
Current Address: Bataan
Informant: Patient, Wife, Niece, Nephew
Reliability: 70%
“Namamaga ang mga kasukasuhan sa kamay,
tuhod, at hinlalaki sa paa (swelling of the hands,
knees and big toe of R/L foot)”
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10 years PTA
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4 months PTA
10 years history of recurrent monoarthritis
– No proper consult was done; self-medicated with
paracetamol 500mg + ibuprofen 200mg (Alaxan),
paracetamol (Biogesic) 500mg, Amoxicillin 500mg
(duration of symptoms, interval between onset of symptoms,
duration of intake, frequency of intake #tabs/day,
frequency of attack, efficacy/ duration of relief from
symptoms, compliance-if every how many hrs)
patient slipped and sustained an injury to the R/L hand or wrist
in an attempt to break his fall
• admitted at a local hospital in Bataan
• confined and was given unrecalled medications
• relieved from the pain (from medications or through
massaging “hilot”? Was swelling also relieved)
2 weeks PTA
-patient accidentally stepped on a sharp object and
cleaned the wound site with guava leaves and
betadine and then applied hydrogen peroxide with
penicillin
-recurrence of joint pain and swelling; self-medicated
with Mefenamic acid 500 mg and amoxicillin 500 mg
which provided relief (duration blah… blah…)
1 week PTA
-progression of joint pain and swelling, graded 10/10
with limitation of movement
ADMISSION (August 24, 2010)
• No major hospitalization, unrecalled immunizations
• No allergy, no previous transfusion
• (-) DM, PTB, Asthma, Cancer
Family History
•
not clear to the patient
Personal and Social History
•Cigarette smoker since 10 years old (unrecalled number of sticks)
•Alcoholic beverage drinker ( 2 bottles; 3x a week and occasional gin
drinker 2-3 bottles/week)
•Diet: mixed and prefers meat and vegetables
•Denies illicit drug use
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General: no fever, no weight loss, (-)anorexia, (-) weakness, (-) insomnia
HEENT: no blurring of vision, no eye redness, pain, itchiness, no excessive
lacrimation, no ear pain nor tinnitus, no ear discharge, no epistaxis, no nose
discharge, no anosmia, no obstruction nor sinusitis, no mouth sores, fissures,
bleeding, no dental carries, no throat irritation,
Pulmonary: no hemoptysis, no coughing, no dyspnea, no chest wall
abnormality
Gastrointestinal: (+) abdominal distention, no abdominal pain, no melena nor
hematochezia, no changes in bowel habits
Genitourinary: no hematuria, no dysuria, no urinary frequency, no hesitancy,
no incomplete voiding
Endocrine: no heat or cold intolerance, no polyphagia, no polydipsia, no
polyuria, no thyroid enlargement
Musculoskeletal: see HPI, (+) ulcers on the medial side of the left foot
Hematologic: no abnormal bleeding, easy bruising
• General Survey: conscious, coherent, ambulatory, not in cardiorespiratory
distress, normal speech, appropriate thought process and content and welloriented as to time, place and date
• Vital Signs
– Systemic BP: (RUE) 170/100
(LUE) 170/100
– PR: 74 beats/minute
– RR: 17 cycles/minute
– Temperature (axillary): 37.2oC
• Anthropometric mesaurement
-Ht: 5’1” Wt kg 71 kgs BMI: 29.9
• Skin: Warm, moist skin, no active dermatoses, no jaundice
• HEENT: Pale palpebral conjunctivae, anicteric sclera, pupils
