DRUGS CAUSING

vasculitis, scleroderma, gout, tendon rupture 2

Hyperthermia, Hirsutism 3

Myopathies 4

Osteoporosis & SIADH 5

Aplastic Anemia 6

Hyperprolactinemia 7

Seizures 8

Drugs with Risk of Hemolysis in G6PD Deficiency pts 9

Phototoxicity 10

Thrombocytopenia 11

Drugs Associated with Edema 12

Myalgia 13

Table 331-2 Drug-Induced Musculoskeletal conditions

Arthralgias
Quinidine, cimetidine, quinolones, chronic acyclovir, interferon, IL-2, nicardipine, vaccines, rifabutin, aromatase and H!Vprotease inhibitors
Myalgias/myopathy
Glucocorticoids, penicillamine, hydroxychloroquine, AZT, lovastatin, simvastatin, pravastatin, clofibrate, interferon, IL-2, alcohol, cocaine, taxol, docetaxel,
colchicine, quinolones, cyclosporine, protease inhibitors
Tendon rupture/tendinitis
Quinolones, glucocorticoids, isotretinoin
Gout
Diuretics, aspirin, cytotoxics, cyclosporine, alcohol, moonshine, ethambutol
Drug-induced lupus
Hydralazine, procainamide, quinidine, phenytoin, carbamazepine, methyldopa, isoniazid, chlorpromazine, lithium, penicillamine, tetracyclines, TNF inhibitors,
ACE inhibitors, ticlopidine
Osteonecrosis
Glucocorticoids, alcohol, radiation, bisphosphonates
Osteopenia
Glucocorticoids, chronic heparin, phenytoin, methotrexate
Scleroderma
Vinyl chloride, bleomycin, pentazocine, organic solvents, carbidopa, tryptophan, rapeseed oil
Vasculitis
Allopurinol, amphetamines, cocaine, thiazides, penicillamine, propylthiouracil, montelukast, TNF inhibitors, hepatitis B vaccine,
trimethoprim/sulfamethoxazole

Abbreviations:ACE, angiotensin-converting enzyme; IL-2, interleukin 2; TNF, tumor necrosis factor.

Hirsutism

Table 387- 11 Drug- Induced Myopathies

I
Drugs Major Toxic Reaction
Lipid -lowering agents Drugs belonging to all three of the maj or classes of lipid -lowering agents can produce a spectrum of toxicity: asymptomatic
serum creatine kinase elevation, myalgias, exercise-induced pain, rhabdomyolysis, and myoglobinuria.
Fibric acid derivatives
HMGCoA reductase inhibitors
Niacin (nicotinic acid)

Glucocorticoids Acute, high-dose glucocorticoid treatment can cause acute quadriplegic myopathy. These high doses of steroids are often
combined with nondepolarizing neuromuscular blocking agents but the weakness can occur without their use. Chronic steroid
administration produces predominantly proximal weakness.
Nondepolarizing Acute quadriplegic myopathy can occur wit h or wit hout concomitant glucocorticoids.
neuromuscular blocking
agents
Zidovudine Mitochondrial myopathy with ragged red fibers.
Drugs of abuse All drugs in this group can. lead to widespread muscle breakdown, rhabdomyolysis, and myoglobinuria.

Alcohol Local injections cause muscle necrosis, skin induration, and limb contractures.
Amphetamines

Cocaine

Heroin
Phencyclidine
Meperidine

Autoimmune toxic myopathy Use of this drug may cause polymyositis and myasthenia gravis.
d-Penicillamine
Amphophilic cationic drugs All amphophilic drugs have the potential to produce painless, proximal weakness associated with autophagic vacuoles in the
muscle biopsy.
Amiodarone
Chloroquine

Hydroxychloroquine

Antimicrotubular drugs This drug produces painless, proximal weakness especially in the setting of renal failure. Muscle biopsy shows autophagic
vacuoles.
Colchicine
Drugs causing SIADH

iTable 107-3 Some Drugs and Chemicals Associated with Aplastic Anemia
Agents that regularly produce marrow depression as major toxicity in commonly employ ed doses or normal exposures:
Cytotoxic drugs used in cancer chemotherapy: a lkyla ting agents, antimetabolites, antimitotics, some antibiotics
Agents that frequently but not inevitably produce marrow aplasia:
Benzene
Agents associated with aplastic anemia but w ith a relatively low probability:
Chloramph eni col

Insecticides

Antiprotozoals: quinacrine and chloroqufne, mepacrine

Nonsteroidal anti-inflammatory drugs (including p h enylbutazone,

indomethacin, ibuprofen, sulindac, aspirin)

Anticonvulsa nts (hydantoins, carbamazepine, phenacemide, felbamate)

Heavy metals (gold, arsenic, b ismuth, mercury)

Sulfonamides: some antibiotics, a n tithy roid drugs ( methimazole, methylthiouracil, propylthiouracil), antidiabetes drugs ( tolbutamide ,
chlorpropamide) , carbonic anhydrase inhibitors ( acetazolamide and methazolamide)

Ant ihistamines (dmetidine, chlorpheniramine)

d-Penicillamin e

Estrogens (in pregnancy and in h igh doses in animals)

Agents whose association with aplastic anemia is more tenuous"

Other antibiotics (streptomycin, tetracydine, methicillin ,

mebendazole, t rimethoprim/ sulfamethoxazole, flucytosine)

Sedatives and tranquilizers ( chlorpromazine, prochlorperazine,

piperacetazine, chlordiazepoxide, meprobamate, methyprylon)

Allopurinol

Methyldopa

Quinidine

Uthium

Guanidine

Potassium perchlorate

Thiocyanate

Carbimazole
of prolactin

Table 369 - 5 Drugs and Other Substances that Can Cause Seizures
Alkylating agents (e.g., bus.u lfan, chlorambucil)
Anti mal arials (chloroquine , mefloquine)
Antimic robials/ antivirals
B-lactam and related compounds
Quinolones
Acyclovir
Isoniazid
Gancidovir
An esthetics and analgesics
Meperidine
Tramadol
Local anesthetics
Dietary supplements
Ephedra (ma huang)
Gingko
Immunomodulatory drugs

Cyclosporine
OKT3 (monoclonal antibo dies t o T cells )
Tacro limus
Interferons
Psychotropics
Antidepressants
Antipsychotics
Lithium
Rad iographic contrast agents
Theophylline
Sedative-hypno t ic drug withdrawal
Alcohol
Barbiturates (short-acting)
Benzodiazepines (short-acting)
Drugs of abuse
Amphetamine
Cocaine
Phencyclidine
Table 106- 5 Drugs t hat Carry Risk of Clinical Hemolysis in Persons with G6PD Deficiency
Definite Risk Possible Risk Doubtful Risk
Antimalarials Primaquine Chloroquine Quinine
Dapsone/ chlorproguanil*

Sulphonamides/sulphone,s Sulfamethoxazole Sulfasalazine Sulfisoxazole

Others Sulfadimidine Sulfadiazine
Dapsone
Antibacterial/antibiotics Cotrimoxazole Ciprofloxacin Chloramphenicol
Nalidixic acid Norfloxacin p-Aminosalicylic acid
Nitrofurantoin
Niridazole
Antip yretic/ analgesics Acetanilide Acetylsalicylic acid high dose (>3 g/ d) Acetylsalicylic acid ( <3 g/d)
Phenazopyridine Acetaminophen
Phenacetin
Othe r Naphthalene Vitamin K analogues Doxorubicin
Methylene blue Ascorbic acid > 1 g Probenecid
Rasburicase
 Topical Systemic

s
Table 1"15- 1 Drugs Reported ~~ Definitely or Probably causing"Isolated Thrombocytopenia
Abciximab I buprofen
Acetaminophen I opanoic acid
Aminoglutethimide Levamisole
Aminosalicylic acid Linezolid
Amiodaron.e Meclofenamate
Amphotericin 8 Methicillin
Ampicillin Methyldopa
Carbamazepine Nalidixic acid
Chlorpropamide Naproxen
Danazol Oxyphenbutazone
Capt opril Phenytoin
Cimetidine Piperacillin
Diatrizoate meglumine (Hypaque Meglumine.) Procainamide
Diclofenac Quinine
Digoxin Quinidine
Dipyridamole Rifampin
Eptifibatide Simvastatin
Ethambutol Sulfa-containing drugs
Famotidine Tamoxifen
Fluconazole Tirofiban
Furosemide Trimethoprim/ sulfamethoxazole
Glyburide Valproic acid
Gold Vancomycin
Hydrochlorothiazide
Imipenem/Cilastatin
Table 36-1 Drug~ Associate!! with Edema Formation
Nonsteroidal anti-inflammat ory drugs
Antihypertensive a gents
Direct arterial/arte riolar vasodilators
Hydralazine
Clonidine
~1ethyld opa

Guanethidine
Minoxidil
Calcium channel ant agonists
o;-Adrenergic antagonists
Thiazolidinediones
Steroid hormones
Grucocorticoids
Anabolic steroids
Estrogens
Progestins
Cyclosporine
Growth hormone
Immunotherapies
I nterleukin 2
OKT3 monoclonal antibody
 CNS

Actions of Opioid Receptors & Peripheral and Central Vertigo 15

Causes of Episodic Generalized Weakness, & Spinal cord levels 16

Cerebellar Ataxia, Sensory Ataxia, and Frontal Gait Disorders 17

Clinical Features of Parkinson's Disease 18

Mesial Temporal Lobe Epilepsy Syndrome features 19

Neurotrophic Factors, & Causes of Ptosis 20

Neurologic Channelopathies 21

Indications and contraindications for rTPA in stroke 22

Neurologic Diseases in Patients with HIV Infection 23

Differentiation of the Major Dementias & C/F of Aphasias 24

EMG Features Axonal Degeneration vs Segmental Demyelination 25

Table 21-1 Features of Peripheral and Central Vertigo

Sign or Symptom Peripheral (Labyrinth or Vestibular Nerve) Central (Brainstem or Cerebellum)
Direction of associated nystagmus Unidirectional; fast phase opposite lesion Bidirectional (direction-changing) or
unidirectional
Purely horizontal nystagmus Uncommon ~1ay be present
without torsional component
Purely vertical or purely torsional Never presentb May be present
nystagmus
Visual fixation Inhibits nystagmus No inhibition
Tinnitus and/or deafness Often present Usually absent
Associated central nervous system None Extremely common (e.g., diplopia, hiccups,
abnormalities cranial neuropathies, dysarthria)
Common causes Benign paroxysmal positional vertigo, infection (labyrinthitis), vestibular Vascular, demyelinating, neoplasm
neuritis, Meniere's disease, labyrinthine ischemia, trauma, toxin

Table 393-1 Actions of Opioid Receptors

Receptor Type Actions

Mu (~)(e .g ., morphine) Analgesia, reinforcement euphoria, cough and appetite suppression, decreased respirations, decreased GI motility, sedation,
hormone cbanges, dopamine and acetylcholine release
Kappa (11:) (e.g., Dysphoria, decreased GI motility, decreased appetite, decreased respiration, psychotic symptoms, sedation, diuresis, analgesia
butorphanol)
Delta (b.) (e.g., Hormone changes, appetite suppression, dopamine release
etorphine)
Corresponding Vertebral Body
Cerebellar Ataxia Sensory Ataxia Frontal Gait
 Table 372-1 Clinical Features of Parkinso n 's Disease

Cardinal Features Other Mot or Features Nonmot or Features

Bradykinesia Micrograpbia Anosmia

Rest tremor Masked facies (hypomimia) equalize Sensory distu rbances (e.g., pa in)
Rigidity Reduced e ye blink Mood d isorders (e.g., depression)

Gait disturbance/ postural instab ility Soft voice (hypophonia) Sle ep d isturbances
Dysphagia Autonomic dist u rbances
Freezing Orthostat ic hypotension
Gastro inte stinal d ist u rbances

Genito urinal dist u rbances

Sexual dysfunction
Cognitive impairment/Dement ia

1
Table 372-6 Hyperkinetic Movement Disorders

Tre"'IO' Rhyth11icosc llstion of a !:odr :art due tointerMi::ent "''Uscle contrac: ons
9/:tona JnvoLntar1 :atte ed sustained or repea:ednuscle ccntrac:ons often a:s3catedwi:1 tll'istin; moverrents and ab ornal postlve:
P.the::s s Slew, ds:sl, writhi g, involun:sry110'/ements ll'~h a prcpensity toaffe:t :e arm; and -ands
Chorea Ra:id, senipLrposeful, gracefu, dsnce ike on:atterned iniolu tarymovemen~s invol;inJ distal cr p:cx mal11uscle goups
\lyoclcnus SU:'den, :rief (<:CO 11:), jerk~ike, arrhythrric rru:cle t11itcl'es
Tic Brief, epeated, sterect'fPed m;sde contractio s tha: ere cfte sLppressible:Canbe :irrple and invol1e a sinJIErru:cle ;roup or cumplex and
afect a sngE o' moto :ctiv~ies
Table 369-3 C.h aracteristic.s of the Mesial Temporal Lobe Epilepsy Syndrome
History
History of febrile seizures Rare generalized seizures
Family history of epilepsy Seizures may remit and reappear
Early onset Seizures often intractable

Clinical observations
Aura common Postictal diso rientation

Behavioral arrest/stare Memory loss

Complex automatisms Dysphasia (with focus in dominanthemisphere)
Unilateral posturing

laboratory studies
Unilateral or bilateral: anterior temporal spik es on EEG
Hypometabolism on interictal PET
Hypoperfusion on interictal SPECT
Material-specific memory deficits on intracranial amobarbital (Wada) test
MRI findings
Small hippocampus with increased signal on T2-weighted sequences
Small temporal lobe
Enlarged temporal horn
Pathologic findings
Highly selective loss of specific cell populations within hippocampus in most cases

Abbreviations: EEG, electroencephalogram; PET, positron em ission t omography; SPECT, single photon emission computed t omography.
Table 366-3 Neurotrophic Factors
Neurotrophin family Table 387- 1 Neuromuscular causes of Ptosis or Ophthalmoplegi~

Nerve growt h factor Peripheral Neuropathy

Brain-derived neurotrophic factor Guillain-Barre syndrome

Neurotrophin -3 Miller-Fisher syndrome

Neuromuscular Junctionr
Neurotrophin-4
Botulism
Neurotrophin-6
Lambert-Eaton syndrome
Cytokine family
Myasthenia gravis
Ciliary neurotrophic factor
Congenital myasthenia
Leukemia inhibitory factor
Myopathy
Interleukin 6 Mitochondrial myopathies
cardiotrophin-1 Kearns-Sayre syndrome
Transforming growth factor B family Progressive external ophthalmoplegia
Glial-derived neurotrophic family Oculopharyngeal and oculopharyngodistal muscular dystrophy
Neurturin Myotonic dystrophy (ptosis only)
Persephin Congenital myopathy

Fibroblast growth factor family Myotubular

Hepatocyte growth factor Nemaline (ptosis only)

Hyperthyroidism/Graves' disease (ophthalmoplegia without ptosis)
Insulin-like growth factor (IGF) family
Hered itary inclusion body myopathy type 3
IGF l
IGF-2
Table 366- 1 Examples of Neurologic Channelopathies

Category Disorder Mutated Gene Chap. Ref.

Genetic
Episodicataxia-1 K KCNA1 373
Episodicataxia-2 ca CACNLlA
Spinocerebellar ataxia-6 Ca CACNL1A

Migraine Familial hemiplegic migraine 1 ca CACNLlA 14

Familial hemiplegic migraine 3 Na SCN1A

Epilepsy Benign neonatal familial oonvulsions K KCNQ2, KCNQ3 SCNlB 369

Generalized epilepsy wit~ febrile convulsions plus Na

Periodi: paralysis Hyperkalemic periodic paralysis Na SCN4A 387

Hypokalemic periodic paralysis Ca CACNL1A3

Myotoria Myotonia congenita Cl QCNl 387

Paramyotonia congenita Na

Deafness Jervell and Lange-Nielsen syndrome (deafness, prolonged QT interval, and arrhythmia) K KCNQl , KCNEf 30
Autosomal dominant pro~ressive deafness K KCNQ4
1-----
Autoimmune
Paraneoplastic L.imbic encephalitis Kv1 101
Acquired neuromyotonia Kv1 101
Cerebellar ataxia ca (P/Q type) 10 1
Lambert-E.aton syndrome ca (P/Q type) 101
Table 370-1 Administration of I ntravenous Recombinant Tissue Pl~sminogen Activator (Rtpa) for Acute Ischemic Stroke (Ais)a
Indication Contraindication
Clinical diagnosis of stroke Sustained BP > 185/110 mm Hg despite treatment
Onset of symptoms to t ime of drug administration s:3 h Platelets <100,000; HCT <25%; glucose <50 or >400 mg/ dl
CT scan showing no hemorrhage or edema of >1/3 of the MCA territory Use of heparin within 48 h and prolonged PIT, or elevated INR
Age " 18 years Rapidly improving symptoms
Consent by patient or surrogate Prior stroke or head injury within 3 months; prior intracranial hemorrhage
Major surgery in preceding 14 days
Minor stroke symptoms
Gastroint estinal bleeding in preceding 21 days
Recent myocardial infarction
Coma or stupor

Administration of rtPA
Int ravenous access with two peripheral IV lines (avoid arterial cr central line placement)
Review eligibility for rtPA
Administer 0.9 mg/kg IV (maximum 90 mg) IV as 10% of total dcse by bolus, followed by remainder of total dose over 1 h
Frequent cuff blood pressure monitoring
No other antithrombotic'treatment for 24 h
For decline in neurologic status or uncontrolled blood pressure, stop infusion, give cryoprecipitate, and reimage brain emergent ly
Avoid urethral catheterization for " 2 h
Table 189-13 Neurologic Diseases in Patients with HIV Infection
Opportunistic infections Myelopathy