ERTL 2-3mm, no exophthalmos, no tragal tenderness, no aural
discharge, supple neck, no distended neck veins, no palpable
cervical lymph nodes, thyroid gland not enlarged
• Pulmonary: Symmetrical chest expansion, no subcostal
retractions, unimpaired tactile and vocal fremiti ,(+) crackles
on both lower lung bases, no wheezes, no rhonchi, resonant,
clear breath sounds
• Cardiovascular: Adynamic precordium, AB at 5th LICS MCL, no
heaves, no lifts, no thrills, S1>S2 apex,S2>S1 base; Pulses were
full and equal in all extremities, (+) bipedal edema, no cyanosis
and clubbing
• Gastrointestinal: flabby abdomen, normoactive bowel sounds,
tympanitic upon percussion, no masses palpated, (+) fluid wave,
Traube’s space not obliterated, Liver span: 10cm, , (-) murphy’s
sign
• Genitourinary: (-) CVA tenderness
• Musculoskeletal: deformed joints on the wrist, (+) swelling on the
wrists to hands, ankles to feet, warm to touch
• Neurologic Exam
• Mental status: Conscious, awake, alert GCS 15
• Pupils 2-3mm, isocoric ERTL, EOMs full and equal, no ptosis, no nystagmus
• No facial asymmetry, can shrug shoulders, can turn head against
resistance
• MMT: 5/5 all extremities
• No sensory deficits
• Can do FTNT, APST
• Reflexes:
• Superficial: (+) Gag and corneal reflex
• Deep Tendon: (++) on all extremities
• No Babinski, nuchal rigidity, Brudzinski, Kernig’s
Physical Examination
Physical Examination
Physical Examination
Physical Examination
Physical Examination
COMPLETE BLOOD COUNT
*8/24
Posttransfusion
UNIT
REFERENCE RANGE
Hemoglobin
48
117
G/L
120-170
X 10^12/L
4.0-6.0
RBC
HCT
0.16
0.36
0.37-0.54
MCV
U^3
87 + - 5
MCH
Pg
29 + - 2
g/dl
34 + - 2
MCHC
30
32.50
RDW
11.6 – 14.6
MPV
fL
7.4 – 10.4
PLATELET
802
450
x 10^9 / L
150 – 450
WBC
19.8
8.50
x 10^9 / L
4.5 – 10.0
NEUTROPHILS
0.89
0.80
METAMYELOCYTES
0.01
BANDS
0.01
SEGMENTED
0.89
0.80
0.50 – 0.70
LYMPHOCYTES
0.06
0.13
0.20 – 0.40
MONOCYTES
0.02
EOSINOPHILS
0.03
DIFFERENTIAL COUNT
BASOPHILS
0.50 – 0.70
0.00 – 0.05
0.00 – 0.07
0.07
0.00 – 0.05
0.00 – 0.01
*Peripheral smear : Hypochromic with anisocytosis and poikilocytosis
8/24
Creatinine
2.86
Sodium
123
Potassium
4.96
iPO4
4.5
Intact PTH
8.2
Ionized Calcium 1.66
Fasting Blood
78.97
Sugar
BUN
65.70
SGPT
36.91
Uric Acid
13
2.29
132.48
Reference
0.5-1.2
137-147mmol/L
3.8-5mmol/L
2.3-4.7 mg/dL
1.12-1.32
70-110 mg/dL
3.89
8-23 mg/dL
3.8-5 U/L
2.7-7.3
Total
Cholesterol
Triglycerides
HDL
LDL
Total Protein
Albumin
Globulin
HbA1c
8/24
119.78
Reference
130.33
22.03
68.20
7.00
2.57
4.43
7.90
10-90 mg/dL
150-250 mg/dL
6-7.8 g/dL
3.2-4.5 g/dL
2.3-3.5 g/dL
4.0-6.0
Other Ancillary procedures:
• Fecal occult blood test – (+)
• ECG – Sinus rhythm with left ventricular
hypertrophy
• Urinalysis: albumin- negative, sugar –
negative, RBC-0-2/hpf, Pus cell-1-4/hpf
• X-ray of the foot – suggestive of osteomyelitis
SALIENT FEATURES
SUBJECTIVE DATA
OBJECTIVE DATA
Age: 60
BP 170/100
(+) swelling on the wrists to hands,
ankles to feet, warm to touch
Presence of joint deformities
Presence of ulcers on the legs
(+) Bipedal edema
(+) Fluid wave
Low Hgb and Hct on CBC with
anisocytosis and poikilocytosis
Increased BUN and creatinine
Sex: M
Swelling of joints of hands, feet and legs
Recurrent joint pains
Limitation of movements
Alcoholic beverage drinker
Diagnosed to have gouty Arthritis
Differential Diagnosis
Patient
Septic arthritis
• 60 y/o
• Male
• No age predilection
• No sexual predilection
• Recurrent joint pains
• Limitation of
movements
• Alcoholic beverage
drinker
• (+) swelling on the
wrists to hands, ankles
to feet, warm to touch
• Presence of joint
deformities
• (+) Hyperuricemia
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Chronic tophaceous gout
• Older age group
• M>F before
menopause; M=F after
menopause
Acute joint pains
• Recurrent joint pains
Limitation of
• Limitation of
movements
movements
N/A
• (+) Alcoholic beverage
drinker
Warm to touch; swelling • swelling on the wrists to
on involved joints
hands, ankles to feet
• (+/-) joint deformity
• (-) Hyperuricemia
• Presence of joint
deformities
• (+) Hyperuricemia
Differential Diagnosis
Patient
Diabetic Foot
Ruptured Tophi
• Presence of ulcers on
the foot with white
chalky substance
Ulcers without white
chalky substance
Ulcers with white chalky
substance
Anemia due to:
NSAID
Gastropathy
Chronic Kidney
Disease
Hypochromic and
microcytic anemia
(↓ iron)
Normocytic and
normochromic
anemia
(↓EPO)
(+) FECAL OCCULT
BLOOD TEST
+
-
Chronic NSAID use
(Alaxan-paracetamol+ibuprofen;
Mefenamic acid)
+
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<20-25%
20 to 30%
Patient
Hypochromic microcytic
anemia
Hct 16%
Hawkey CJ. Non-steroidal anti-inflammatory drug gastropathy: causes and treatment. Scand J Gastroenterol Suppl. 1996;220:124-7.
CATHERINE S. SNIVELY, M.D.,et.al. Chronic Kidney Disease: Prevention and Treatment of Common Complications. Am Fam Physician. 2004 Nov 15;70(10):1921-1928.
Main Diagnosis
• Acute gouty arthritis on top of chronic
tophaceous gout
• Ruptured tophi with secondary bacterial
infection of the foot with osteomyelitis
• Anemia secondary to occult GI bleeding
probably due to NSAID gastropathy
• Chronic kidney disease secondary to gout
Differential Diagnosis
Patient
Septic arthritis
• 60 y/o
• Male
• No age predilection
• No sexual predilection
• Recurrent joint pains
• Limitation of
movements
• Alcoholic beverage
drinker
• (+) swelling on the
wrists to hands, ankles
to feet, warm to touch
• Presence of joint
deformities
• (+) Hyperuricemia
•
•
•
•
Chronic tophaceous gout
• Older age group
• M>F before
menopause; M=F after
menopause
Acute joint pains
• Recurrent joint pains
Limitation of
• Limitation of
movements
movements
N/A
• (+) Alcoholic beverage
drinker
Warm to touch; swelling • swelling on the wrists to
on involved joints
hands, ankles to feet
• (+/-) joint deformity
• (-) Hyperuricemia
• Presence of joint
deformities
• (+) Hyperuricemia
Differential Diagnosis
Patient
Diabetic Foot
Ruptured Tophi
• Presence of ulcers on
the foot with white
chalky substance
Ulcers without white
chalky substance
Ulcers with white chalky
substance
Anemia due to:
NSAID
Gastropathy
Chronic Kidney
Disease
Hypochromic and
microcytic anemia
(↓ iron)
Normocytic and
normochromic
anemia
(↓EPO)
(+) FECAL OCCULT
BLOOD TEST
+
-
Chronic NSAID use
(Alaxan-paracetamol+ibuprofen;
Mefenamic acid)
+
-
<20-25%
20 to 30%
Patient
Hypochromic microcytic
anemia
Hct 16%
Hawkey CJ. Non-steroidal anti-inflammatory drug gastropathy: causes and treatment. Scand J Gastroenterol Suppl. 1996;220:124-7.
CATHERINE S. SNIVELY, M.D.,et.al. Chronic Kidney Disease: Prevention and Treatment of Common Complications. Am Fam Physician. 2004 Nov 15;70(10):1921-1928.