Toxoplasmosis Vacuolar myelopathy

Cryptococcosis Pure sensory ataxia

Progressive multifocal leukoencephalopathy Paresthesia/ dysesthesia

Cytomegalovirus Peripheral neuropathy
Syphilis Acute inflammatory demyelinating polyneumpathy (Guillain-Barre
syndrome)
Mycobacteriumtuberculosis
Chronic inflammatory demyelinating polyneuropathy (CIDP)
HTLV-1infection
Mononeuritis multiplex
Amebiasis
Distal symmetric polyneuropathy
Neoplasms
Myopathy
Primary CNS lymphoma
Kaposi's sarcoma

Result of HIV-1 infection

Aseptic meningitis
HIV-associated neurocognitive disorders, including
HIVencephalopathy/AIDS dementia complex
Table 26- 1 Clinical Features of Aphasias and Related Conditions

Comprehension Repetition of Spoken l anguage Naming Fluency

Wernicke's Impaired Impaired Impaired Preserved or increased
Broca' s Preserved (except grammar) Impaired Impaired Decreased
Global Impaired Impaired Impaired Decreased
Conduction Preserved Impaired Impaired Preserved
Nonfluent (motor) transcortical Preserved Preserved Impaired Impaired
Fluent (sensory) transcortical Impaired Preserved Impaired Preserved
Isolation Impaired Echolalia Impaired No purposeful speech
Anomie Preserved Preserved Impaired Preserved except for word-finding pauses
Pure word deafness Impaired only for spoken language Impaired Preserved Preserved
Pure alexia Impaired only for reading Pr eserved Preserved Preserved

Table 371- 4 Clinical Differentiation of the Major Dementias

Disease First Symptom Mental Status Neuropsychiatry Neurology Imaging

AD Memory loss Episodic memory loss Initially normal Initially normal Entorhinal cortex and
hippocampal atrophy
FTD Apathy; poor judgment/insight, Frontal/executive, Apathy, disinhibition, May have vertical gaze Frontal, insular, and/or
speech/language; hyperorality language; spares drawing hyperorality, euphoria, palsy, axial rigidity, temporal atrophy; spares
depression dystonia, alien hand, or posterior parietal lobe
MND
DLB Visual hallucinations, REM sleep Drawing and Visual hallucinations, Parkinsonism Posterior parietal atrophy;
disorder, delirium, Capgras' frontal/executive; spares depression, sleep hippocampi larger than in AD
syndrome, parkinsonism memory; delirium prone disorder, delusions
CJD Dementia, mood, anxiety, Variable, frontal/executive, Depression, anxiety Myoclonus, rigidity, Cortical ribboning and basal
movement disorders focal cortical, memory parkinsonism ganglia or thalamus
hyperintensity on
diffusion/flair MRI
Vascular Often but not always sudden; Frontal/executive, cognitive Apathy, delusions, anxiety Usually motor slowing, Cortical and/or subcortical
variable; apathy, falls, focal slowing; can spare memory spasticity; can be normal infarctions, confluent white
weakness matter disease

Abbreviations: AD, Alzheimer's disease; CBD, cortical basal degeneration; CJD, Creutzfeldt-Jakob disease; DLB, dementia with Lewy bodies; FTD,
frontotemporal dementia; MND, motor neuron disease; PSP, progressive supranuclear palsy.
Table 384-3 Electrophysiologic Feat ures: Axonal Degeneration vs . Segmental Demyelination

Axonal Degeneration Segmental Demyelination

Motor Nerve Conduction Studies
CMAP amplitude Decreased Normal (except with CB)
Distal ,latency Normal Prolonged
Conduction velocity Normal Slow
Conduction block Absent Present
Temporal disper sion Absent Present
F wave Normal or absent Prolonged or Absent
H reflex Normal or absent Prolonged or Absent
Sensory Nerve Conduction Studies
SNAP amplitude Decreased Normal
Distal latency Normal Prolonged
Conduction velocity Normal Slow
Needle EMG
Spontaneous activity
Fibrillations Present Absent
Fasciculations Present Absent
Motor unit pat e ntials
Recruitment Decreased Decreased
Morphology Long duration/ polyphasic Normal
 IMMUNOLOGY

HLA and its assoc diseases part1 27

HLA and its assoc diseases part2 28

Complement Deficiencies and Associated Diseases 29

Amyloidosis 30

ANA Patterns and Clinical Associations 31

Systemic sclerosis and limited cutaneous sclerosis 32

Organ involvement in systemic and limited sclerosis 33

Immunologically Mediated Blistering Diseases 34

Dermatomyositis, Polymyositis, Inclusion body myositis 35

Lupus nephritis 36

jTable 315- 1. Sign ifican t HLA Cl ass I and C lass I I Associations w i th Di sease
Marker Gene Strength of Association
Spondyloa rth ropathies
Ankylosing spon dylitis 827 8 "2702,-04, -05 ++ + +
Reiter's syndrome 827 ++ + +
Acute anterior uveitis 827 ++ +
Reactive arthritis (Yerslnia, SalmoneHa, ShigeUa, Chla mydia) 827 +++
Psoriabc spondylitis 827 +++
Collagen- Vascular Diseases
Juvenrle arthritis, pauciarticular DRS ++

DRS ++

Rheumatoid arthntis DR4 DRB1"0401, -04, -05 +++

Sjogren's syndrome DR3 ++
Systemic lupus erytt.ematosus
Wh1te DR3 +
Japanese DR2 ++
Autoimmune Gut and Skin
Gluten-sensit ive e nteropathy (celia c d isease) DQ2 DQA1.0501 ++ +
DQ8 10201
Chronic active h epatitis DR3 ++
Dermatit is herpetiformis DR3 ++ +
Psoriasis vulgaris Cw 6 ++
Pemphigus vulgaris DR4 DRB10402 ++ +
DQl DQ8 1.0503
Bullous pemphigoid varian t DQ7 DQ81.0301 +
Autoimmune Endoc,r ine
Type 1 diabetes mellitus DQS DQ81.0302 +++
DR4 DRB1"0401, -04
++
DR3
DR2 DQ81 o602
_..
Hyperthyroidism ( Graves') 88 +
DR3 +
Hyperthyroidism (Japanese) 8 35 +
Adrenal Insufficiency DR3 ++
+
+
++

+++
++++
++
++++
Table 314- 17. Complement Deficiencies and Associated Diseases
Component Associated Diseases
Classic Pathway
Clq, Clr, CIS, C4 Immune-complex syndromes,"' pyogenic infections
C2 Immune-complex syndromes," few with pyogenic infections
Cl Inhibitor Rare immune-complex disease, few with pyogenic infections
C3 and Alternative Pathway C3
C3 Immune-complex syndromes,"' pyogenic infections
D Pyogenic infections
Properdin Neisseria infections
I Pyogenic infections
H Hemolytic uremic syndrome
Membrane Attack Complex
CS,C6,C7,C8 Recurrent Neisseria infections, immune-complex disease
C9 Rare Neisseria infections

"Immune-complex syndromes include systemic lupus erythematosus (SLE) and SLE-Iike syndromes, glomerulonephritis, and vasculitis syndromes.
Table 112-1 Amyloid Fibril Proteins and Their Clinical Syndromes

Term Precursor Clinical Syndrome Clinical Involvement

Systemic Amyloidoses
AL Immunoglobulin light chain Primary or myeloma associated" Any

AH Immunoglobulin heavy chain Primary or myeloma associated (rare) Any

AA Serum amyloid A protein Secondary; reactiveb Renal, any

AB2M B2-~1icroglobulin Hemodialysis-associated Sy1ovial membrane, bone

ATIR Transthyretin Familial :mutant) Cardiac, peripheral and autonomic nerves

Senile ststemic (wild type.)

AApoAI Apolipoprotein AI Familial Hepatic, renal

AApoAII Apolipoprotein All Familial Renal
AGel Gelsolin Familial Corneas, cranial nerves, renal
AFib Fibrinogen kt. Familial Renal
ALys Lysozyme Familial Renal
ALECT2 Leukocyte chemotactic factor 2 ? Renal
Localized Amyloidoses
AB Amyloid B protein Alzheimer's disease; Down syndrome
ACys Cystatin c Cerebral amyloid angiopathy CI\S, vascular
APrP Prion protein Spongiform encephalopathies Cl\5
Al APP Islet amyloid polypeptide (amylin) Diabetes-associated Pancreas
ACal Calcitonin Medullary carcinoma of the thyroid Thyroid
AANF Atrial natriuretic factor Age-related Cardiac atria
APro Prolactin Endocrinopathy Pituitary
Table 323-2 Subsets of Systemic Sclerosis (Sse): Limited Cutaneous Sse versus Diffuse cutaneous Sse

Features limited Cutaneous SSe Diffuse Cutaneous SSe

Skin involvement Indolent onset. Rapid onset. Diffuse: fingers, extremities, face, trunk; rapid
progress1on
Limited to fingers, distal to elbows, face; slow
progression

Raynaud' s phenomenon Precedes skin involvement; associated with critical Onset coincident with skin involvement, may be mild
ischemia

Musculoskeletal Early arthralgia, fatigue Severe arthralgia, carpal tunnel syndrome, tendon friction rubs

Pulmonary fibrosis Occasional, moderate Frequent, early and severe

Pulmonary arterial Frequent, late, may be isolated May occur, often in association with pulmonary fibrosis
hypertension

Scleroderma renal crisis Very rare Occurs in 15%; early

Calcinosis cutis Frequent, prominent May occur, mild

Characteristic autoantibodies Anticentromere Antitopoisomerase I (Scl-70), anti-RNApolymerase III

Table 323-4 Internal Organ Involvement: limited Cutaneous and Diffuse Cutaneous Forms of Systemic Sclerosis

Features Limited Cutaneous SSe (%) Diffuse Cutaneous SSe(%)

Skin involvement go* 100

Raynaud's phenomenon 99 98

Esophageal involvement 90 80

Pulmonary fibrosis 35 65

Pulmonary arterial hypertension 15 15

Myopathy 11 23

Cardiac involvement 9 12

Scleroderma renal crisis 2 15

Table S4-1 I mmunologically Mediated Blistering Diseases
Disease Clinical Histology Immunopathology Autoantigensa
Pemphigus Crusts and shallow erosions on scalp, Acantholytic blister formed Cell surface deposits of IgG on Dsg1
foliaceus central face, upper chest, and back in superficial layer of keratinocytes
epidermis
Pemphigus Flaccid blisters, denuded skin, Acanth'olytic blister formed Cell surface deposits of IgG on Dsg3 (plus Dsg 1 in patients
vulgaris oromucosal lesions in suprabasal layer of keratinocytes with skin involvement)
epidermis
Paraneoplastic Painful stomatitis with Acantholysis, keratinocyte Cell surface deposits of IgG and C3 Plakin protein family members
pemphigus papulosquamous or lichenoid necrosis and vacuolar on keratinocytes and (variably) and desmosomal cadherins
eruptions that progress to blisters interface dermatitis similar immunoreactants in epidermal (see text for details)
BMZ
Bullous Large tense blisters on flexor surfaces Subepidermal blister with Linear band of lgG and/or C3 in BPAGl,BPAG2
pemphigoid and trunk eosinophil-rich infiltrate epidermal BMZ
Pemphigoid Pruritic, urticarial plaques, rimmed by Teardrop -shaped, Linear band of C3 in epidermal BMZ BPAG2 (plus BPAG l in s.ome
gestationis vesiCles and bullae on the trunk and subepidermal blisters in patients)
extremities dermal papillae; eosin'ophil
rich infiltrate
Linear IgA Pruritic small papules on extensor Subepidermal blister with Linear band of IgA in epidermal BMZ BPAG2 (see text for specific
disease surfaces; occasionally larger, arciform neutrophil-rich infiltrate details)
blisters
Cicatricial Erosive and/or blistering lesions of Subepidermal blister that Linear band of IgG, IgA, and/or C3 in BPAG2, laminin -332, or others
pemphigoid mucous membranes and possibly the may or may not include a epidermal BMZ
skin; scarring of some sites leukocytic infilt rate
Epidermolysis Blisters, erosions, scars, and milia on Subepidermal blister that Linear band of IgG and/or C3 in Type VII collagen
bullosa acquisita sites exposed to trauma; widespread, may or may not include a epidermal BMZ
inflammatory, tense blisters may be leukocytic infiltrate
seen initially
Dermatitis Extremely prurit ic small papules and Subepidermal blister with Granular deposit s of IgA in dermal Epidermal transglut aminase
herpetiformis vesicles on elbows, knees, buttocks, neutrophils in dermal papillae
and posterior neck papillae

aAutoantigens bound by these patients' autoantibodies are defined as follows: Dsg1, desmoglein 1; Dsg3, desmoglein 3; BPAG 1, bullous pemphigoid
antigen 1; BPAG2, bullous pemphigoid antigen 2.
Abbreviation: BMZ, basement membrane zone,
Table 388-1 Features Associated with Inflammatory Myopathies

Characteristic Polymyositis Dermatomyositis Inclusion Body Myositis

Age at onset >18 years Adulthood and childhood >50 years
Familial a.ssociation No No Yes, in some cases
Extramuscular manifestations Yes Yes Yes
Associated conditions
Connective tissuediseases Yes" Scleroderma and mixed connective tissue disease (overlap syndromes) Yes, in up to 20% of cases 8

Systemic autoimmune diseasesb Frequent Infrequent Infrequent

Malignancy No Yes, in up to 15% of cases No

Viruses Yes' Unproven Yes'

Drugsd Yes Yes, ra rely No

Parasites and bacteriae Yes No No

Table 283-3 Classification for l upus Nephritis
Class I Minimal mesangial Normal histology with mesangial deposits
Class Mesangial Mesangial hypercellularity with expansion of the mesangial matrix
II proliferation
Class Focal nephritis Focal endocapillary extracapillary proliferation with focal subendothelial immune deposits and mild mesangial
III expansion
Class Diffuse nephritis Diffuse endocapillary extracapillary proliferation with diffuse subendothelial immune deposits and mesangial
IV alterations
Class Membranous Thickened basement membranes with diffuse subepithelial immune deposit s; may occur with class Ill or IV lesions and is
v nephritis sometimes called mixed membranous and proliferative nephritis
Class Sclerotic nephritis Global sclerosis of nearly all glomerular capillaries
VI
 HEMATOLOGY

Diagnosis of Microcytic Anemia 38

DD for Iron overload states & Dry tap 39

Diagnosis of von Willebrand Disease & causes of Massive spleenomegaly 40

Causes of Erythrocytosis 41

Causes of Thrombocytosis & Megaloblatic anemia 42

Classification of Hemolytic Anemias & Sickle cell disease 43

Clinical Situations with Predominantly Intravascular Hemolysis 44

Diagnosis of Hypoproliferative Anemias & thalassemia 45

Characteristics of Blood Components & Platelet disorders 46

LMW heparin over heparin, Features of GPIIb IIIA Antagonists, etc. 47

Comparison of LMWH and Fondaparinux 48

Diagnosis of Chronic Eosinophilic Leukemia and Hypereosinophilic Syndrome 49

Table 103--4 Diagnosis of Microcytic Anernia

Tests Iron Inflammation Thalassemia Sideroblastic

Deficiency Anemia
Smear Micro/hypo Normal Micro/hypo with targeting Variable
micro/hypo
51 <30 <50 Normal to high Normal to high
TIBC >360 <300 Normal Normal
Percent saturation <10 10-20 30-80 30-80
Ferritin (~g/L) <15 30-200 50-300 50-300
Hemoglobin pattern on Normal Normal Abnormal with Bthalassemia; can be normal with IX Normal
electrophoresis thalassemia
Table e21-3 Differential Diagnosis oif "Dry Tap"-Inability to Aspirate Bone Marrow
Dry taps occur in about 4% of attempts and are associated with :
~1 etastati c carcinoma infiltrat ion 17%
Chronic my eloid leukemia 15%
Myelofibrosis 14%
Hairy cell leukemia 10%
Acute leukemia 10%
Lymphomas, Hodgkin's disease 9%
Normal marrow Rare

Acquired I ron Overload

Iron-loading anemias Chronic liver disease
Thalassemia major Hepatitis C
Sideroblastic anemia Alcoholic cirrhosis, especially when advanced
Chronic hemolytic anemias Nonalcoholic steatohepatitis
Transfusional and parenteraliron overload 'Porphyria cutanea tarda
Dietary iron overload Dysmetabolic iron overload syndrome
Post-portacaval shunting

Miscellaneous
Iron overload in sub-Saharan Africa
Neonataliron overload
Aceruloplasminemia
Congenital atransferrinemia
Table 115-2 Laboratory Diagnosis of von Willebrand Disease
Type aPTT VWF Antigen VWF Activity FVIII Activity Multimer
~ ~
1 Nl or t Normal distribution, decrea;ed n quantity
~ ~
2A Nl or t 4 Loss of high- and inter11ediate-MW multimers
~ ~
28. Nl or t 4 Loss of high-fVW multiners
~ ~
21~ Nl ort 4 Normal distribution, decrea;ed n quantity
tt H
21~ NI 0' 4b Nl or ~ Normal distribution
tt ~4 .~ H
3 Ab;ent

Table 59-,3 Diseases Associated with Massive Splenomegaly

Chronic nweiC~id leukemia
Lymphomas
Hairy cell leuk emia
Myelofibrosis with myeloid
metaplasia
Polycythemia vera
Gaucher's disease
Chronic lymphocytic leukemia
Sarcoidosis
Autoimmune hemolytic anemia
Diffuse splenic hemangiomatosis

The spleen extends greater than 8 em below left costal marg in and/or weighs more than iooo g.
Table 108-2 Causes of Erythrocytosis
Relative Erythrocytosis
Hemoconcent ration secondary to dehydrat ion, diuret ics, ethanol abuse, androgens or tobacco abuse
Absolute Erythrocytosis
Hypoxia Tumors
Carbon monoxide intoxication Hypernephroma

High oxygen-affinity Hepatoma

hemoglobin Cerebellar hemangioblastoma

High altitude Uterine myoma

Pulmonary disease Adrenal tumors

Right t o left cardiac or Meningioma

vascular shunts Pheochromocytoma

Sleep apnea syndrome Drugs

Hepatop,ulmonary syndrome Androgens

Renal Disease Recombinant erythropoi.e tin

Renal artery stenosis Familial (with normal hemoglobin function)

Focal sclerosing or membranous glomerulon ephritis Erythropoietin receptor mutation