Main Diagnosis
• Acute gouty arthritis on top of chronic
tophaceous gout
• Ruptured tophi with secondary bacterial
infection of the foot with osteomyelitis
• Anemia secondary to occult GI bleeding
probably due to NSAID gastropathy
• Chronic kidney disease secondary to gout
Present Medications
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Omeprazole 40 mg tab OD
Amlodipine 10 mg tab OD
Clindamycin 300 mg cap q 6
Ciprofloxacin 250 mg tab BID
Given Colchicine as follows to treat acute
gout: 2 tabs now then 1 tablet after 6 hours
• Cold compress x 10-15 mins TID on inflamed
joints
Pathophysiology of Gout
Gout
• Metabolic or renal disease
• Middle-aged to elderly men and
postmenopausal women
• Results from hyperuricemia
• Characterized by episodes of inflammatory
arthritis due to deposition of Monosodium
urate (MSU) crystals in and around joints
Hyperuricemia
• Serum urate concentration >6.8 mg/dl (men
>7 mg/dl, women >6 mg/dl)
• Causes
– Increased urate production
– Decreased uric acid excretion
– Combination of the two
Purine metabolism
Uric acid elimination
Group C1
Risk factors of Gout
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Obesity
Alcohol use
Family Hx
History of Kidney Disease
Diet
Others
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–
–
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–
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Medications (low dose Aspirin, Pyrazinamide, Ethambutol)
Lead exposure
Hypertension
Diabetes
Hyperlipidemia
Arterioslcerosis
Group C1
Pathogenesis of Hyperuricemia and
Gout
Stages of Gout
• Asymptomatic Hyperuricemia:
– (-) symptoms,
– uric acid levels are high and it needs to be taken care
of so that the uric acid does not precipitate out of
blood and then become crystallized in kidneys or the
joints.
• Acute gout or acute gouty arthritis:
– Uric acid begins to crystallize and deposits in joint
spaces
– (+) pain and swelling
• Intercritical gout:
– attack of gout has subsided
– no symptoms but it is because the body's immune
system is stabilizing itself for more attacks on the uric
acid crystals which form because of the high
concentration of blood
• chronic gout:
– worst and most destructive stage of the disease
– permanent damage to the joints
– kidney damage
Complications:
Tophi:
• Join deformities
• Carpal tunnel syndrome (flexor tendons of
hands and wrist)
• Compression of spinal cord and peripheral
nerves
Gouty Nephropathy
• Severity correlates with the duration and
magnitude of the elevation of the serum uric
acid concentration
• presence of crystalline deposits of uric acid
and monosodium urate salts in kidney
parenchyma obstruction and inflammation
to lymphocytic infiltration, foreign-body
giant cell reaction,fibrosis
Nephrolithiasis
• In gout - urine pH is usually <5.4
• In acidic urine, the protonated form of uric
acid predominates and is soluble in urine only
in concentrations of 100 mg/L.
• >100mg supersaturation stones
NSAID Gastropathy
NSAIDS
• Weak organic acids that inhibit biosynthesis of
prostaglandins
• Anti-inflammatory, analgesic, antipyretic,
antiplatelet effects
• Ex: Aspirin, Ibuprofen
Prostaglandin
• Regulate the release of mucosal bicarbonate
and mucus
• Inhibit parietal cell secretion
• Important in maintaining mucosal blood flow
• Epithelial cell restitution
Complications:
•
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Bleeding
Perforation
Penetrating Ulcer
Gastric Outlet Obstruction
Chronic NSAID use
NSAID gastropathy
Bleeding
Clinical Signs:
(-) Hematemesis
(-) Melena
Laboratory Findings:
Hgb – 48 g/L
Hct-.16
Reticulocyte ct - 33
Peripheral smear – Hypochromic with
anisocytosis and poikilocytosis
Fecal occult blood test – (+)
Management
Main Diagnosis
• Acute gouty arthritis on top of chronic
tophaceous gout
• Ruptured tophi with secondary bacterial
infection of the foot with osteomyelitis
• Anemia secondary to occult GI bleeding
probably due to NSAID gastropathy
• Chronic kidney disease secondary to gout
Panel B:
Patient with
ACUTE GOUT
ARTHRITIS
Acute Gouty Arthritis
•Identify and treat precipitants of gout flare*
•Do NOT start Allopurinol
•If the patient is already taking allopurinol, do not change its dose.