Postrenal t ransplantation VHL mutations (Chuvash polycythemia)

Renal cyst s 2,3-BPG mut at ion

Bartter's syndrome Polycythemia vera

Table 108- 5 Causes of Thrombocytosis
Tissue inflammation: collagen vascular disease, inflammatory bowel disease Hemorrhage

Malignancy Iron deficiency anemia

Infection Surgery
f\'lyeloproliferative disorders: polycythemia vera, primary myelofibrosis, essential thrombocytosis, Rebound: Correction of vitamin B12 or folate deficiency,
chronic myelogenous leukemia post -ethanol abuse

Myelodysplastlc disorders: Sq-syndrome, idiopathic refractory sideroblastlc anemia Hemolysis

Postsplenectomy or hyposplenism Familial: Thrombopoietin overproduction, constitutive Mpl
activation

.
Table 105- 1 Causes of Megaloblastic Anemia
Cobalamin deficiency or abnonmalities of cobalamin metabolism (see Tables 105- 3 and 105- 4)
Folate deficiency or abnormalities of folat e met abolism (see Table 105- 5)
Therapy with antifolate drugs (e.g., methotrexate)
Independent. of either cobalamin or folate deficiency and refractory t o cobalamin and folate therapy:
Some cases of acute myeloid leukemia, myelodysplasia
Therapy with drugs interfering with synthesis of DNA [e.g., cytosine arabinoside, hydroxyurea, 6-mercaptopurine, az.idothymidine (AZT))
Orotic aciduria (responds to uridine)
Thiamine-responsive
Table 106- 1 Classification of Hemolytic Anemias *
Intracorpuscular Defects Extracorpuscular Factors
Hereditary Hemoglobinopathies Familial (atypical) hemolytic uremic syndrome

Enzymopathies

Membrane-cytoskeletal defects

Acquired Paroxysmal nocturnal hemoglobinuria (PNH) Mechanical destruction (microangiop athic)

Toxic agents

Drugs

Infectious

Autoimmune

Table 104-2 Clinical Features of Sickle Hemoglobinopathies

Condition Clinica l Abnormaliti e.s Hemoglobin Level g /L MCV, Hemoglobin

(g/dl) fl Electrophoresis
Sickle cell trait None; rare painless hematuria Normal Normal Hb S/A:40/60
Sickle cell Vasoocdusive crises with infarction of spleen, brain, marrow, kidney, lung; aseptic 70 - 100 (7-10) 80- Hb 5/A: 100/0
anemia necrosis of bone; gallstones; priapism; ankle ulcers 100
Hb F:2- 25%

S/ Vasoocdusive crises; aseptic necrosis of bone 70-100 (7-10) 60-80 Hb S/A: 100/0
6 thalassemia
Hb F:l-10%

S/6+ Rare crises and aseptic necrosis 100- 140 (10- 14) 70-80 Hb S/A:60/ 40
thalassemia
Hemoglobin SC Rare crises and aseptic necrosis; painless hematuria 100- 140 (10- 14) 80 - Hb S/A:S0/ 0
100
Hb C:SO%
Table 106- 6 Diseases/ Clinical Situations with Predominantly Intravascular Hemolysis
Onset/Time Course Main Mechanism Appropriate Diagnostic Comments
Procedure
Mismatched blood Abrupt Nearly always ABO Repeat cross-match
transfusion incompatibility
Paroxysmal nocturnal Chronic with acute Complement (C)-mediated Flow cytometry to display a Exacerbations due to C activation through any
hemoglobinuria (PNH) exacerbations destruction of CD59(-) red CD 59(-) red cell population pathway
cells
Paroxysmal cold Acute Immune lysis of normal red Test for Donath-Landsteiner Often triggered by viral infection
hemoglobinuria (PCH) cells antibody
Septicemia Very acute Exotoxins produced by Blood cultures Other organisms may be responsible
Clostridium perfJjngens
Microangiopathic Acute or chronic Red cell fragmentation Red cell morphology on Different causes ranging from endothelial
blood smear damage to hemangioma to leaky prosthetic
heart valve
March hemoglobinuria Abrupt Mechanical destruction Targeted history taking
Favism Acute Destruction of older fraction of G6PD assay Triggered by ingestion of large dish of fava
G6PD-deficient red cells beans; but trigger can be infection or drug
instead
 Table 103 - 6 Diagnosis o f Hypopro liferative Anemias

Tests Iro n Deficiency I nflammation Renal Disease H y pometabolic States

Anemia Mild to severe Mild Mild to severe Mild

MCV (fl) 60- 90 80- 90 90 90

Morphology Norma -micro cytic Normocytic Normocytic Norm ocytic

51 <30 <50 Normal No rma l

TIBC > 360 <300 Normal Normal

Saturation (%) <10 10-2 0 Normal Norm al

Serum ferritin (?gjL) <15 30-200 115-150 Normal

Iron stores 0 2- 4+ 1- 4 + No rm al

Abbreviations: MCV, m ea n corpuscula r volu me; 51, serum iron; TIBC, t ota l ir on -bindin g capacity.

Table 104- 4 The cz: Thalassemias

Condition Hemoglobin A, Ofo Hemoglobin H ( 8 4 ), A> Hemoglobin level, g/l (g/dl ) MCV, fl
Normal 97 0 150 (15) 90
Silent thalassemia: 4:1./cz:cz: 98-100 0 150 (15) 90
Thalassemia trait: 85-95 Rare red blood cell inclusions 120-130 ( 12-13) 70-80
-cz:/ 4:1. homozygous cz:-thal-2
or
--1= heterozygous cz:-thal-1
Hemoglobin H disease: 70-95 5-30 60-100 (6-10) 60-70
--/ 4:1. heterozygous cz:-thal-1/cz:-thal-2
Hydrops fetal is: 0 S-lOb Fatal in utero or at birth
--1-- homozygous a -thal-1

'When both o; alleles on one chromosome are deleted, the locus is called o;-thal-1; when only a single cz: allele on one chromosome is deleted, the locus is calle
:>:-thal-2.
Table 113- 2 Characteristics of Selected Blood Components

Component Volume, Content Clinical Re.sponse

ml
PRBC 180-200 RBCs with variable leukocyte cont ent and small amount of Increase hemoglobin 10 g/ L and hematocrit 3o/o
plasma
Plat elets 50 - 70 5.5 x 10 10/ RD unit Increase plat elet count S000-10,000frl

200-400 :>3 " 10 l l/SOAP product CCI :.10 " 109 / L within 1 hand :.7.5" 109/L within 24 h
posttransfusion

FFP 200- 250 Plasma proteins- coagulation factors, proteins C and S, Increases coagulation factors about 2%
antithrombin
Cryoprecipit ate 10-15 Cold-insoluble plasma proteins, fibrinogen, factor VIII, vWF Topical fibrin glue, also 80 IU factor VIII

Table 58-1 Primary Hemostatic (PJatel et P l ug) O i.sorders

D efects of P l atelet Adhesion
Von W illebrand d is ease
Be r nard-Soul ier syndrom e ( absen ce o f d y s f uncti o n of G plb - IX- V)
Defects .o f P l atelet A ggregati on
G la nzm ann's thrombasthen ia (ab sence or d ysf unctio n of Gpiibiiia)
Afibrinogenem ia
D efects of P l atelet SecreUon
Decreas ed cyclooxygenas e activ it y
Drug-indu.ced ( a spi r i n , nonsteroidal anb-inflammatory agents, t h ien opyr i d ine s )
I nherited
Granule storage pool defects
I nherited
Acq u ir ed
Non-specif ic inh erite d secretory defects
Non-specif i c d r ug effects
Uremia
P l a tel et coating ( e . g., p a r aprotein , penici ll in)
Defect o f P l atelet C o agu l ant Acti vity
Scott's s y ndrome
 Table 118-5 Advantages of LMWH over Heparin

Advantage Consequence
Better bioav<Oilability and longer half-life after subcutaneous injection Can be given subcutaneously once or twice daily for both prophy axis and treatment
Dose-independent clearance Simplified dosing
Predictable a1ticoagulant response Coagulation monitoring is unnecessary in most patients
Lower risk of heparin-induced thrombocytopenia Safer than heparin for short- or long -term administration
Lower risk of osteoporosis Safer than heparin for e:<tended administration

Table 118-1 Features of GPIIb/ IIIA Antagonists

Feature Abciximab Eptifibatide Tirofiban
Description Fab fragment of humanized mouse monoclonal antibody Cyclical KGD-containing heptapeptide Nonpeptidic RGD mimetic
Specific for GP!Ib/ IIIa No Yes Yes
Plasma half-life Short (min) Long (2.5 h) Long (2.0 h)
Platelet-bound half-life Long (days) Short (s) Short (s)
Renal clearance No Yes Yes

Table 118-7 Comparison of the Properties of Lepirudin, Bivalirudin, and Argatroban

Lepirudin Bivalirudin Argatroban

Mole<:uJar mass 7000 1980 527
Site(s) of interaction wit h thrombin Active site and e.xosite 1 Active site and exosite 1 Active site
Renal clearance Yes No No
Hepat ic metabohsm No No Ye.s
Plasma half-life (min) 60 25 45
LMWH Fondaparinux
5
 KIDNEY

Laboratory Findings in Acute Renal Failure 51

Indications for steroids in Interstitial nephritis 52

Types of MPGN 53

causes of FSGS 54

stages of CKD & Factors affecting Theophylline clearance 55

causes of anema in CKD 56

Index Prerenal Azotemia Oligurk: Acute Renal F11ilure

:1
Table 283-5 Focal Segmental Glomer ulosclerosis
Primary focal segmental glomerulosclerosis
Secondary focal segmental glomeculosclerosis

Viruses : HI V/Hepatitis 8/ Parvovirus

Hypertensive nephropathy
Reflux nephropathy

Cholesterol emboli
Drugs: Heroin/ analgesics/ pamidronate
Oligomeganephronia
Renal dysgenesis
Alpert's syndrome
Sickle cell disease
Lymphoma
Radiation nephritis
Familial podocytopathies

NPHS1 mutation/ nephrin

NPHS2 mutation/ podocin
TRPC6 mutation/cation channel
ACTN4 mutation/actinin
o;-Galactosidase A deficiency/ Fabry's disease
N-acetylneuraminic acid hydrolase deficiency/nephrosialidosis
 Table 280-1 elassification of Chronic Kidney Disease (CKD)

Stage GFR, ml/min per 1.73 m 2

0 >90a

1 , gob
2 60- 89
3 30- 59
4 15- 29
5 <15

Table 254- 4 Factors Affecting Clearance of Theophylline

Increased Clearance
Enzyme induction (rifampicin, phenobarbitone, ethanol)
Smoking (tobacco, marijuana)
Highprotein, tow-carbohydrate diet
Barbecued meat
Childhood
Decreased Cleilrance
Enzyme inhibition (cimetidine, erythromycin, ciprofloxacin, allopurinol, zileuton, zafirlukast)
Congestive heart failure
Liver disease
Pneumonia
Viral infection and vaccination
High carbohydrate diet
Old aqe
II
 INFECTIOUS DISEASES

Gram positive and gram negative organisms 59

DNA viruses 60

Anaerobic Human Flora 61

Microbial Ligand-Receptor Interactions 62

Classification of Streptococci 63

Causes of community acquired pneumonia 64

Bacterial Food Poisoning 65

Intestinal Pathogenic E. Coli 66

Pathogens causing lung cavitations & risk factors for active TB 67

Legionnaires disease & common skin infections 68

Rickettsial Infections 69

Viral Hemorrhagic Fever (HF) Syndromes 70

IRIS & serologic features of EBV infections 71

Enterovirus Serotypes and it s diseases 72

Congenital rubella syndrome & diseases caused by parvovirus B19 73

Clinical Features of Genital Ulcers 74

Vaginal Infections, it s features and management 75

Infections after solid organ Transplantation 76

Infections after Hematopoietic Stem Cell Transplantation and Renal transplant 77

Lab features of chronic hepatitis 78

Serologic pattern of hep B infecation and it s interpretation 79

Inidications for ART & causes of BM suppression in HIV pts 80

Characteristics of Plasmodium Species & complications of Pf malaria 81

Characteristics features of Filariae 82

African Trypanosomiases 83

Diagnosis of Intestinal Protozoal Infections & Trematode infections 84

Category of bio terrorizing agents 85

Gram-Negative Organisms
only

Gram-Positive Organisms
Table 164- 1 Anaerobic Human Flora: An Overview

Anatomic Site Total Anaerobic/ Aerobic Potential Pathogens

Bacteria Ratio

Oral cavity
Saliva 108 -10 9 1:1 Fusobacterium nucleatum, Prevote/la melaninogellica, Prevotella ora/is group, Bacteroides
ureolyticus group, Peptostreptococcus ; pp.
Tooth surface 1010_10 11 1:1
Gingival crevices 1011-1012 10 3: 1

Gastrointestinal
tract
Stomach 0-10 5 1: 1 Bacteroides spp. (principally members of the 8. fragi/is group), Prevote/la spp., Clostridium spp.,
Peptostreptococcus spp.
Jejunum/ileum 10"- 10 7 1: 1
Terminal ileum and 1011- 1012 103: 1
colon

Female genital tract 107- 109 10: 1 Peptostreptococcus spp., Bacteroides s~p .., Prevotella bivia
Table 120- 1. Examples of Microb ial Ligand-Receptor Interactions
Microorganism Type of Microbial liga nd Host Receptor
V ira l Pathogens
Influenza virus Hemagglutinin Sia lic acid
Measles vir us
Vaccine strain Hemagglutinin CD46/ moesin
Wild-tyoe strains Hemaoolutinin Sionalino lymphocytic activat ion molecule (SLAM)
Human herpesvirus type 6 ? CD46
Herpes simplex vir us Gly coprot ein C Heparan sulfa te
HIV Su.rface glycoprotein CD4 and chemokine receptors (CCRS and CXCR4)
Epstein -Barr virus Envelope prote in CD2 1 (CR2)
Adenovirus Fiber protein Coxsackie-adenovirus receptor (CAR)
Coxsackiev in ls Viral coat prote ins CAR and maj o r h istocompatibility class I ant igens
Bacter ia l Pathogens
Neisseria spp_ Pili Membr ane co-facto r pr otein (CD46}
Pseudomonas aeruginosa Pili and flagella Asialo-GM1
Lipopolysaccharid e Cystic fibrosis transmembrane conductance r egula tor (CFTR)

Escherichia coli Pili Ceramides/ m annose and digalactosyt residues

Streptococcus pyogenes Hyaluronic acid capsule. CD44
Yersini.; spp. lnvasin/ accessory invasin locus R1 I ntegrins

Bordetella pertussis Filamentous hemagglutinin CR3

Legionella pneumophila Adsorbed C3bi CR3
My.cobac.terium tuberculosis Adsorbed C3bi CR3; DC-SIGW
Fungal Pathogens
Blastomyces dermati tidis WI-1 Possibly matrix proteins and integrins
candida albicans Intlp Extracellular matrix proteins
Prot ozoal Pathogens
Plasmodium vivax Merozoite fo rm Duffy Fy antigen
Plasmodium fakiparum Erythrocyte-binding protein 17 5 (EBA-17 5) Glycophorin A
Entamoeba N stoly.tica Surface lectin N-Acetylglucosamine
Table 136-1 Classification ol Streptococci

Lancefield Group Representative Speci.es Heri10lytia Typical Infections

Pattern
A s. pyogenes B Pharyngitis, impetigo, celluliti;, scarlet fever
8 S. agalactiae B Neonatal sepsis and meningitis, puerperal infection, urinary tract
infection, diabetic ulcer infection, endocarditis
C,G s. dysgalactiae subsp. equisjmj/is B Cellulitis, bacteremia, endocarditis
D Enterococci: E. faecalis; E. iaecium usually Urinary tract infection, nosocomial bacteremia, endocarditis
nonhemolytic
Nonenterococci: S. bovis Usually Bacteremia, endocarditis
nonhemolytic
o;
Variable or Viridans streptococci: 5. sar:guis; 5. mitis Endocarditis, dental abscess, brain abscess
nongroupable
Intermedius or milleri group 5. intermedius, S. Variable Brain abscess, visceral abscess
anginosus, S. constellatus
Anaerobic streptococcib: Peptostreptococcus Usually Sinusitis, pneumonia, empyema, brain abscess, liver abscess
magnus nonhemolytic
 Hospitalized Patients
Outpatients Non-ICU ICU
Table 128- 4 Bacterial Food Poisoning

I ncubation Period, Symptoms Common food Sources

Organism
1-6 h
Staphylococcus aureus Nausea, vomiting, diarrhea Ham, poultry, potato or egg salad, mayonnaise, cream
pastries
Bacillus cereus

8- 16 h
Clostridium perfringens Abdominal cramps, diarrhea Beef, poultry, legumes, gravies
(vomiting rare)
B. cereus Abdominal cramps, diarrhea Meats, vegetables, dried beans, cereals
(vomiting rare)
>16 h
Vibrio cholerae Watery diarrhea Shellfish, water
Enterotoxigenic Escherichia Watery diarrhea Salads, cheese, meats, water
coli
Enterohemorrhagic E. coli Bloody diarrhea Ground beef, roast beef, salami, raw milk, raw
vegetables, apple juice
Salmonella Inflammatory diarrhea Beef, poultry, eggs, dairy products
Campy]obacter jejuni Inflammatory diarrhea Poultry, raw milk
Shigella spp. Dysentery Potato or egg salad, lettuce, raw vegetables
Vibrio parahaemolyticus Dysentery Mollusks, crustaceans
Table 149-2 Intestinal Pathogenic E. Coli
Pathotype8 Epidemiology Clinical Syndromeb Defining Molecular Trait Responsible Genetic Element"
STEC/EHEC Food, water, person-to-person; all Hemorrhagic colitis, Shiga toxin Lambda-like Stxl- or Stx2-encoding
ages, industrialized countries hemolytic-uremic bacteriophage
syndrome

ETEC Food, water; young children in and Traveler's diarrhea Heat-sta~le and -labile enterotoxins, Virulence plasmid(s)
travelers to developing countries colonization factors

EPEC Person-to-person; young children and Watery diarrhea, Localize<:. adherence, attaching and EPEC adherence factor p lasmid
neonates in developing countries persistent diarrhea effacing lesion on intestinal pathogenicity island [locus for
epit helium enterocyte effacement (LEE)]

EIEC Food, water; children in and travelers Dysentery Invasion of colonic epit helial cells, tvlultiple genes contained primarily in
to developing countries intracellular multiplication, cell -to-cell a large virulence plasmid
spread

EAEC ?Food, water; children in and t ravelers Traveler's diarrhea, Aggregative/ diffuse adherence, Chromosomal or plasmid-associated
to developing ccountries; all ages, acute diarrhea, virulence factors regulated by AggR adherence and toxin genes
industrialized countries persistent diarrhea
 Table 165- 1 Risk Factors for Active Tuberculosis among Persons Who Have Been Infected with Tubercle Bacilli

Factor Relative Risk/ Odds<'

Recent infection ( <1 year) 12.9
Fibrotic lesions (spontaneously healed) 2-20
Comorbidity
HIV infection 21->30
Silicosis 30
Chronic renal failure/ hemodialysis 10-25
Diabetes 2- 4
I V drug use 10-30
Immunosuppressive treatment 10
Gastrectomy 2-5
Jejunoileal bypass 30-60
Posttransplantation period (renal, cardiac) 20- 70
Tobacco smoking 2- 3
Malnutrition and severe underweight 2
Table 258- 2 Micr obial Pathogens Causing Cavitary Lung I n fection
I
Aspiration-Prone Host
Anaerobic bacteria plus microaerophilic and/ or anaerobic streptoco~ci, Gemefla spp .
Embolic (endovascular) lesions: usually Staphylococcus aureus, Pseudomonas aeruginosa, Fusobdcterium necrophorum
Endemic fungi: Histoplasma, Blastomyces, Coccidioides spp .
Mycobacteria: M. tuberculosis, M. kansasii, M. avium
Immunocompromised Host
M. tuberculosis, Nocardia asteroides, Rhodococcus equi, Legionella spp ., P. aeruginosa, Enterobacteriaceae (especially Klebsiella pneumoniae), Aspergillus
spp., Cryptococcus spp .
Previously Healthy Host
Bacteria: 5. aureus, bs. mifferi, K. pneumoniae, group A Streptococcus; Gemella, Legionella, and Ac.tinomytes spp.
Parasites: !Entamoeba hlsto/yt/ca, Paragonimus westermanl, Strongyloides stercora/is
 Table 147-1 Clinical Clues Suggestive of Legionnaires ' Disease

Diarrhea
High fever (>40C; > 104F)
Numerous neut rophils but no organisms revea led by Gram's staining of respirat ory secretions
Hyponatremia (serum sodium level <131 mg/dL)
Failure to respond t o B-lactam drugs (penicillins or cephalosporins) and aminoglycoside antibiotics
Occurrence of illness in an environment in which the poTable water supply is known to be contaminated with Legionella
Onset of symptoms within 10 days after discharge from the hospital

Table 52-5 Common Skin Infections

I
Clinical Features Etiologic Agent Treatment
Impetigo Honey-colored crusted papules, plaques, o bullae Group A streptococcus and Systemic or topical
Staphylococcus aureus antistaphylococcal antibiotics
Dermatophytosis Inflammatory or noninflammatory annular scaly plaques; may have Trichophyton, Topical azoles, systemic griseofulvin,
hair loss; groin involvement spares scrotum; hyphae on KOH Epidermophyton, or t erbinafine, or azoles
preparation Microsporum sp.
Candidiasis Inflammatory papules and plaques with satellite pustules, frequently Candida albicans and other Topical nystatin or azoles; systemic
i1 intertriginous areas; may involve scrotLim; pseudohyphae on KOH Candida sp . azoles for resistant disease
preparation
Tinea versicolor Hyper- or hypopigmented scaly patches on the trunk; characteristic Mafassezia furfur Topical selenium sulfide lotion or
mixture of hyphae and spores ("spaghetti and meatballs") on KOH azoles
preparation
Table 174-1 Feat ures of Selected Rickettsial Inf ertions

D isease -Organism T ransmission Geograph_

i c Range Incubation Duration, Rash, Eschar, Lymphadenopathy>
Pe riod, Days % OJb
Days
Rocky Mountain Rkkettsia Tick b ite: Dermacentor United States 2 -14 10-20 90 <1 +
spotted fever rickettsii ander son !, D. variabilis
Amblyomma caj ennen se, A. Central/ South
dure o/;;tum Am~ri ca

Rhip iceph alus san guineus Mexico, Br azil,

United States
Mediter ranean R. c onorii Tick b ite: R. sang.uineus, R. Southern Europe, 5- 7 7 -14 97 50 +
spotted fever pum;J;o Africa, Middle East ,
Central Asia
Afr ican tick-bite fever R. aFricae Tick b ite: A. hebraeum , A. Sub-Saharan 4 -10 ? 50 90 ++++
va riegatum Africa, West Indies
~1aculatum disease R.. parker! A. m aculatum United States, 2 -10 ? 88 94 ++
South America
Rickettsialpox R. a kari Mite bite : Uponyssoides United States, 10-1 7 3 -1 1 100 90 +++
sanguin eus Ukraine, Turkey,
Mexico, Croatia
Tick-borne R. slovaca Tick b ite: Dermacent or Eu r ope 7- 9 17- 180 5 10 0 ++++
lymphadenopathy m arginatus, D. r eticularis
Flea-borne spotted R. {<,lis Flea ( m<>ehanism Worldwide 8 -16 8 -16 80 15 -
feve r undetermined) : Ctenocep halides
Felis
Epidemic typhus R. prowazekii Louse feces : Pediadus Worl dwide 7-14 10-18 80 None -
huma nus corporis , fleas and lice
of flying squirrels, or
recrudescence
~1urine typhus R.. typ hi Flea feces : Xenopsylla cheopis, w orldwide 8 -1 6 9-18 80 None -
C. Felis, ot hers
Human Ehrlic hia Tick bite: Amblyomma Unit e d States 1-21 3 -2 1 26 None ++
monocytotropic chaffeen sis am ericanum, D. variabili s
ehrlichiosis
Ew ingii ehrlichiosis E. ewingii Tick b ite: A. am er icanum United States None
Human Anapl asma Tick b ite: Ixodes scapu/aris, I . United States, 4 -8 3 -14 Rare None -
granulocytotropic ph agocytophifum ricinus, I . padftcus, I . Europe, Asia
anaplasmosis persulcatus
Scrub typhus Orien tia Mite bite : Leptotrombidium Asia, Australia, 9 -18 6 -21 50 35 +++
tsu tsugamus h i deliense, others New Guinea, Pacific
I slands
Q fever Coxieffa burnetii Inhalation of aer o so ls of Worldwide 3-30 5 -5 7 <1 None -
infected parturit ion m aterial
(sheep, dogs, other s) ,
ingestion of infected milk o r
Table 196-4 Viral Hemorrhagic Fever (HF) Syndromes and Their Dist ribution

Disease Incubation Case-Infection Ratio Case-Fatality Geographic Range Target Population

Period, Days Rate, Ofo
Lassa fever 5-16 Mild infections probably 15 west Africa All ages, both sexes
comm on
South American HF 7- 14 Most infections (more 15-30 Selected rural areas of Bolivia, Bolivia: Men in countryside; all ages, both
than h alf) result in Argentina, Venezuela, and Brazil sexes in villages
disease
Argentina: All ages, both sexes; excess
exposure and disease in men

Venezuela: All ages, both sexes

R,ift Vall ey fever 2- 5 N1:1oo N5o Sub-Saharan Africa, Madagascar, All ages, both sexes; more often
Egypt diagnosed in men; preexisting liver
disease may predispose
Crimean -Congo HF 3- 12 :o1:5 15- 30 Africa, ~1iddle East, Turkey, Balka ns, All ages, both sexes; men mor e exposed
southern region of former Soviet in some settings
Union, western China
HF with renal 9- 35 Hantaan, >1: 1.25; Hantaan, 5- 15; Worldwide, depending on rodent Excess of male patients (partially due to
syndrome Puumala, 1:20 Puumala, <1 reservoir greater exposure); mainly adults
Hantavirus N7- 28 Very high 40 -50 Americas Excess of male patients due to some
pulmonary occupational exposure; mainly adults
syndrome
Marburg or Ebola 3- 16 High 25-90 Sub-Saharan Africa All ages, both sexes; children less
HF exposed
Yellow fever 3-6 1:2-1:20 20 Africa, South America All ages, both sexes; adults more
exposed in jungle setting; preexisting
flavivirus immunity may cross-p rotect
Dengue HF/dengu e 2- 7 Nonimmune, 1: 10,000; <1 with Tropics and subtropics worldwide Predominantly children; previous
shock syndrome heterologous immune, supportive heterologous dengue infection
1:100. treatment predisposes to HF
Kyasanur 3- 8 Variable 0.5-10 Mysore State, India/western Siberia Variable
Forest/Omsk HF
 Table 189-11 Characteristics of Immune Reconstitution Inflammatory Syndrome (IRIS)
Paradoxical worsening of clinical condition is seen foUowing the initiation of antiretroviral therapy
Occurs weeks to months following the initiation of antiretroviral therapy
Is most common in patients starting therapy with a CD4t Tcell count under 50/iJ,l who experience a precipitous drop in viral load
Is frequently seen in the setting of tuberculosis
Can be fatal

Table 181- 2 Serologic Features of EBV-Associated Diseases

Result in Indicated Test
Anti VCA Anti EA
Condition Heterophile IgM I gG EA O EA R Anti EBNA
Acut e infectious mononucleosis + + ++ + - -
Convalescence - + - +
Past infection - - + - - +
Reactivation with immunodeficiency - - ++ + +

Burkitt's lymphoma - - +++ ++ +

Nasopharyngeal carcinoma - - +++ ++ +
Table 191-1 Manifestations Commonly Associated With Enterovirus Serotype.s-
Serotype( s) of Indicated Virus
Manifestation Cox sackievirus Echovirus ( E) and Enterovirus ( Ent)
Acute hemorrhagic conjunctivitis A24 E7Q
Aseptic meningitis A2, 4, 7, 9, 10; 81-5 E4, 6, 7, 9, 11, 13, 16, 18, 19, 30, 33; Ent70, 71
Encephalitis A9; 81-5 E3, 4, 6, 7, 9, 11, 18, 25, 30; Ent71
Exanthem A4, 5, 9, 10, 16;81,3-5 E4- 7, 9, 11, 16- 19, 25, 30; Ent71
Generalized disease of the newborn 81 - 5 E4- 6, 7, 9, 11, 14, 16, 18, 19
Hand-foot-and-mouth disease AS, 7, 9, 10, 16; 81, 2, 5 Ent71
Herpangina A1-10, 16, 22; 81-5 E6, 9, 11, 16, 17, 25, 30; Ent71
Myocarditis , pericarditis A4, 9, 16; 81-5 E6, 9, 11, 22
Paralysis A4, 7,9; 81-5 E2-4, 6, 7, 9, 11, 18, 30; Ent70, 71
Pleurodynia A1, 2, 4, 6, 9, 10, 16; 81-6 E1 - 3, 6, 7, 9, 11, 12, 14, 16, 19, 24, 25, 3Q
Pr I~U I.I IUr lid A9, 16; 61-5 E6, 7, 9, 11, 12, 19, 20, 30; Enl68 , 71
Table 193 - 1 Common Transient and Per manent Manifestations in Infants With Congenital Rubella Syndrome
I
Transient Manifestations Permanent Manifestations
Hepatosplenomegaly Hearing impairment/deafness
Interstitial pneumonitis Congenital heart defects (patent ductus arteriosus, pulmonary arterial
stenosis)
Thrombocytopenia with purpura/petechiae (e.g., dermal erythropoiesis, or Eye defects (cataracts, cloudy cornea, microphthalmos, pigmentary
"blueberry muffin syndrome") retinopathy, congenital glaucoma)
Hemolytic anemia
Bony radiolucencies

Intrauterine growth retardation ~1icrocephaly

Adenopathy
Meningoencephalitis Central nervous system sequelae (mental and motor delay, autism)

Table 184-1 Diseases Associated with Human Parvovirus 819 Infection and Methods of Diagnosis
Disease Host(s) l gM IgG PCR Quantitative PCR
Fifth disease Healthy children Positive Positive Positive >10 3 IU/ mL

Polyarthropathy Healthy adults (more often Positive within 3 Positive Positive >103 IU/ mL
syndrome women) months of onset
Transient aplastic crisis Patients wit h increased Negative/ positive Negative/ posit ive Positive Often > 10 12 IU/ ml , but rapidly
erythropoiesis decreases

Persistent anemia/pure Immunodeficient or Negative/weakly Negative/weakly Positive Often >10 1 2 IU/ mL, but should be
red-cell aplasia immunocompetent patients positive positive > 106 in the absence of treatment

Hydrops fetalis/congenital Fetus ( <20 weeks) Negative/ positive Positive Positive amniotic n/ a
anemia fluid or tissue
Table 130-7 Clinical Features of Genital Ulcers

Feature Syphilis Herpes Chancroid lymphogr anuloma Venereum Oonovanosis

Incubation period 9-90 days 2-7 days 1-14 days 3 days-6 weeks 1-4 weeks (up to 6
months)
Early primary Papule Vesicle Pustule Papule, pustule, or vesicle Papule
lesions
No. of lesions Usually one Multiple Usually multi~le, may Usually one; often not detected, Variable
coalesce despite lymphadenopathy
Diameter 5-15 mm 1-2 mm Variable 2-10 mm Variable
Edges Sharply demarcated, Erythematous Undermined, agged, Elevated, round, or oval Elevated, irregular
elevated, round, or oval irregular
Depth Superficial or deep Superficial Excavated Superficial or deep Elevated
Base Smooth, nonpurulent, Serous, erythematous, Purulent, bleeds easily Variable, nonvascular Red and velvety,
relatively nonvascular nonvascular bleeds readily
Induration Firm None Soft Occasionally firm Firm
Pain Uncommon Frequent ly tender Usually very tender Variable Uncommon
Lymphadenopathy Firm, nontender, Firm, tender, often Tender, may suppurate, Tender, may suppurate, None;
bilateral bilateral with initial loculated, usually 'unilateral loculated, usually unilateral pseudobuboes
episode
!Table 130-5 Diagnostic features and Management of Vaginal I nfedion
I
Feature Normal Vaginal Vulvovaginal Candidiasis Trichomonal Vaginitis Bacterial Vaginosis
Examination
Etiology Uninfected; lactobacilli candida albicans Trichomonas vagina/is Associated with Gardnerella vagina/is,
predominant various 3naerobic and/ or noncultured
bacteria, and mycoplasmas
Typical symptoms None Vulvar itching and/or irritation Profuse purulent discharge ; Malodorous, slightly increased discharge
vulvar itching
Discharge
Amount Variable; usu3lly scant Scant Often profuse Moderate
Color" Clear or translucent White White or yellow White or gray
Consistency Nonhomogeneous, Clumped; adherent plaques Homogeneous Homogeneous, low viscosity; uniformly
floccular coats vaginal walls
Inflammation of None Erythema of vaginal epithelium, introitus; Erythema of vaginal and None
vulvar or vaginal vulvar dermatitis, fissures common vulvar epithelium ; colpitis
epithelium macularis
pH of vaginal Usually .:4.5 Usually .:4.5 Usually ;,5 Usually >4.5
fluid0
Amine ("fishy") None None May be present Present
odor with 10%
KOH
Microscopy'" Normal epithelial cells; Leukocytes, epithelial cells; mycelia or Leukocytes; motile Clue cells; few leukocytes; no lactobacilli
lactobacilli pseudomycelia in up to 80% of c. trichomonads seen in 80- or only a few outnumbered by profuse
predominant a/bicansculture-positive persons with 90% of symptomatic patients, mixed microbiota, nearly always including
typical symptoms less often in the absence of G. vagim/isplus anaerobic species on
symptoms Gram's stain (Nugent's score ;, 7)
Other laboratory rsolation of Candida spp . Isolation ofT. vagina/is or
findings positive NAArd
Usual treatment None Azole cream, tablet, or suppository- Metronidazole or tinidazole, 2 Metronidazole, 500 mg PO bid for 7 days
e.g., miconazole ( 100-mg vaginal g orally (single dose)
Metronidazole gel, 0.75%, one applicator
suppository) or clotrimazole (100-rrg Metronidazole, 500 mg PO bid
(5 g) intravaginally once daily fer 5 days
vaginal tablet) once daily for 7 days for 7 days
Clindamf cin, 2% cream, one full applicator
Fluconazole, 150 mg orally (single dose)
vaginal!~ each night for 7 days

Usual None None; topical treatment if candida! Examination for STD; None
management of dermatitis of penis is detected treatment. with
sexual partner metronidazole., 2 g PO (single.
dose)
Table 132-5 Common Infections after Solid organ Transplantation, by Site of Infection
1
Period after Transplantation
Infected Site Early ( <1 Month) Middle ( 1- 4 Months) l ate ( >6 Months)
Donor organ Bacterial and fungal infections of the graft, CMV infection EBV infection (may present in allograft orga1)
anastomotic sit e, and surgical wound
Systemic Bacteremia and candidemia (often resulting CMV infection (fever, bone marrow CMV infection, especially in patients given early
from central venous catheter colonization) suppression) posttransplantation prophylaxis; EBV proliferative
syndromes (may occur in donor organs)
l ung Bacterial aspiration pneumonia with Pneumocystis infection; CMV pneumonia Pneumocystis infection; granulomatous lun~
prevalent nosocomial organisms associated (highest risk in lung transplantation); diseases (nocardiae, reactivated fungal and
with intubation and >edation (highest risk Aspergillus infection (highest ri~k in lung mycobacterial diseases)
in lung transplantation) transplantation)
Kidney Bacterial and fungal (Candida) infections Renal transplantation: BK virus infection Renal transplantation: bacteria (late urinary tract
(cystitis, pyelonephrtis) associated with (associated with nephropathy); JC virus infections, usually not associated with
urinary tract catheters (highest risk in infection bacteremia); BK virus (nephropathy, graft failure,
kidney transplantation) generalized vasculopathy)
Liver and biliary Cholangitis CMV hepatitis CMV hepatitis
tract
Heart Toxoplasma gondii infection (highest risk T. gondli (highest risk in heart transplantation)
in heart transplantation)
Gastrointestinal Peritonitis, especial!~ after liver Colitis secondary to Clostridium difficile Colitis secondary to c. difficile infection (risk can
tract transplantation infection (risk can persist) persist)
Central nervous Listeria (meningitis); T. gondii infection Listeria meningitis; Cryptococcus meningitis;
system Nocardia abscess; JC virus-associated PML
Table 132- 3 Common Sources of Infections. after Hematopoietic Stem Cell Transplantation