•Ice compress (20 min x 4x/day up to one week)
Any contraindications
to colchicine/ NSAID/
COX-2 selective
inhibitor
Y
•REFER TO RHEUMATOLOGIST
•Start Prednisone 30 mg single dose on day 1, reduce
dose by 5 mg daily and discontinue by day 7
•Intravenous or intramuscular steroids are options
N
Colchicine 0.5 mg/tab 1
tab TID-QID ± NSAID/
COX-2 selective inhibitor ±
analgesic
On day 7, is
the arthritis
RESOLVING
N
Y
•Discontinue NSAID/
COX-2 inhibitor/ Steroids
•Start or adjust Colchicine
0.5 mg/tab 1 tab BID
Go to Panel C
(Intercritical
and Chronic
Gout
•Review adherence to meds
• Recheck if precipitants have
been adequately treated
•REFER TO
RHEUMATOLOGIST
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
Known precipitants of gout flares
•
•
•
•
•
Stress
Hospital admission or surgery
Infection
Dehydration
Drugs/ Medication (aspirin <1g/day,
pyrazinamide, ethambutol, diuretics, etc)
• Irregular intake of urate lowering medications
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
Panel C:
Patient with
INTERCRITICAL/
CHRONIC GOUT
Intercritical and Chronic
Gouty Arthritis
•Start Colchicine 0.5 mg/tab 1 tablet BID
•Prescribe lifestyle modifications*
•Correct modifiable risk factors
Is there an
INDICATION to
start Allopurinol?
N
•Instruct patient on colchicine
use to avert flare
•Monitor/ observe for
indications to start allopurinol
Y
Is crea
clearance <80
mL/min?
Y
REFER TO
RHEUMATOLOGIST/
NEPHROLOGIST
N
•Baseline crea, uric acid every 1-3
months & ALT every 6 months
•Start Allopurinol at 50-100 mg once
daily, to be titrated by 50-100 mg
every 2-4 weeks
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
On periodic
monitoring, is
SUA <6mg/dL?
Y
Any flare in
between visits?
Y
N
N
Has allopurinol
300 mg/day
been used?
•Maintain on allopurinol and
colchicine
•Check lifestyle
•Check adherence to
medications
•REFER TO
RHEUMATOLOGIST
•Maintain allopurinol
•May discontinue colchicine
•Continue periodic monitoring
of SUA, crea
Y
•Review the diagnosis of GOUT
•REFER TO RHEUMATOLOGIST
N
•Continue titration of
allopurinol
•Maintain colchicine
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
Lifestyle modifications that should be
prescribed to all patients with gout
• Low to moderate purine diet
• Intake of more fluid (at least 2 L/day if without
contraindication)
• Avoidance of alcoholic beverages
• Maintenance of appropriate body mass index
• Engagement in low-to-moderate aerobic
exercises at least 45 minutes per day 4 times a
week
Indications for starting urate lowering
therapy
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•
•
•
Recurrent arthritis, at least 2 episodes
Presence of tophaceous deposits
Radiographic evidence of chronic gout
Recurrent uric acid nephrolithiases
Febuxostat
• inhibitor of xanthine oxidase, it is structurally
different from allopurinol
• has an alternate mechanism of enzyme
inhibition, and is more potent
Love, BL et al. (2010). Urate-lowering therapy for gout:
focus on febuxostat. Pharmacotherapy 30(6):597-608
Febuxostat
• Unlike allopurinol, which undergoes oxidation to the
active metabolite oxypurinol and interacts
chemically with the molybdenum center of xanthine
oxidase
• febuxostat remains unchanged and inhibits xanthine
oxidase by binding in a narrow channel leading to the
molybdenum center of the enzyme.
• By this mechanism, febuxostat is able to inhibit both
the reduced and oxidized form of xanthine oxidase
to produce sustained reductions in SUA levels.
Love, BL et al. (2010). Urate-lowering therapy for gout:
focus on febuxostat. Pharmacotherapy 30(6):597-608
Gaffo, AL and Saag KG. (2009). Febuxostat: the evidence for its
use in the treatment of hyperuricemia and gout. Core Evid 4:25-36
Rilonacept
• Being evaluated as a therapeutic drug
candidate for the prevention of gout flares in
patients who are initiating uric acid- lowering
therapy
• Fusion protein designed to attach to and
neutralize IL-1 before IL-1 can bind to cell
surface receptors and generate signals that
trigger inflammation
Rilonacept
• Currently indicated in the U.S. for the
treatment of Cryopyrin-Associated Periodic
Syndroms (CAPS), including Familial Cold
Auto-inflammatory Syndroms (FCAS) and
Muckle-Wells Syndroms (MWS) in adults and
children 12 and older
PRE-SURGE
• PREventive Study against URate-lowering drug-induced
Gout Exacerbations 1 and 2
• Evaluating the mean number of gout flares per patient over
the first 16 weeks of initiation og allopurinol therapy.
• Approximately 240 patients are being randomized on a
1:1:1 basis in each study to receive one of the following
regimens:
– Rilonacept 160mg as an initial loading dose, followed by weekly
80mg subcutaneous injections
– Rilonacept 320mg as an initial loading dose, followed bu weekly
160mg subcutaneous injections
– Weekly placebo injections
Preliminary results of PRE-SURGE 1
• Patients who received rilonacept at a weekly
dose of 160mg had an 80% decrease in mean
number of gout flares compared to the
placebo group over the 16 week treatment
period (0.21 flares vs 1.06 flares, p<0.0001)
• Patients who received rilonacept at a weekly
dose of 80mg had a 73% decrease compared
to the placebo group (0.29 flares vs 1.06
flares, p<0.0001)
Preliminary results of PRE-SURGE 1
• Adverse events that occurred at a frequency
of at least 5% in any study group were:
– Injection site reaction
– Upper respiratory tract infection
– Lower respiratory tract infection
– Musculoskeletal pain/discomfort
– headache
Global RE-SURGE
• REview of Safety Using Rilonacept in preventing
Gout Exacerbations study
• Evaluating the safety of rilonacept vs placebo
over 16 weeks in 1,200 patients at risk for gout
flares from uric-acid lowering treatment,
including allopurinol, febuxostat, probenecid, or
sulfinpyrizone
• About 300 patients receive placebo, 900 patients
receive rilonacept as an initial 320mg loading
dose, followed by weekly 160mg subcutaneous
injections
Rilonacept with NSAIDs
• Compared to indomethacin, there was no
significant benefit from combining
indomethacin with rilonacept
• Measured by the primary endpoint of the
average intensity of gout pain from 24-72
hours after initiation of treatment.
Wound Management
• Debridement may be accomplished by sharp,
mechanical, enzymatic, and/or autolytic measures.
• Wounds should be cleaned initially and each dressing
changed by a nontraumatic technique.
• Use normal saline
• Selection of a dressing should ensure that the ulcer
tissue remains moist and the surrounding skin dry.
• Give tetanus prophylaxis
James, WD, et al. (2006). Andrews’ Diseases of
the skin: Clinical Dermatology, 10th ed.
Cellulitis
• Initial empiric therapy should cover both
staphylococci and streptococci.
• Intravenous penicillinase-resistant penicillins
or a first-generation cephalosporin are usually
effective
James, WD, et al. (2006). Andrews’ Diseases of
the skin: Clinical Dermatology, 10th ed.
Osteomyelitis
• Empiric therapy guided by findings on Gram’s
stain or chosen to cover the most likely
pathogens
• Should include agent active against anaerobes
in the setting of a decubitus ulcer or diabetic
foot infection
Fauci, AS, et al. (2008). Harrison’s
Principles of Internal Medicine, 17th ed
Fauci, AS, et al. (2008). Harrison’s
Principles of Internal Medicine, 17th ed
• initial empiric therapy to cover gonococci, S.
aureus, and streptococci, pending culture
results
• ceftriaxone or cefotaxime
Firestein, GS, et al. (2008). Kelley’s
Textbook of Rheumatology, 8th ed
PNDF Vol II, 3rd ed (2006)
3rd gen cephalosporins
• more stable to hydrolysis by beta-lactamases than 2nd
generation cephalosporins.
• wider spectrum and greater potency against gram-negative
organisms especially for Enterobacteriaceae
• treating serious gram-negative bacillary infections including
sepsis and meningitis when microorganisms are resistant to
customarily used drugs or when aminoglycosides are
contraindicated
• cefotaxime and ceftriaxone - gram-positive organisms and
beta-lactamase producing Proteus, Klebsiella, Serratia, H.
influenzae, Enterobacter, N. gonorrheae and S. typhi
PNDF Vol II, 3rd ed (2006)
GI bleeding
Feldman, M et al. (2006). Sleisenger & Fordtran's
Gastrointestinal and Liver Disease, 8th ed.
GI Bleeding
• Treatment of patients with fecal occult blood
depends on the underlying disorder.
• NSAIDs should be discontinued if possible
• PPIs are more effective than H2 receptor
antagonists and misoprostol
Feldman, M et al. (2006). Sleisenger & Fordtran's
Gastrointestinal and Liver Disease, 8th ed.