Period after Transplantation

Infection Site Early ( <1 Month) Middle ( 1- 4 Months) l ate (>6 Months)
Disseminated Aerobic bacteria (gram-negative, gram- NO<Ardia, Candida, Aspergillus, EBV Encapsulated bacteria (Streptococcus pneumoniae,
positive) Haemophilus influenzae, Neisseria meningitidis)
Skin and mucous HSV HHV-6 vzv
membranes
Lungs Aerobic bacteria (gram-negative, gram- CMV, seasonal respiratory viruses, Pneumocystis, s. pneumoniae
positive), Candida, Aspergillus, other molds, Pneumocystis, Toxoplasma
HSV
Gastrointestinal tract Clostridium diffici/e CMV, adenovirus EBV, CMV
Kidney BK virus, adenovirus
Brain HHV-6 HHV-6, Toxoplasma Toxoplasma, JC virus (rare)
Bone marrow HHV-6

Table 282- 5 The Most Common Opportunistic I nfections in Renal T ransplant Recipients
Peritransplant ( < 1 month) l ate ( >6 months)

Wound infections Aspergillus NOC<Jrdia

Herpesvirus BK virus (polyoma)

Oral candidiasis Herpes zoster

Urinary t ract infection Hepatitis B

Early ( 1-6 mont hs) Hepatit is c

Pneumocystis C<irinii
Cytomegalovirus

Legionel!a Usteria
Hepatitis B

Hepatitis c
Tab le 306- 1 Clinical and l aboratory Features of Chronic Hepatit is
I

Type of hepatitis Diagnostic test( s) Autoantibodies Therapy

Chr onic hepatitis 8 H8sA:g, I gG anti-H8c, HBeAg, H8V DNA Uncommon IFN-c::, PEG IFN-
c:; lamivudine adefovir entecavir telbivudine tenofoyir

Chr onic hepatitis Ant i-HCV, HCV RNA Anti-LKM1 PEG IFN..cz: ribavirin Telaprevirl
c 8oceprevir1

Chr onic hepatitis Ant i-HDV, HDV RNA, H8sAg, I gG anti-H8c Anti-LKM3 I FN..cz:, PEG IFN..cz:c
D

Autoimmune ANAb (homogeneous), :anti-LKM 1 ( ) ANA, anti-LKM 1 ant i- Prednisone, azat hioprine
hepatitis Hyperglobulinemia SLAe

Drug-associated - Uncommon Withdraw drug

Cryptogenic All negative None Prednisone (?'), azathioprine (?)

a Ant ibodies t o liver-kidney microsomes t ype 1 (autoimmLJne hepatitis type II and some cases of hepatit is C)

b Antinuclear antibody (autoimmune hepatit is type I )

c Clinical t rials suggest b enefit of IFN..cz: ther apy; PEG IFN-c:: is as effective, if not mo re so.

d Expected approval dat e 2011.

e Antibodies t o soluble liver antigen (aut oimmune hepatitis type III)

Abbr eviations: H8c, hepatitis 8 core ; H8eAg, hepatitis 8 e antigen; H8sAg, hepatit is 8 surface antigen ; H8V, hepatitis 8 virus; Hcv, hepatitis C virus;
HDV, hepatitis D virus; IFN..cz:, interferon..cz:; I gG, immunoglobulin G; LKM, liver-kidney microsome;
PEG-I FN..cz:, pegylated in.terferon..cz:; SLA, soluble liver antigen.
Table 304-5 Commonly Encountered Serologic Patterns of Hepatitis B Infection

HBsAg Anti- Anti- HBeAg Anti- Interpretation

HBs HBc HBe

+ - JgM + - Acute hepatitis B, high infectivity

+ - JgG + - Chronic hepatitis B, high infectivity

+ - lgG - + Lat e acute or chronic hepatitis 8, low infectivityH8eAg-negative ("precore-mutant") hepatitis 8 (chronic
or, arely, acute)
+ + + +I- +I- 1. HBsAg of one subtype and heterotypic anti - HBs (common)

2. Process of seroconversion from HBsAg to anti- HBs (rare)

- - JgM +I- +I- 1. Acut e hepatitis 8

2. Anti- HBc "window"

- - l gG - +I- 1. Low- level hepatitis 8 carrier

2. Hepatitis 8 in remote past

- + JgG - +I- Recovery from hepatitis B

- + - - - 1. Immunization with H8sAg (after vaccination)

2. Hepatitis 8 in the remote past (?)

" False- positive

Table 189- 23 Indications for the I nitiation of Antiretr ovlral Therapy in Patients with HIV Infecti01

I. Acute infection syndrome

II. Chronic in fection

A. Symptomatic disease (including HIV-associated nephropathy)

B. Asymptomatic disease

1. CD4+ T cell count <SOO,fll.L"

2. Pregnancy

III. Postexposure prophylaxis

Table 189-12 causes of Bone Marrow Suppression in Patients With HI V I nfection

HI V infection Medicat ions
Mycobacterial infections Zidovudine
Fungal infections Dapsone
8 19 parvovirus infection Trimethoprim/ sulfamethoxazole
Lymphoma Pyrimethamine
5-Fiucytosine
Gancidovir
Interferon o:
Trimetrexate
Foscamet
Table 210-1 Characteristics of Plasmodium Species Infecting Humans
I
Finding for Indicated Speciesa
Characteristic P. fa/ciparum P. vivax P. ovale P. malariae
Duration of intrahepatic 5.5 8 9 15
phase (days)
Number of merozoites 30,000 10,000 15,000 15,000
released per infected
hepat ocyt e
Duration of erythrocytic 48 48 50 72
cycle (hours)
Red cell preference Younger cells (but can Reticulocytes and cells up to 2 weeks Reticulocytes Older cells
invade celts of all ages) old
Morphology Usually only ring formsb; Irregularly s1aped large rings and Infected erythrocytes, enlarged Band or rectangular
banana-shaped trophozoites; enlarged erythrocytes; and oval with tufted ends; forms of trophozoites
gametocytes SchUffner's dots SchUffner's dots common
Pigment color Black Yellow-brown Dark brown Brown-black
Ability to cause relapses No Yes Yes No

Table 210-4 Relative Incidence of Severe Complications of Faldparum Malaria

c omplicat i on Nonpregnant Adult s Pregnant Women Children
Anemia + ++ +++
Convulsions + + +++
Hypoglycemia + +++ +++
Jaundice +++ +++ +
Renal failure +++ + ++ -

Pulmonary edema ++ + ++ +
Table 2 18- 1 Characteristics of the Filariae

Organism Periodicity Distribution Vector location of Adult Microfilarial Sheath

location
Wuchereria Nocturnal Cosmopolitan areas worldwide, including South Culex, Anopheles Lymphatic t issue Blood +
bancroft/ America, Africa, southern Asia, Papua New Guin ea, (mosquit oes)
China, Indon esia
Subperiodic Eastern Pacific Aedes (mosquitoes) Lymphatic tissue Blood +
Brug/a malay/ Nocturnal Southeast Asia, Indonesia, India Mansonia, Anopheles Lymphatic tissue Blood +
(mosquitoes)
Subperiodic Indonesia, Southeast Asia Coquillettidia, Mansonia Lymphatic tissue Blood +
(mosquitoes)
B. timori Nocturnal Indonesia Anopheles Lymphatic tissue Blood +
(mosquitoes)
Loa loa Diurnal West and Central Africa Chrysops (deerflies) Subcutaneous tissue Blood +
Onchocerca None South and Central America, Africa Simulium (blackflies) Subcutaneous tissue Skin, eye -
volvulus
Mansonella None South and Central America Culicoides (midges~ Undetermined site Blood -
ozzardr
Caribbean Simulium (blackflies)
M. perstans None South and Central America, Africa Culicoides (midges) Body cavities, Blood -
mesentery, perirenal
tissue
M. streptocerca None West and Central Africa Culicoides (midges) Subcutaneous tissue Skin -
Table 2 13-1 Comparison o f West African and East African Trypanosomiases

Point of Comparison West African ( Gambiense) East African ( R/Jodesiense)

Organism T. b. gambiense T. b. r/Jodesiense
Vectors Tsetse flies (palpalis group) Tsetse flies (morsitans group)
Primary reservoir Humans Antelope and cattle
Human illness Chronic (late CNS disease) Acute (early CNS disease)
Duration of illness Months to years <9 months
Lymphadenopathy Prominent Minimal
Parasitemia Low High
Diagnosis by rodent inoculation No Yes
Epidemiology Rural populations Wor<ers in wild areas, rural popLJiations, tourists in game parks
Table 215- 1 Diagnosis of Intestinal Protozoal Infections
Parasite Stool O+P" Fecal Acid-Fast Stai n Stool Antigen I mmunoassays Other
Giardi a + +
cryptosporidium - + +
Isospora - +
cydospora - +
Micro sporidia - Special fecal st ains, t issue biopsies

Table 219-1 Major Human Trematode Infe.c tions.

Trematode Transmission Endemic Are.a(s)

Blood Flukes
Schis tosoma mans oni Skin penetration by cercariae released from snails Africa, Sout h America, Middle East
S. japonicum Skin penetration by cercariae released from snails China, Philippines; Indonesia
S. inteficafatum Skin penetration by cercariae released from snails West Africa
S. m ekongi Skin penetration by cercariae released from snails Southeast Asia
S. haematobium Skin penetration by cercariae released from snails Africa, ~~iddle ::ast
Biliary (Hepatic) Flukes
C!onofiChis sinensis Ingestion of metacercariae in freshwater fish Far East
Opisthorchis viverrini Ingestion of metacercariae in freshwater fish Far East, Thai and
0. felineus Ingestion of metacercariae in freshwater fish Far East, Europe
Fasciola hepatica Ingestion of metacercariae on aquatic plants or in water Worldwide
F. gigantica Ingestion of metacercariae on aquatic plants or in water Sporadic, Africa
Intestinal Flukes
Fasdo!opsis bus ki Ingestion of metacercariae on aquatic plants Southeast Asia
Heterophyes h eterophyes Ingestion of metacercariae in freshwater or brac.kish-w ater fish Far East, North Africa
lung Flukes
Paragonimus westermani Ingestion of metacercariae in crayfish or crabs Global except North America and Europe
Table 221-2 CDC Category A, 8, and c Agents
Category A
Anthrax (BaciNus anthracis)
Botulism (Clostridium botulinum toxin)
Plague (Yersinia pestis)
Smallpox (Variola major)
Tularemia (Francisella tular ensis)
Viral hemorrh3gic fevers
Arenaviruses: Lassa, New World (~1achupo, Junin, Guanarito, a1d Sabia)
Bunyaviridae: Crimean-Congo, Rift Valley
Filoviridae : Ebola, Marburg
Category B
Brucellosis (Brucella spp.)
Epsilon toxin Jf Clostridium perfringens
Food safety threats (e.g., Salmonella spp., Escherichia coli

0157: H7, Shigella~

Glanders (Bwkholderia mallei)

Melioidosis (8. pseudomallei)
Psittacosis ( C~lamydophila psittad)
Q fever (Coxiella bumetit)
Ricin toxin fro11 Ricinus communis (castor beans)
Staphylococcal enterotoxin B
Typhus fever (Rickettsia prowazekit)
Viral encephalitis [.alphaviruses (e.g., Venezuelan, eastern, and western equjne. encephalitis))
Water safety threats (e.g., Vibrio choferae, Cryptosporidium parvu:n)
Category C
Emerging infectious diseases threats such as Nipah, hantavirus, SARS coronavirus, and pandemic influenza.
 ANTIMICROBIAL THERAPY

Antibiotic Regimens for Prophylaxis of Endocarditis in Adults 88

Empirical Therapy of Bacterial Meningitis & H.pylori regimen 89

community acquired pneumonia 90

antibiotics for health care assoc pneumonia 91

Endocarditis Caused by HACEK Group Organisms 92

Enteric Fever in Adults 93

Leptospirosis Treatment and Chemoprophylaxis 94

Treatment of Active Tuberculosis in Adults 95

Plague treatment and Prophylaxis 96

Malaria Treatment Regimens 97

Treatment of severe Malaria 98

Prophylaxis of Malaria 1 99

Prophylaxis of Malaria 2 100

African Trypanosomiases & Amebiasis 101

Indications for Changing Antiretroviral Therapy in Patients with HIV Infection 102

Staphylococcal Infections and it s treatment 103

Trt plan for chronic hepatitis B 104

Leptospirosis Treatment and Chemoprophylaxis 105

Tables 124- 7 Antibiotic Regimens for Prophylaxis of Endocarditis in Adults with High-Risk Cardiac LesionsOI,b
A. Standard oral regimen

1. Amoxicillin: 2 g PO 1 h before procedure

B. Inability to take oral medication

1. Ampicillin: 2 g IVor IM within 1h before procedure

c. Penicillin allergy
1. Clarithromycin or azithromycjn: 500 mg PO 1h before procedure

2. Cephalexin': 2 g PO 1 h before procedure

3. Clindamycin: 600 mg PO 1h before procedure

D. Penicillin allergy, inability to take oral medication

1. Cefazolin' or ceftriaxone': 1g IV or IM 30 min before procedure

2. Clindamycin: 600 mg IVor IM 1 h before procedure

Dosing for children: for amoxicillin, ampicillin, cephalexin, or cefadroxil, use 50 mg/kg PO; cefazolin, 25 mg/kg IV; clindamycin, 20 mg/kg PO, 25 mg/kg IV;
clarithr.omycin, 15 mg/kg PO; and vancomycin, 20 mg/kg IV.
Table 361-1 Antibiotics Used in Empirical Therapy of Bacterial Meningitis and Focal CNS Infectionsa
Indication Antibiotic
Preterminfants to infants <1 month Ampicillin +cefotaxime
Infants 1-3 mo Ampicillin +cefotaxime or ceftriaxone
Immunocompetent children >3 mo and adLits <55 Cefotaxime, ceftriaxone or cefepime +
vancomycin
Adults >55 and adults of any age with alcoholismor other debilitating illnesses Ampicillin +cefotaxime, ceftriaxone or cefepime +
vancomycin
Hospital-acquired meningitis, posttraumaticor postneurosurgery me1ingitis, neutropenic patients, or Ampicillin +ceftazidime or meropenem+
patients with im~aired cell-mediated immunity vancomycin

!Table 151-2 Recommended Treatment Regimens f,o r Helicobacter Pylori

Regimen ( Duration) Drug 1 Drug 2 Drug 3 Drug 4
Regimen 1: OCM (7- 14 days) Omeprazole 0 (20 mg
bid)
Clarithromycin (500 mg bid) Metronidazole (500 mg bid) -
Regimen 2: OCA (7- 14 days) Omeprazoleb (20 mg Clarithromycin (500 mg bid) Amoxicillin ( 1 g bid) -
bid)
Regimen 3: OBTM (14 days)< Omeprazole& (20 mg Bismuth subsalicylate (2 tabs Tetracycline HCI (500 mg Metronidazole (500 mg
bid) qid) qid) tid)
Regimen 4d: sequential (5 days + 5 Omeprazoleb (20 mg Amoxicillin 1 g bid
days) bid)
Omeprazoleb (20 mg Clarithromycin (500 mg bid) Tinidazole (500 mg bid)
bid)
Regimen s: OAL (10 days) Omeprazole 0 (20 mg Amoxicillin (1 g bid) Levofloxacin (500 mg qid)
bid)
Table 257- 4 Empirical" Antibiotic Treatment of Community- Acquired Pneumonia
Outpatients
Previously healthy and no antibiotics in past 3 months
A macrolide [ clarithromycin (SOd mg PO bid) or azithromycin (500 mg PO once, then 250 mg qd)) or
Doxycycline ( 100 mg PO bid)
Comorbidities or antibiotics in past 3 months: select an alternative from a different class
A respiratory fluoroquinolone [moxifloxacin (400 mg PO qd), gemifloxacin (320 mg PO qd), levofloxacin ( 750 mg PO qd)) or
A B-lactam [preferred: high-dose amoxicillin (1 g tid) or amoxjcillin/clavulanate (2 g bid); alternatives : ceftriaxone (1-2 g IV qd), cefpodoxime (200 mg
PO bid), cefuroxime (500 mg PO bid)) plus a macrolide"
In regions with a high rate of "high-level" pneumococcal macrolide resistance, b consider alternatives listed above for patients with comorbidities.
Inpatients, Non-ICU
A respiratory fluoroquinolone [moxifloxacin (400 mg PO or I V qd), gemifloxacin (320 mg PO qd), levofloxacin (750 mg PO or I V qd))
A B-lactam< [ cefotaxime (1-2 g I V qSh), ceftriaxone (1-2 g IV qd), ampicillin (1-2 g IV q4-6h), ertapenem ( 1 g I V qd in selected p atients)) plus a
macrolided [ oral clarithromycin or azithromycin (as li.s ted above for previously healthy patients) or I V azithromycin ( 1 g once, then 500 mg qd))
Inpatients, ICU
A B-lactam [ cefotaxime ( 1-2 g I V qSh), ceftriaxone (2 g I V qd), ampicillin-sulb.actam (2 g I V q8h)) plus
Azit hromycin or a fluoroquinolone (as listed above for inpatients, non-ICU)
Special Concerns
If Pseudomonas is a consideration
An antipneumococcal, antipseudomonal B-lactam [piperacillin/ tazobactam (4.5 g I V q6h), cefepime (.1-2 g IV q12h), imipenem (500 mg IV q6h),
meropenem ( 1 g I V qSh)) plus either ciprofloxacin (400 mg IV q12h) or levofloxacin ( 750 mg I V qd)
The above B-lactams plus an aminoglycoside [ amikacin ( 15 mg/ kg qd) or tobramycin (1.7 mg/ kg qd) and azithromycin]
The above B-lactams'plus an aminoglycoside plus an antipneumococcal fluoroquinolone
If CA-MRSA is a consideration
Add linezolid (600 mg I V q12h) or vancomycin ( 1 g I V q12h).

aooxycycline \100 _mg PO bid) is an alternative to the. macrolide.

bMI Cs of > 16 ~g/mL in 25% of isolates.
<A respiratory fluoroquinolo.ne should be used for penicillin-allergic patients.
dooxycycline (100 mg I V q12h) is an alternative to the macrolide.