Anemia
• Blood transfusion
• normal daily blood loss of 0.5 to 1.5 mL/day, a stool weight of
150 g, and a circulating hemoglobin level of 15 g/dL, the usual
stool hemoglobin concentration is 0.5 to 1.5 mg/g of stool.
• under normal circumstances, a total of 0.25 to 0.75 mg of
elemental iron is lost because of gastrointestinal bleeding
daily.
• A small amount of iron is also lost in sloughed intestinal cells
and from minute amounts of bleeding, making the average
daily iron loss approximately 1 mg
• The absorptive capacity of the small intestine for iron can
increase dramatically in response to iron depletion but
normally is limited.
Feldman, M et al. (2006). Sleisenger & Fordtran's
Gastrointestinal and Liver Disease, 8th ed.
• iron deficiency results only when iron loss
exceeds absorption, usually when blood loss
exceeds 5 to 10 mL/day over many weeks.
• When diagnosis of iron deficiency anemia is
established
• iron therapy should be instituted
• Ferrous sulfate, 325 mg orally two to three
times daily, is recommended
Hypertension
• Diuretics – contraindicated in hyperuricemia, gout
• Anti-adrenergics
– Alpha Adrenoceptor Blockers - salt and/or water depleted
may exhibit a sudden, drastic drop in standing BP after the
first dose
– Beta Adrenoceptor Blockers – relative contraindication
insulin-requiring diabetes; renal failure; lipid disorders
– Adrenergic Neuron Blockers – contraindicated in patient
with PUD
– Centrally Acting Anti-hypertensives – 2nd or 3rd line with
multiple drug regimen
Fauci, AS, et al. (2008). Harrison’s
Principles of Internal Medicine, 17th ed
PNDF Vol II, 3rd ed (2006)
Hypertension
• Direct Vasodilators – precaution in renal or
hepatic impairment
• Calcium Channel Blockers
• Angiotensin Converting Enzyme (ACE)
Inhibitors – contraindicated in renal failure
• Angiotensin 2 Receptor Blockers (ARB) –
precaution in renal insufficiency
Fauci, AS, et al. (2008). Harrison’s
Principles of Internal Medicine, 17th ed
PNDF Vol II, 3rd ed (2006)
Calcium Channel Blockers
• Reduce vascular resistance through L-channel
blockade, which reduces intracellular calcium and
blunts vasoconstriction
• NIFEDIPINE 5-10 mg q8h,
• Amlodipine 5-10 mg daily
• Felodipine Initially, 5 mg once daily, PO; titrated
slowly to 10 mg once daily.
• Nicardipine Start with 10 mg 3x/d PO
• Nimodipine PO 60 mg q4h.
Fauci, AS, et al. (2008). Harrison’s
Principles of Internal Medicine, 17th ed
PNDF Vol II, 3rd ed (2006)
Thank you!!!
Jordan, KM, et al. (2007). Guideline for Management
of Gout. British Society for Rheumatology
In the absence of
contraindications
Ice compress 20
min x 4x/day up
to one week
0.5 mg/tab TIDQID
initially at 30 mg
and rapidly tapered
over 6 days can be
given as alternative
Allopurinol started at 100 mg/day 2 weeks after the pain
and swelling has subsided.
Dose is titrated by 50-100 mg/day every 2 to 4 weeks to
achieve SUA <6 mg/dL.
The maximum dose of allopurinol is 300 mg/day.
SUA and serum creatinine should be periodically
monitored.
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
Jordan, KM, et al. (2007). Guideline for Management of Gout.
British Society for Rheumatology
Jordan, KM, et al. (2007). Guideline for Management
of Gout. British Society for Rheumatology
Absence of response after a week should
prompt re-evaluation of the diagnosis and
referral to a rheumatologist
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
Jordan, KM, et al. (2007). Guideline for Management of Gout.
British Society for Rheumatology
• In the absence of contraindications, i.e.. renal impairment or
gastrointestinal ulcers, the use of colchicines, traditional nonsteroidal anti-inflammatory drugs (NSAIDs), OR selective cyclooxygenase 2 (COX-2) inhibitors is recommended for the treatment
of acute gouty arthritis.
• The expert panel recommends that colchicines (500 mcg tab)
should not exceed 4 tablets in divided doses per day.
• Prednisone, initially at 30 mg and rapidly tapered over 6 days can
be given as alternative if colchicines, traditional NSAIDs or COX-2
inhibitors are contraindicated or not tolerated by the patient
• Absence of response after a week should prompt re-evaluation of
the diagnosis and referral to a rheumatologist
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
• Ice compress is recommended in combination with
pharmacologic agents for relief of joint pain and swelling of
acute gouty arthritis
• Serum uric acid (SUA) level should be reduced to and
maintained at <6 mg/dL (0.36 mmol/L)
• Continuous long term therapy with allopurinol is advised to
achieve a target SUA level of <6 mg/dL
• Allopurinol should be started at 100 mg/day 2 weeks after the
pain and swelling of gouty arthritis has subsided. The dose is
titrated by 50-100 mg/day every 2 to 4 weeks to achieve SUA
<6 mg/dL. The maximum dose of allopurinol is 300 mg/day.
SUA and serum creatinine should be periodically monitored.
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
• A referral to an internist or rheumatologist is recommended if
SUA persistently remains > 6 mg/dL despite maximum dose.
• Colchicine should be used at 0.5 mg/tab OD BID to prevent
gout flares when initiating urate-lowering therapy with
allopurinol. This should be maintained for 3-6 months from
the last occurrence of gout flare and after the optimal SUA
target is achieved. In the event that adverse events like
diarrhea occur, a lower dose of colchicines should be used.
NSAIDs should not be used for prevention of gout flares.
• Dietary modification (to promote weight loss) and avoidance
of alcohol should be prescribed.
• Low impact exercises (walking, biking, swimming, ballroom
dancing) may also be advised.
Li-Yu J, et al. (2008) Philippine Clinical Practice Guidelines for
Management of Gout. Phil. J. Internal Medicine, 46:165-173
Management of acute gout
(1) Affected joints should be rested and analgesic, antiinflammatory drug therapy commenced immediately, and
continued for 1–2 weeks.
(2) Fast-acting oral NSAIDs at maximum doses are the drugs of
choice when there are no contraindication.
(3) In patients with increased risk of peptic ulcers, bleeds or
perforations, co-prescription of gastro-protective agents
should follow standard guidelines for the use of NSAIDs and
Coxibs.
(4) Colchicine can be an effective alternative but is slower to
work than NSAIDs. In order to diminish the risks of adverse
effects (especially diarrhea) it should be used in doses of 500g
bd–qds.
Jordan, KM, et al. (2007). Guideline for Management
of Gout. British Society for Rheumatology
(5) Allopurinol should not be commenced during an acute attack
but in patients already established on allopurinol, it should be
continued and the acute attack should be treated
conventionally.
(6) Opiate analgesics can be used as adjuncts.
(7) Intra-articular corticosteroids are highly effective in acute
gouty monoarthritis and i.a., oral, i.m or i.v corticosteroids can
be effective in patients unable to tolerate NSAIDs, and in
patients refractory to other treatments.
(8) If diuretic drugs are being used to treat hypertension, an
alternative antihypertensive agent should be considered, but
in patients with heart failure, diuretic therapy should not be
discontinued.
Jordan, KM, et al. (2007). Guideline for Management
of Gout. British Society for Rheumatology
Given in ward
•
•
•
•
•
Omeprazole 40 mg tab OD
Amlodipine 10 mg tab OD
Clindamycin 300 mg cap q 6
Ciprofloxacin 250 mg tab BID
Given Colchicine as follows to treat acute
gout: 2 tabs now then 1 tablet after 6 hours
• Cold compress x 10-15 mins TID on inflamed
joints
ANTIGOUT
• For acute gout
• COLCHICINE
Oral: 500 mcg tablet
• NSAIDs
• For chronic gout
• ALLOPURINOL Oral: 100 mg and 300 mg tablet
PNDF Vol. I, 7th ed. (2007)
•
•
•
•
•
•
•
•
2.4 NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs)
2.4.1 Non-selective COX inhibitors
IBUPROFEN
NAPROXEN
diclofenac
indometacin
ketoprofen
mefenamic acid
• 2.4.2 Selective COX 2 inhibitor
• CELECOXIB
PNDF Vol. I, 7th ed. (2007)