For penicillin-allergic patients, .use a respiratory fluoroquinolone and aztreonam (2 g I V q8h).

Table 257-8 Empir ical Antibiotic Treatment of Health Care - Associated Pneumonia
Patients without Risk Factors for MDR Pathogens
Ceftriaxone (2 g IV q24h) or
Moxifloxacin (400 mg IV q24h), ciprofloxacin (400 mg IV q8h), or Levofloxacin (750 mg IV q24h) or
Ampicillin/ sulbactam (3 g IV q6h) or
Ertapenem ( 1 g IV q24h)
Patients with Risk Factors for MDR Pathogens
1. A B-lactam:

Ceftazidime (2 g IV q8h) or cefepime (2 g IV q8-12h) or

Piperacillin/ tazobactam (4.5 g IV q6h), imipenem (500 mg IV q6h or 1 g I V q8h), or meropenem (1 g IV q8h) plus

2. A second agent active against gram-negative bacterial pathogens:

Gentamicin or tobramycin (7 mg/kg IV q24h) or amikacin (20 mg/kg IV q24h) or

Ciprofl0xacin (400 mg IV q8h) or levofloxacin (750 mg IV q24h) plus

3. An agent active against gram -positive bacterial pathogens:

Linezolid (600 mg IV q12h) or

Vancomycin (15 mg/kg, up to 1 g IV, q12h)

Abbreviation: MDR, multidrug-resistant.

Table 146- 1 Treatment of Endocarditis caused by HACEK Group Organismsa
Organism I nitial Therapy Alternative Agents Comments
Haemophilus species, Ceftriaxone (2 g/ d) Ampicillin/sulbactam (3 g .of Ampicillin an aminoglycoside can be used if the
Aggregatibacter ampicillin q6h) .or organism does not produce B-lactamase.'
actinomycetemcomitans fluoroquinolonesb
Cardiobacterium hominis Ceftriaxone (2 g/d) Ampicillin/sulbactam (3 g of Penicillin ( 16- 18 mu q4h) or ampicillin (2 g q4h)
ampicillin q6h) should be used if the organism is susceptible.
Eikenella corrodens Ampicillin (2 g q4h) Ceftriaxone (2 g/d) or The organism is t ypically resistant t o clindamycin,
fluoroquinolonesb metronidazole, and aminoglycosides.
Kingel/a kingae Ceftriaxone (2 g/ d) Fluoroquinolonesb The prevalence of B-lactamase-producing strains is
or ampicillin/sulbactam (3 g of increasing. Efficacy for inva.sive infections is best
ampicillin q6h) demonstrated for first-line treatments.
Table 153- 1 Antibiotic Therapy f o r Enteric Fever in Adult s
Indicafjon Agent Dosage ( Route) Duration, Days
Empirical Treatment
Ceftriaxone 1-2 g/ d (I V) 7-14
Azithromycin 1 g/ d (PO) 5
Fully Susceptible
Ciprofloxacinb (first line) 500 mg bid (PO) or 400 mg q 12h (IV) 5-7
Amoxicillin (second line) 1 g tid (PO) or 2 g q6h (I V) 14
Chloramphenicol 25 mg/ kg tid (PO or IV) 14-21
Trimethoprim-sulfamethoxazole 160/ 800 mg b id (PO) 7-14
Multidrug-Resistant
Ciprofloxacin 500 mg bid (PO) or 400 mg q 12h (IV) 5-7
Ceftriaxone 2-3 g/ d (I V) 7-14
Azithromycin 1 g/ d (PO)c 5
Nalidixic Acid-Resistant
Ceftriaxone 2-3 g/ d (I V) 7-14
Azithromycin 1 g/ d (PO) 5
High-dose ciprofloxacin 750 mg bid (PO) or 400 mg q8h (IV) 10-14
IT,..h ... 111-1 Treatment and Chemoprophylaxis of Leptospirosis in Adultsil

Indication Regimen

Treatment

Mild leptospirosis Doxycycline (100 mg PO bid) or

Amoxicillin (500 mg PO tid) or
Ampicillin (500 mg PO t id)

Moderate/severe leptospirosis Penicillin ( 1.5 million units IV or JM q6h) or

Ceftriaxone (1 g/d IV) or
Cefotaxime (1 g IV q6~)

Chemoprophylaxisb

Doxycycline (200 mg PO once a week) or

Azit hromycin (250 mg PO once cr t wice a week)
f<ilile 166- 2 Simplified Approach to Treatment of Active Tuberculosis in Adults
I
Culture Intensive Phase Continuation Phase Extension of Total Treatment
Results
Culture HRZE for 2 month;, daily or intermittent HR for 4 months, daily or 5 d/wk To 9 months, if 2 months of Z is not completed or culture
positive (with dose adjustment) conversion is prolonged and/or cavitation is documented
or
HR for 4 months, intermittent
(with dose adjustment)

Culture HRZE for 2 month; 2 months To 6 months, if patient is infected with HIV
negative
Resistant to RZE or S (Qb) for 6 months .. . Prolonged culture conversion, cavitation
H
Resistant to HZEQb (! A<) for 2 11onths HEQ(S) for 10-16 months Prolonged culture conversion, delayed response
R
Resistant to ZEQb(IA<) alternative agents for 18- ... Prolonged culture conversion
HRd 24 months
 T able. 159-2 Guidelines for t he Treatment of Pl ague

Drug Dai ly Dose Interval, h Rout e

Gentamicin
Adult S mgfl<g'" 24 IM/ N
3- S mgfl<g 8 ( 2-mg/ kg loading dose followed by 1.7 mg/ kg t id, then by 1 mgfl<g t id as soon as clinically indicat ed} IM/ N
Child S mgfl<g'" 24 IM/N
7.S mg/ kg 8 ( 2.S mgfl<g t id) IM/ N
Streptomycin
Adult 2g 12 IM
Child 30 mg/kg 12 IM
Doxycycli ne
Adult 200 mg 12 or 24 PO/ IV
Child :.8 years 4.4 mg/ kg 12 or 24 PO/ IV
Tet racycline
Adult 2g 6 PO/ IV
Child :.8 years 2S-SO mgfl<g 6 PO/ IV
Chloramphenicol
Adult SO mg/kg 6 PO/ IV
Child :.1 year SO mgjkg 6 PO/ IV

Table 159-3 Guidelines for Plague Prophylaxis

Drug Daily Dose Interva l, h Route

Doxycycline
Adult 200 mg 12 or 24 PO
Child :.8 y If weight is :.45 kg, give adult dosage; if <45 kg , g ive 2.2 mgfl<g PO bid (maximum, 20Q mg/ d) 12 PO
Tetracycline
Adult 1-2 g 6 or 12 PO
Child :.8 y 25 - 50 mg/ kg 6 or 12 PO
Ciprof loxacin
Adult 1g 12 PO
Child 40 mg/kg 12 PO
Tr imethoprim -sulfamethoxazole
Adult 320 mej' 12 PO
Child :22 months 8 mg/ kg 12 PO
Table 210- 6 Regimens for the Treatment of Malaria

Type of Disease or Treatment IRegimen( s)

Uncomplicated Malaria
Known chloroquine-sensitive strains of Chloroquine (10 mg of base/kg stat followed by 5 mg/kg at 12, 24, and 36 h or by 10 mg/kg at 24 hand 5
Plasmodium vivax, P. malariae, P. ovate, P. mg/ kg at 48 h)
know/esi, P. falciparum
or
Amodiaquine (10-12 mg of base/kg qd for 3 days)

Radical treatment for P. vivax or P. ovate In addition to chloroquine or amodiaquine as detailed above, primaquine (0.5 mg of base/ kg qd) should be
infection given for 14 days to prevent relapse. In mild G6PD deficiency, 0.75 mg of base/kg should be given once
weekly for 6-8 weeks. Primaquine should not be given in severe G6PD deficiency.
Sensitive P. fafciparum malariab Artesunate< (4 mg/kg qd for 3 days) plus sulfadoxine (25 mg/ kg)fpyrimethamine (1.25 mg/kg) as a single
dose
or
Artesunate< (4 mg/kg qd for 3 days) plus amodiaquine ( 10 mg of base/kg qd for 3 days)d

Multidrug-resistant P. falciparum malaria Either artemether -lumefantrine< (1.5/9 mg/ kg bid for 3 days with food)

or
Artesunate< (4 mg/kg qd for 3 days)
plus
Mefloquine (25 mg of base/kg-either 8 mg/kg qd for 3 days or 15 mg/kg on day 2 and then 10 mg/kg on day
3)d

Second-line treatment/treatment of imported Either artesunate< (2 mgfkg qd for 7 days) or quinine (10 mg of salt/kg tid for 7 days)
malaria
plus 1 of the following 3:
1. Tetracycline (4 mg/kg qid for 7 days)

2. Doxycycline (3 mg/ kg qd for 7 days)

3. Clindamycin ( 10 mg/kg bid for 7 days)

or
Atovaquone-proguanil (20/8 mg/kg qd for 3 days with food)
Table 210- 8 Drugs Used in the Prophylaxis of Malaria

Drug Usage Adult Dose Pediatric Dose Comments

Atovaquone/proguanil Prophylaxis in areas 1 adult tablet 5-8 kg : 1/2 Begin 1-2 days before travel to malarious areas. Take daily at the
(Malarone) with chloroquine- or PO" pediatric tabletb same time each day while in the malarious areas and for 7 days after
mefloquine-resistant daily leaving such areas. Atovaquone-proguanil is contraindicated in
Plasmodium persons with severe renal impairment (creatinine clearance rate <30
;,S- 10 kg . 3/4
falciparum mL/min). In the absen;e of data, it is not recommended for children
pediatric tablet weighing <:5 kg, pregrant women, or women breast-feeding infants
daily weighing <5 kg . Atovaquone/proguanil should be taken with food or a
:> 10-20 kg: 1 milky drink.
pediatric tablet
daily
:>20-30 kQ : 2
pediatric tablets
daily
;,30-40 kg: 3
pediatric tablets
daily
:o40 kg : 1 adult
tablet dai y

Chloroquine phosphate Prophylaxis only in 300 mg of base 5 mg/kg cf base Begin 1-2 weeks before travel to malarious areas . Take weekly on the
(Aralen and generic) areas wit h (500 mg of salt) (8.3 mg o' saltjkg) same day of the week while in the malarious areas and for 4 weeks
chloroquine-sensitive PO once weekly PO once weekly, after leaving such areas. Chloroquine phosphate may exacerbate
P. falciparum< or P. up to maximum psoriasis.
v/vax only adult dose of 300
mg of base
Doxycycline (many Prophylaxis in areas 100 mg PO qd " 8 years of age : 2 Begin 1-2 days before travel to malarious areas. Take daily at the
brand names and with chloroquine- or mg/kg, u~ to adult same time each day while in the malarious areas and for 4 weeks
generic) mefloquine-resistant dose after leaving such areas. Doxycycline is contraindicated in children <8
P. fa/c/parum< years of age and in pregnant women.
Hydroxychl,roquine An alternative to 310 mg of base 5 mg of base/kg Begin 1-2 weeks before travel to malarious areas. Take weekly on the
sulfate (Piaquenil) chloroquine for (400 mg of salt) (6.5 mg o' saltjkg) same day of the week while in the malarious areas and for 4 weeks
primary prophylax s PO once weekly PO once weekly, after leaving such areas. Hydroxychloroquine may exacerbate
only in areas with up to maximum psoriasis.
chloroquine-sensitive adult dose of 310
P. fa/ciparum<or P. mg of base
vivax only
Mefloquine (Lariam and Prophylaxis in areas 228 mg of base s9 kg: 4.6 mg of Begin 1- 2 weeks before travel to malarious areas. Take weekly on the
generic) with chloroquine (250 mg of salt) base/kg (5 mg of same day of the week while in the malarious areas and for 4 weeks
resistant P. PO once weekly salt/kg) PO once after leaving such areas. Mefloquine is contraindicated in persons
fa/ciparum weekly allergic to this drug or related compounds (e.g., quinine and quinidine)
and in persons with active or recent depression, generalized anxiety
10- 19 kg: 1/4
tablet once weekly disorder, psychosis, schizophrenia, other major psychiatric disorders,
or seizures. Use with caution in persons with psychiatric disturbances
1
20- 30 kg: /2 or a history of depression. Mefloquine is not recommended for persons
tablet once weekly with cardiac conduction abnormalities.

31-45 kg: 3/4

tablet once weekly
:.46 kg: 1 tablet
once weekly

Primaquine For prevention of 30 mg of base 0.5 mg of base/kg Begin 1-2 days before travel to malarious areas. Take daily at the
malaria in areas with (52.6 mg of salt) (0.8 mg of saltjkg) same time each day while in the malarious areas and for 7 days after
mainly P. vivax PO qd PO qd, up to adult leaving such areas. Primaquine is contraindicated in persons with
dose; should be G6PD deficiency. It is also contraindicated during pregnancy and in
taken with food lactation unless the infant being breast-fed has a documented normal
G6PD level.
Primaquine Used for presumptive 30 mg of base 0.5 mg of base/kg This therapy is indicated for persons who have had prolonged
antirelapse therapy (52.6 mg of salt) (0.8 mg of exposure to P. vivax and/or P. ova/e. It is contraindicated in persons
(terminal prophylaxis) PO qd for 14 saltjkg), up to with G6PD deficiency as well as during pregnancy and in lactation
to decrease risk of days after adult dose, PO qd unless the infant being breast-fed has a documented normal G6PD
relapses of P. vivax departure from for 14 days after level.
and P. ovate the malarious departure from
area the malarious area
Clinical Stage
I (Normal CSF) II (Abnormal CSF)

Duration,

3
Table 135-3 Anti microbial Therapy fo r Staphylo<:;occal Infectionsa
Se,n s itiv ity/ Res istance of Drug o f Cho ice A lternati v e ( s ) Comments
Isola te
Parent eral Therapy for Serious Infections
Sens itive t o penicillin Penicillin G (4 mU N a fcill in or oxa cill in ( 2 g q 4h), Fe w er than 5/o of iso la tes a re sensitive to p enicillin.
q4h) cefa zo lin (2 g q 8h), van comycin (1
g q12hb)
Sen s itiv e t o m ethicillin N a fcillin or oxa cillin Cefazolin ( 2 g q8 h 0 ) , v ancomy cin Pat ients with pen ici llin allergy can b e t r eated w ith a ce phalosporin if
( 2 g q4h ) ( 15-20 m gfl<g q8-12hb) the a lle rgy does not in v o lv e an a nap h y lactic o r a ccelerated reaction;
desensitization to B-lactam s m ay be indica ted in selected cases of
s erious infection when m a x ima l bacte r icidal activity is n eeded ( e .g. ,
prosthetic valv e endocarditisd) . Ty pe A B-lactamase may rapidly
h y drolyze cefazo lin a nd re duce its e fficacy in e ndoca rdit is. Vancomycin
is a les s effective o ption.
Re sistan t to methicillin V a ncomy cin (15-20 D aptom ycin ( 6 m g / kg q 2 4hb,") for Sen sitiv ity t esting is necessary bef o r e an a lternativ e d rug is u sed .
m g/ k g q8 - 12hb) bacte remia, endocardit is, a nd Adjunctiv e d r ugs (th ose that should b e use d only in combin ation w ith
com p licated skin infections; o t h e r antim icrobia l agents) include gentam icin ( 1 m gfl<g q 8hb),
lin ezo lid (600 mg q12h except: 400 r ifampin ( 3 00 mg PO q8h ), and fusidic acid ( 5 00 m g q8h; not r eadily
m g q 12h for u n comp licated sk in a v a ilab le in the U n ited State s) . Fo r so m e serious infections, h igher
infections); q uin upristin/ dalfopr ist in doses of d apt omycin hav e b een used. Quinupristin/ dalfopr is tin is
(7.5 mg/ k g q8h ) b actericidal against methicillin - resistant isolates u nles s the strain is
res istant to e rythr omycin or clindam y cin. T h e eJficacy of a dju nctiv e
therapy is n ot w e ll established in many settin gs. Both linezolid and
quinup rist in / d a lfop ristin hav e had in v itro activity aga in st most VISA
and V RSA stra ins. See f ootnote for treatment of p r o sthetic- valv e
endocardit is d
Resis tant to meth icillin with Uncerta in Sam e a s for meth icillin-resistant Sa me a s f or methicillin-resis tant strains; check ant ib iotic
intermediate or comp le te strains; check antibiotic s u sceptibilit ie s
resis tance to v a ncomy cine suscep t ib ilities
Not y et kn'o wn ( i.e ., v a ncomycin ( 15-20 - Em p ir ica l t herapy is g iv en w hen the su sce ptib ility of the isola te is not
e mpirical therapy) m g / k g q8 - 12h~ k n own. V a ncom ycin w ith or w ithout a n a m inogly coside is
recomme nded for suspected communit y - or hosp ital-acq uired
Stap hy!OCO<Xus a u reus infections becau se o f the incre as e d frequ ency
o f methicillin -resistant strains in the commu n it y.
O ral Therap y for Skin an<:! Soft Tissue Infections
Sensitive t o meth icillin D iclox a cillin ( 500 Min ocycline o r doxycyclin e ( 100 m g It is im porta nt to know the a ntib iotic suscep tibility o f isola tes in t h e
m g q id ), cephale x in q12h0 ), TMP-SMX (1 o r 2 ds table ts s pecific geo graphic r e g ion. All d rain age s h ould b e cu lt u r ed .
( 500 mg q id ) bid ) , clinda mycin ( 3 00- 450 m gfl<g
t id )
Resistant to m ethicillin Clinda mycin ( 3 00- I t is im po rtant to know the antibiotic susceptibility o f isola te s in the
450 m g/ kg tid ), s pecific geo graphic r egion . All d rain age s h ould b e cult u r ed .
TM P-SMX (1 or 2 d s
tablets b id ) ,
m inocycline o r
doxycycline ( 100
m g q12hb),
linezo lid ( 4 00-600
m g bid )
Table 306-4 RecommeJJdations for Treatment of Chronic: Hepatitis sa
HBeAg Clinical HBV DNA ALT Recommendation
status ( IU/ ml )

HBeAg- b >2 x10 4 <2. x No treat ment; monitor . I n patients >40, wit h family history of hepatocellular carcinoma,
reactive ULNC and/or ALT persistently at the high end of the t wofold range, liver biopsy may help in
decision to treat

Chronic hepatitis >2 X 10 4 d >2 X Treat"

ULNd

Cirrhosis >2 X 10 3 <or > Treat" with oral agents, not PEG IFN
compensated ULN

<2 X 10 3 >ULN Consider treatment'

Cirrhosis Detectable <or > Treat" with oral agentsg, not PEG IFN; refer for liver transplantation
decompensated ULN

Undetectable <or > Observe; refer for liver t ransplantation

ULN

HBeAg- b S:2 X 10 3 s:ULN I nactive carrier; t reatment not necessary

negative

Chronic hepatitis >10 3 1->2 X Consider liver biopsy; treat" if biopsy shows moderate t o severe inflammation or fibrosis
ULNd

Chronic hepatitis >10 4 >2. x Treat";

ULNd

Cirrhosis >2 X 1Q3 <or > Treat" wit h oral agents, not PEG IFN
compensated ULN

<2 X 10 3 >ULN Consider treatment'

Cirrhosis Detectable <or > Treat" with oral agentsg, not PEG IFN; refer for liver t ransplantation
decompensated ULN

Undetectable <or > Observe; refer for liver t ransplantat ion

ULN
Table 171-1 Treatment and Chemoprophylaxis of leptospirosis in Adultsa
Indication Regimen

Treatment

Mild leptospirosis Doxycycline ( 100 mg PO bid) or

Amoxicillin (500 mg PO tid) or
Ampicillin (500 mg PO tid)

Moderate/severe leptospirosis Penicillin (1.5 million units IVor IMq6h) or

Ceftriaxone (1 g/d IV) or

Cefotaxime (1 g IV q6h)

Chemoprophylaxisb

Doxycycline (200 mg PO once a week) or

Azithromycin (250 mg PO once or twice a week)
 CVS

Blood Pressure Classification & BMI 107

ADR of CVS drugs 108

Drugs used in Hypertensive emergencies & Prophylaxis duration for RHD 109

Cardiac Tamponade from Constrictive Pericarditis and Similar Clinical Disorders 110

NYHA and canadian classification & Systolic HTN with wide PP 111

Factors Precipitate Acute Decompensation in Pts with Chronic Heart Failure 112

Indications for Early Invasive Strategy in IHD 113

Indications for Cardiac Catheterization and Coronary Angiography 114

Indications for Surgery in Patients with Endocarditis 115

 Table 247- 1 . Blood Pressure Classjfication

Blood Pr essure Classificat ion Systolic, mmHg Diast olic, mmHg
Normal <120 and <80
Prehypertension 120- ! 39 or 80- 89
Stage 1 hypertension 140- 159 or 90-99
Stage 2 hypertension ~160 or ~ 100
Isolated systolic hypertension ~1 40 and <90

Tab le 76- 1 Body Mass Index (BMI) and Nutrit ional Status

BMI Nutritional Status

>30 kg/ m2 Obese

>25-30 kg/ m2 Overweight

20-25 kg/ m2 Normal

<18 .5 kg/ m2 Moderate malnutrition

<16 kg/ m2 Severe malnutrition

< 13 kg/r:n 2 Lethal in males

< 11 kg/ m2 Lethal in females

Table 247-10. Usual Intravenous Doses of Antihypertensive Agents Used in Hypertensive Emergencies.*
Antihypertensive Intravenous Dose
Agent
Nitroprusside Initial 0.3 (~g/kg)/min; usual 2- 4 (~g/kg)/min; maximum 10 (~g/kg)/min for 10 min
Nicardipine Initial 5 mg/h; titrate by 2.5 mg/h at 5- 15 min intervals; max 15 mg/h
Labetalol 2 mg/min up to 300 mg or 20 mg over 2 min, then 40-80 mg at 10-min intervals up to 300 mg total
Labetalol 2 mg/min up to 300 mg or 20 mg over 2 min, then 40-80 mg at 10-min intervals up to 300 mg total
Esmolol Initial 80- 500 ~g/kg over 1min, then 50- 300 (~g/kg)/min
Phentolamine 5-15 mg bolus
Nitroglycerin Initial s ~g/min, then titrate by 5 ~g/min at 3- 5-min intervals; if no response is seen at 20 ~g/min, incremental increases of 10- 20 ~g/min
may be used
Hydralazine 10-50 mg at 30-min intervals

-
Table 322-3 American Heart Association Recommendations for Duration of Secondary Prophylaxis*
Category of Patient Duration of Prophylaxis

Rheumatic fever without carditis For 5 years after the last attack or 21 years of age (whichever is longer)

Rheumaticfever with carditis but no residual valvular disease For 10 years after the last attack, or 21years of age (whichever is longer)

Rheumatic fever with persistent valvular disease, evident clinically or on For 10 years after the last attack, or 40 years of age (whichever is longer).
echocardiography Sometimes lifelong prophylaxis.

*These are only recommendations and must be modified by individual circumstances as warranted. Note that other organizations have slightly different
recommendations (see www.worldheart.orgjrhd for links).
T~ble 239- 2 Featur es That Distinguish cardiac Tamponade from Constrictive Pericarditis ~nd Similar Clinical Disord e.ts

Characteristic Tamponade Constrictive Pericarditis Restrictive Cardiomyopathy RVMI

Clin ical
Pulsus paradoxus Common Usually absent Rare Rare
Jugular veins
Pmminent y descent Absent Usually present Rare Rare
Pmminent x descent Present Usually present Present Rare
Kussmaul's sign Absent Present Present Present
Third heart sound Absent Absent Rare May be present
Pericardial knock Absent Often present Absent Absent
Electrocardiog ram
Low ECG voltage May b e pre sent May be present May be present Absent
Electrical alternans May be pre sent Absent Absent Absent
Echocardiography
Thickened pericardium Absent Present Absent Absent
Pericardial calcification Absent Often present Absent Absent
Peri,cardial effusion Present Absent Absent Absent
RV size Usually small Usually normal Usually normal Enlarged
~1 yo cardia! thickness Normal Normal Usually increas.e d Normal
Right atrial collapse and RVDC Present Absent Absent Absent
Increased early filling, 1 mitral flow velocity Absent Present Present May be present
Exaggerated respiratory variation in flow velocity Present Present Absent Absent
CT/MRI
Thickened/ calcific pericardium Absent Present Absent Absent
Cardiac catheterization
Equalization of diastolic pressures Usually pre sent Usually present Usually absent Absent or present
Cardiac biopsy helpful? No No Sometimes No
Table 243- 1. cardiovascular Disease Classification Chart

Class New York Heart Association Functional Classification canadian Cardiovascular Society Functional Classification
I Patients have cardiac disease but without the resulting limitations Ordinary physical activity, such as walking and climbing stairs, does not cause angina.
of physical activity. Ordinary physical activity does not cause undue Angina present with strenuous or rapid or prolonged exertion at work or recreation.
fatigue, palpitation, dyspnea, or anginal pain.
II Patients have cardiac disease resulting in slight limitation of physical Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill,
activity. They are comfortable at rest. Ordinary physical activity walking or stair climbing after meals, in cold, or when under emotional stress or only
results in fatigue, palpitation, dyspnea, or anginal pain. during the few hours after awakening. Walking more than two blocks on the level and
climbing more than one flight of stairs at a normal pace and in normal conditions.
III Patients have cardiac disease resulting in marked limitation of Marked limitation of ordinary physical activity. Walking one to two blocks on the level
physical activity. They are comfortable at rest. Less than ordinary and climbing more than one flight of stairs in normal conditions.
physical activity causes fatigue, palpitation, dyspnea, or anginal
pain.
IV Patients have cardiac disease resulting in inability to carry on any Inability to carry on any physical activity without discomfort-anginal syndrome may be
physical activity without discomfort. Symptoms of cardiac present at rest.
insufficiency or of the anginal syndrome may be present even at
rest. If any physical activity is undertaken, discomfort is increased.

Table 247-2. Systolic Hypertension w ith Wide Pulse Pressure

1. Decreased vascu[ar compliance (arteriosclerosis)
2. I ncreased cardiac output.
a. Aortic regurgitation
b. Thyrotoxicosis.
c. Hyperkinetic heart syndrome.
d. Fever.
e. Arteriovenous fistula
f. Patent ductus arteriosus
Table 234- 4 Factors That May P~ecipitate Acute Decompensation in Patients w ith Chronic Heart Failure
Dietary indiscretion
Myocardial ischemia/ infarction
Arrhythmias (tachycardia or bradycardia)
Discontinuahon of HF therapy
Infection
Anemia
Initiation of medications that worsen HF
Calcium antagonists (verapamil, diltiazem)
Beta b lockers
Nonsteroidal anti-inflammatory drugs
Antiarrhythmic agents [ all class I agents, sotalol (dass III))
Anti-TNF antibodies
Alcohol consumption
Pregnancy
Worsening hypertension
Acute valvular insufficiency
Table 244- 3. Class I Recommendations for Use of an Early Invasive Strategy * I
Class I ( l evel of Evidence: A) Indications
Recurrent angina at rest/low -level activity despite Rx
Elevated TnT or Tnl
New ST-segment depression
Rec. ang na/ ischemia with CHF symptoms, rates, MR
Positive stres.s test
EF < 0.40
Decreased BP
Sustained VT
PC! < 6 months, prior CA.BG
High-risk score
Table 230-1. Indication s for Cardiac Catheter ization and Cor onary Angiogr aphy

Coronary Artery Disease

Asymptomlltic or Symptomatic
High risk for adverse outcome based on noninvasive testing
Sudden cardiac death
Sustained ( >30 sc) monomorphic ventricular tachycardia
Nonsustained ( <30 sc) polymorphic ventricular tachycardia
Symptomatic
Canadian Cardiology Society class Ill or I V angina on medical therap y
Unstable angina-high or intermediate risk
Chest-pain syndrome of unclear etiology and equivocal findings on noninvasive tests
Acute Myocardial Infarction
Reperfusion with primary percutaneous coronary intervention
Persistent or recurrent ischemia
Severe pulmonary edema
Cardiogenic shock or hemodynamic instability
Mechanical complications-mitral regurgitation, ventricular septal defect
Valvular Heart Disease
Suspected valve disease in symptomatic patients-dyspnea, angina, heart failure, syncope
Infective endocarditis with coronary embolization
Asymptomatic patients with aortic regurgitation and cardiac enlargement or ~ ej ection fraction
Prevalve surgery in older patients with coronary artery diseaserisk factors
Congestive Heart Failure
New onset with angina or suspected undiagnosed coronary artery disease
Congenital Heart Disease
Prior to surgical correction, when sympt oms or noninvasive testing suggests coronary disease
Suspicion for congenital coronary anomalies
Forms of congenital heart disease associated with coronary anomalies
Pericardia! Disease
Symptomatic patients with suspected cardiac tamponade or constrictive pericarditis
Cardi.ac Transplantation
Preoperative and postsurgical evaluation
other Conditions
Hypertrophic cardiomyopat hy with angina
Diseases of the aorta when knowledge of coronary artery involvement is necessary for management
or re!a1pse:d
 GIT AND HEPATOBILIARY

Anticopper Drugs for Wilson's Disease & Nazer prognostic Index 117

causes of Macrovesicular steatosis 118

Diagnostic methods for H.pylori & causes of steatorrrhea and tests used 119

Interpretation of Schilling tests 120

Findings in small int mucosal biopsies and it s diseases 121

Lab features of alcoholic hepatitis 122

CT severity index for acute pancreatitis & etiology of IBD 123

 Table 360-3 Prognostic Index of Nazer

Score (in Points)

Laboratory Measurement Normal Value 0 1 2 3 4

Serum bilirubina 0.2- 1.2 mg/dL <5.8 5.8- 8.8 8.8-1 1.7 11.7- 17.5 >17.5
Serum aspartate transferase (AST) 10-35 IU/L <100 100-150 151-200 201-300 >300
Prolongation of prothrombin time (seconds) - <4 4-8 9-12 13-20 >20

au hemolysis is present, the serum bilirubin cannot be used as a measure of liver function until the hemolysis subsides.

Table 360-2 Recommended Anticopper Drugs for Wilson's Disease

I
Disease Status First Choice Second Choice
Initial hepatic
Hepatitis or cirrhosis without decompensation Zinc' Trientine

Hepatic decompensation
Mild Trientineb and zi1c Penicillamineb and zinc
Moderate Trientine and zin: Hepatic transplantation
Severe Hepatic transplantation Trientine and zinc
Initial neurologic/psychiatric Tetrathiomolybdatec and zinc Zinc
Maintenance Zinc Trientine
Presymptomatic Zinc Trientine
Pediatric Zinc Trientine
Pregnant Zinc Trientine

zinc acetate is supplied as Galzin, manufactured by Gate Pharmaceutical. Recommended adult dose for all the above indications is SO mg of elemental zinc
three times daily, each dose separated from food and beverages other than water by at least 1 h, and separated from trientine or penicillamine doses by at
least 1 h.
Table 293-2 Tests f or Detection of H. Pylori
Test Sensitivity/Specificity, Comments
Ofo

I nvasive (Endoscopy/Biopsy Required )

Rapid urease 80- 95/95 - 100 Simple, false negative with recent use of PPi s, antibiotics, or bismuth compounds
Histology 80-90/>95 Re.quires pathology processing and staining; provides histologic information
Culture - I- Time-consuming, expensive, dependent on experience; allows determination of antibiotic susceptibility
Noninvasive
Serology >80/>90 Inexpensive, convenient; not useful for early follow -up
Urea breath >90/ >90 Simple, rapid; useful for early follow-up; false negatives with recent therapy (see rapid urease test);
test exposure to low-dose radiation with 14c test

Stool antigen >90/>90 Inexpensive, convenient; not established for eradication but prGmising

Abbreviation: PPi s, proton pump inhibitors.

Table 294-7 Results of Diagnostic Studies in Different causes of Steatorrhea

o-Xylose Test Schilling Test Duodenal Mucosal Biopsy
Chronic pancreatitis Normal 50% abnormal; if abnormal, normal with pancreatic Normal
enzymes
Bacterial overgrowth Normal or only modestly Often abnormal; if abnormal, normal after antibiotics Usually normal
syndrome abnor11al
Ileal disease Normal Abnormal Normal
Celiac disease Decreased Normal Abnormal: probably "flat"
Intestinal lymphangiectasia Normal Normal Abnormal: "dilated
lymphatics"
' 8co-Cbl With Intrinsic Fador With Pancreatic Enzymes After5 Antibiotics
Table 294- 6 Disease that Can Be Diagnosed by Small-Intestinal Mucosal Biopsies

Lesions Pathologic Findings

Diffuse, Specific
Whipple's disease Lamina propria contains macrophages containing PAS+ material
Agammaglobulinemia No plasma cells; either normal or absent villi ("flat mucosa")
Abetalipoproteinemia Normal villi; epithelial cells vacuolated with fat postprandially
Patchy, Specific
Intestinal lymphoma Malignant cells in lamina propria and submucosa
Intestinal lymphangiectasia Dilated lymphatics; clubbed villi
Eosinophilic gastroenteritis Eosinophil infiltration of lamina propria and mucosa
Amyloidosis Amyloid deposits
Crohn's disease Noncaseating granulomas
Infection by one or more microorganisms (see text) Specific organisms
Mastocytosis Mast cell infiltration of lamina propria
Diffuse, Nonspecific
Celiac disease Short or absent villi; mononuclear infiltrate; epithelial cell damage; hypertrophy of crypts
Tropical sprue Similar to celiac disease
Bacterial overgrowth Patchy damage to villi; lymphocyte infiltration
Folate deficiency Short villi; decreased mi tosis in crypts; megalocytosis
Vitamin 812 deficiency Similar to folat e deficiency
Radiation enteritis Similar to folate deficiency
Zollinger-EIIison syndrome Mucosal ulceration and erosion from acid
Protein -calorie malnutrition Villous atrophy; secondary bacterial overgrowth
Drug-induced enteritis Variable histology

Abbreviation: PAS+, periodic acid- Schiff positive.

Table 307-2 Laboratory Diagnosis of Alcoholic Fatty liver and Alcoholic Hepatitis

Test Comment

AST Increased two - to sevenfold, <400 U/L, greater than ALT

ALT Increased two- to sevenfold, <400 U/L

AST/ALT Usuallpl

GGTP Not specific to alcohol, easily inducible, elevated in all forms of fatty liver

Bilirubin May be markedly increased in alcoholic hepatitis despite modest elevation in alkaline phosphatase

PMN If >5500/J.tl, predicts severe alcoholic ~epatitis when discriminant function >32

Note: AST, aspartate aminotransferase; ALT, alanire aminotransferase; GGTP, gamma-glutamyl transpeptidase; PMN, polymorphonuclear cells.
 Table 295- 1 Epidemiology of lBO

Ulcer ative Colitis Crohn' s Dis ease

Incidence (North Ame rica) pe r person-years 2.2-14.3 : 100,0.00 3.1-14.6:100,000
Age of onset 15-30 & 60-80 15-30 & 60-80
Ethnicity Jewish > non -Jewish white >African American > Hispanic >Asian
Male/ female ratio 1:1 1.1-1.8:1
Smoking May prevent disease May cause disease
Ora l contraceptives No incr eased risk Odds ratio 1.4
Appendectomy Protective Not protectiv e
Monozygotic tw ins 6% concor dance 58% concordance
Dizygotic twins OOJo concordance 4% concordance

"tb1e 313-3 CT Findings and Grading of Acute Pancreatitis [CT severity Index (Ctsi)]

Grade Findings Score

A Normal pancreas: normal size, sharply defined, smooth contour, homogeneous enhancement, ret roperit oneal peripancreaticfat without 0
enhancement
8 Focal or diffuse enlargement of the pancreas, contour may show irregularity, enhancement may be inhomogeneous but t here is no 1
peripancreatic inflammation
c Peripancreatic inflammat ion with intrinsic pancreatic abnormalities 2
D Intrapancreatic or extrapancreatic fluid collections 3
E Two or more large. collections or gas in the pancreas or retroperitoneum 4
Necrosis score based on contrast -enhanced CT
Necrosis,% Score
0 0
<33 2
33- 50 4
:.50 6
DIAGNOSTIC CRITERIA

Table 389-1 Diagnostic Criteria for Chronic Fatigue Syndrome

Characterized by Persistent or Relapsing Unexplained Chronic Fatigue

Fatigue lasts for at least 6 months

Fatigue is of new or definite onset

Fatigue is not the result of an organic disease or of continuing exertion

Fatigue is not alleviated by rest

Fatigue results in a substantial reduction in previous occupational, educational, sooial, and personal activities

Four or more of the following symptoms, concurrently presentfor 6 months:

impaired memory or concentration, sore throat, tender cervical or axillary lymph nodes, muscle pain, pain in several joints, new headaches, unrefreshin
sleep, or malaise after exertion

Exclusion Criteria

Medical condition explaining fatigue

Major depressive disorder (psychoticfeatures) or 9ipolar disorder

Schizophrenia, dementia, or delusional disorder

Anorexia nervosa, bulimia nervosa

Alcohol or substance abuse

Severe obesity (BMI >40)

Table 268-2. Diagnostic Criteria for ALI and ARDS
Oxygenat ion Onset Chest Radiograph Absence of Left Atrial Hyperte.nsion
All : Pa0 2/FI02 .: 300 mmHg Acute Bilateral alveolar or interstitial PCWP .: 18 mmHg or no clinical evidence of increased left
infiltrates atrialpressure

ARDS: Pa0 2/FI0 2 .: 200

mmHg

Abbreviations: All, acut e lung injury,; ARDS, acute respirat ory distress syndrome; FI0 2 , inspired 0 2 percentage; Pa0 2 , arterial partial pressure of 02;
PCWP, pulmonary capillary wedge pressure.

The annual incidences of All and ARDS are estimated to be up to 80/100,000 and 60/100,000, respectively. Approximately 10% of all intensive care
unit (ICU) admissions suffer from acute respiratory failure, with ~20% of these patients meeting criteria for All or ARDS.

Etioloov
Table 255- 3 Diagnostic Features of Allergic Br onchopul monary Aspergillosis (ABPA)
Main diagnost ic criteri a
Bronchial asthma
Pulmonary infiltrates
Peripheral eosinophilia (> 1000/V-L)
Immediate whea l-and-flare response to AspergiJ/us fumigatus
Serum precipitins to A. fumigatus
Elevated ser um lgE
Central bronchiectasis
Other d iagnostic f eatur es
History of brownish plugs Jn sputum
Culture of A. fumigatus from sputum
Elevated IgE (and JgG) class antibodies specific for A. fumigatus
 expected during a

senousness
 Table 327- 1 Diagltostic Criteria ofBehc;ET's Disease

Recurrent oral ulceration .plus two of the following:

Recurrent genital ulceration

.Eye lesions

Skin lesions

Pathergy test

Table344-2 Criteriafor the Diagnosisof Diabetes Mellitus

, SymJtomsof diabetes plus random blocd ~luccse concentraton :<11.1 mmci/L (200 mgfdL)aor

1 Fastingplasmaglucose :<?.0 mrnJI/L (126 11gjdL)bor

1A:C >6.5%cor

1 Two-hour plasrm gluco5e :< 11.1 11no/L(20C ngfdL) curing c;n oral glucose tclerance testd
Table 241- 3 . Clinical I dentification of the Metabolic syndrome - Any Three Risk Factors

Risk Factor Defining Level

Abdominal obesity
Men (waist eireumferenee)b >102 em (>40 in.)

Women >88 em (>35 in.)

Triglyeerides >1.7 mmoi/L ( >150 mg/dL)
HOL cho-lesterol
Men <1 mmoi/L ( <40 mg/dL)
Women <1.3 mmoi/L (<50 mg/ dL)
Blood pressure ::. 130/ :o85 mmHg
Fasting glucose >6.1 mmoi/L (>110 mg/dL)

Table 296-1 Diagnostic Criteria for I rritable Bowel Syndromea

Recurrent abdominal pain or discomfortb at least 3 days per month in the last 3 months associated with two or more of the following:
1. Improvement with defecation

2. Onset associated with a change in frequency of stool

3. Onset associated with a change in form (appearance) of stool

criteria fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis. &Discomfort means an uncomfortable sensation not
described as pain. In pathophysiology research and clinical trials, a pain/discomfort frequency of at least 2 days a week during screening evaluation is
required for subject eligibility. &Jurce: Adapted from Longstreth et al.
T<tble 220-1 Diagnostic Criteria for Human Cysticercosisa
I
1. Absolute criteria
a. Demonstration of cysticerci by histologic or microscopic examination of biopsy material
b. Visualization of the parasite in the eye by funduscopy
c. Neuroradiologic demonstration of cystic lesions containing a characteristic scolex
2. Major criteria
a. Neuroradiologic lesions suggestive of neurocysticercosis
b. Demonstration of antibodies to cysticerci in serum by enzyme-linked immunoelectrotransfer blot
c. Resolution of intracranial cystic lesions spontaneously or after therapy with albendazole or praziquantel alone
3. Minor criteria
a. Lesions compatible with neurocysticercosis detected by neuroimaging studies
b. Clinical manifestations suggestive of neurocysticercosis
c. Demonstration of antibodies to cysticerci or cysticercal antigen in cerebrospinal fluid by ELISA
d. Evidence of cysticercosis outside the central nervous system (e.g., cigar-shaped soft-tissue calcifications)
4. Epidemiologic criteria
a. Residence in a cysticercosis-endemic area
b. Frequent travel to a cysticercosis-endemic area
c. Household contact with an individual infected with Taenia so/ium
Table 385-3 Diagnostic Features of Acute I nflammatory Demyelinating Polyneuropat hy (AIDP)
I. ReQuired for Diag nosis
1. Pr ogressive weakness of variable degree from mild paresis to complet e par alysis
2. Gener alize d hypo- or areflexia
II. Supportive of Diagno sis
1. d inical Features
a. Symptom progression: Moto r weakness rapidly progresses init ially but ceases by 4 weeks. Nadir attained by 2 weeks in 5 0%, 3 week s 8 0%, and 9 0% by
4 weeks.
b. Demonstration of r elative limb symmet ry r egard ing paresis.
c. Mild to mo derate sensory signs.
d. FreQuent cranial nerve involvement : Facial (cran ial nerve VII) 50% an d typically bilateral but asymmetric; occasional involvement of cranial nerves XII, X,
and o ccasionally I II, I V, and VI a s well as Xi.
e . Recovery typically b egin s 2-4 w eeks following plat eau p ha se.
f. Autonomic dysfunction can includ e tachycardia, oth er arrh ythmia s, po stural hypot en sion, hyperten sion, other vasomotor sympt oms.
g. A precedin g g astro intest inal illn ess ( e.g., d iarrhea) or upper resp irato ry tract infection is .common.
Cerebrospina l Fluid Features Su pporting Diagnosis
a . Elevated o r serial e levation of CSF protein.
b. CSF cell count s are <IO mononuclear cell/ mm3

3. Electrodiag nostic Medicine Fin dings Su pportive of Diagno sis

a. 8 0% of p atients have evidence of NCV slowing/conduction b lock at so me time durin g disease process.
b . Patchy reduction in NCV attainin g values less than 60% of normal.
c. Distal motor latency increase may reach 3 t imes normal valu es .
d. F-.waves indicat e proximal NCV slowin g.
e. About 15-20% of p atients h ave normal NCV findings.
f . No ab normalities on nerve conduction stu dies may b e seen for severa l weeks.
III. Findings Reducing Possib ility of Diagno sis
1. Asymmetric weakness
2. Failure of b owe l/bladder symptoms t o r esolve
3. Sever e bowe lfbladder dysfunction at init iat ion of disease
4. Great er t han 5 0 mononuclear cells/ mm3 in CSF
5. Well-d emarcated sensory level
IV. Exclusionary Criteria
1. Diagnosis of other causes of acute neu romuscular w eakness (e.g., my asth enia gravis, b otulism, poliomyelitis, toxic n euro pathy).
3 . Abnormal CSF cytology suggesting carcinomatous invasion of the n erve roots
Tables 124-3 The Duke Criteria for the Clinical Diagnosis of Infective Endocarditis"
Major Cr iteria
1. Positive blood culture

Typical microorganism for infective endocarditis from two separate blood cultures

Viridans streptococci, Streptococcus gilflo/ytlcus, HACEK group, Staphylococcus aureus, or

Community-acquired enterococci in the absence of a primary focus, or

Persistently positive blood culture, defined as recovery of a microorganism consistent with infective endocarditis from:

Blood cultures drawn > 12 h apart; or

All of 3 or a majority of :.4 separate blood cultures, with first and last drawn at least 1 h apart

Single positive blood culture for Cox/elfil burnetil or phase I lgG antibody titer of > 1:800

2. Evidence of endocardial involvement

Positive echocardiogramb

Oscillating intracardiac mass on valve or supporting structures or in the pat h of regurgitant jets or in implanted material, in the absence of an alternative
anatomic explanation, or

Abscess, or

New partial dehiscence of prosthetic valve, or

New valvular regurgitation (increase or change in preexisting murmur not sufficient)

Minor Criteria
1. Predisposition: predisposing heart condition or injection drug use
2. Fever :t38.0C (lll00.4F)
3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway
lesions
4. Immunologic phenomena : glomerulonephritis, Osier's nodes, Roth's spots, rheumatoid factor
5. Microbiologic evidence: posit1ve blood culture but not meeting major criterion as noted previously< or serologic evidence of active infection with organism
consistent with Infective endocard1t1s

oefimte endocarditiS IS defined by documentation of two ma)or cntena, of one major critenon and three m1nor cr1ter1a, or of five m1nor cntena. See text for
further details.
Table 321- 1 Classification Criteria for Rheumatoid Arthritis

Score

Joint involvement 1 1arge joint (shoulder, elbow, hip, knee, ankle) 0

2- 10 large joints 1

1- 3 small joints (MCP, PI~, Thumb IP, MTP, wrists) 2

4- 10 small joints 3

>10 joints (at least 1 small joint) 5

Serology Negative RF and negative ACPA 0

Low-positive RF or low-positive anti -CCP antibodies (,.;3 times ULN) 2

High-positive RF or high-positive antiCCP antibodies (>3 times ULN) 3

Acute-phase reactants Normal CRP and normal ESR 0

Abnormal CRP or abnormal ESR 1

Duration of sympt oms <6 weeks 0

;,6 weeks 1
Table 319-3 Diagnostic Criteria for Systemic lupus Erythematosus
Malar rash Fixed erythema, flat or raised, over the malar eminences

Discoid rash Erythematous circular raised pat ches with adherent keratotic scaling and follicular plugging; atrophic scarring may occur

Photosensitivity Exposure to ultravblet light causes rash

Oral ulcers Includes oral and nasopharyngeal ulcers, observed by physician

Arthritis Nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion

Serositis Pleuritis or pericarcitis documented by ECG or rub or evidence of effusion

Renal disorder Proteinuria >0.5 g/d or .f3+, or cellular casts

Neurologic disorder Seizures or psychosis without other causes

Hematologic disorder Hemolytic anemia cr leukopenia (<4000/llol) or lymphopenia (<1500/lloL) orthrombocytopenia(<lOO,OOO/IloL) in the absence of
offending drugs

Immunologic disorder Anti-dsDNA, anti-Sn, and/or anti-phospholipid

Antinuclear An abnormal titer of ANA by immunofluorescence or an equivalent assay at anv point in time in the absence of drugs known to
antibodies induce ANAs

If :.4 of these criteria, well documented, are present at any time in a patient's history, the diagnosis is likely to be SLE. Specificity is - 95%; sensitivity is
-75%.
Table 111- 2 Diagnostic Criteria for Multiple Myeloma, Myeloma variants, and Monoclonal Gammopathy of Undetermined I
Significance
Monoclonal Gammopathy of Undetermined Significance ( MGUS)
M protein in serum <30 g/ L
Bone marrow clonal plasma cells <10%
No evidence of other B cell proliferative disorders

No myeloma-related organ or tissue impairment (no end organ damage, including bone lesions)

Asymptomatic Myeloma (Smoldering Myelomn)

M protein in serum :.30 g/L and/or
Bone marrow clonal plasma cells "10%
No myeloma-related organ or tissue impairment (no end organ damage, including bone lesions) or symptoms

Symptomatic Multiple Myeloma

M protein in serum and/or urine

Bone marrow (clonal) plasma cellsb or olasmacytoma

Myeloma-related organ or tissue impairment (end organ damage, including bone lesions)

Nonsecretory Myeloma
No M protein in serum and/or urine with immunofixation
Bone marrow clonal plasmacytosis :o1C% or plasmacytoma
Myeloma-related organ or tissue impairment (end organ damage, including bone lesions)'

Solitary Plasmacytoma of Bone

No M protein in serum and/or urine<
Single area of bone destruction due to clonal plasma cells
Bone marrow not consistent with multiple myeloma

Normal skeletal survey (and MRI of spi~e and pelvis if done)

No related organ or tissue impairment (no end organ damage other than solitary bone lesion)'
T~ble 267- 1. Calculation of Acute Physiology and Chronic Heal!h Evaluation II (APACHE II)"

Score 4 3 2 1 0 1 2 3
Rectal temperature, oc ~41 39.0- 40 .9 38.S- 36.0- 34.0- 32.0- 30.0-
38.9 38.4 3S.9 33.9 31.9
Mean blood pressure, mmHg :.160 130- 1S9 110- 70- S0-.69
129 109
Heart rate :. 180 140-179 110- 70- 5S-69 40-5
139 109
Respiratory rate ~so 3S-49 2S-34 12- 24 10- 11 6- 9
Arterial pH " 7 .70 7.60- 7.69 7.50- 7.33- 7.25- 7. 15-
7.S9 7.49 7.32 7.24
Oxygenation
If FI 02 > O.S, use (A - a) 0 02 :aSOO 3S0-499 200- <200
349
If F02 " O.S, use Pa 02 " 70 61- 70 S5- 6

Serum sodium, meq/L d80 160- 179 1SS- 1SO- 130- 120- 111-
1S9 1S4 149 129 119
Serum potassium, meq/L :.7.0 6.0-6.9 5.5- 3.S- 3.0- 2.5-
5.9 5.4 3.4 2.9
Serum creatinine, mg/dl " 3.5 2.0-3.4 1.5- 0.6- <0.6
1.9 1.4
Hematocrit :.60 so- 46- 30- 20-
59.9 49 .9 4S.9 29.9
WBC count, 10 3/ ml :.40 20- 1S- 3-14.9 1-2.9
39.9 19.9
MISCELLANEOUS

Table 297- 5 The Staging and Treatment of Hemorrhoids

Stage Description of Classification Treatment
I EnlarQement with bleeding Fiber supplementation Cortisone suppository Sclerotherapy
I! Protrusion with spontaneous Fiber supplementation Cortisone suppository
reduction
IU Protrusion requiring manual reduction Fiber supplementation Cortisone suppository Banding Operative hemorrhoidectomy (stapled or
traditional)
IV Irreducible protrusion Fiber supplementation Cortisone suppository Operative hemorrhoidectomy

Table 353- 2 Guidelines for Surgery in Asymptomatic Primary Hyper parat hyroidisma

Parameter Guideline
Serum calcium (above normal) >1 mg/dL
24-h urinary Ca No indication
Creatinine clearance (calculated) If <60 mL/min
Bone density T score <-2.5 at Any of 3 sitesb
Age <50

Table 165-5 Tuberculin Reaction Size and Treatment of Latent Mycobacterium tuberculosis Infection

Risk Group Tuberculin Reaction Size, mm

HIV-infected persons or persons receiving immunosuppressive therapy :.5
Close contacts of tuberculosis patients :.sa
Persons with fibrotic lesions on chest radiography :.5
Recently infected persons (..:2 years) :.10
Persons with high-risk medical conditionsb :.10
Low-risk persons' :.15
Table 32-4 Alterations of the Tongue

Typeof Change Clinical Features

Size or Morphology Changes
Macroglossia Enlarged tongue that may be part of a syndrome found in developmental conditions such as Down syndrome, Simpson-Golabi-
Behmel syndrome, or Beckwith-Wiedemann syndrome may be due to tumor (hemangioma or lymphangioma), metabolic disease
(such as primary amyloidosis), or endocrine disturbance (such as acromegaly or cretinism)
Fissured ("scrotal") Dorsal surface and sides of tongue covered by painless shallow or deep fissures that may collect debris and become irritated
tongue
Median rhomboid Congenital abnormality of tongue with ovoid, denuded area in median posterior portion of the tongue; may be associated with
glossitis candidiasis and' may respond to antifungals
Color Changes
"Geographic" tongue Asymptomatic inflammatory condition of the tongue, with rapid loss and regrowth of filiformpapillae, le.ading to appearance of
(benign migratory denuded red patches "wandering" across the surface of the tongue
glossitis)
Hairy tongue Elongation of filiformpapillae of the medial dorsal1surface area due to failure of keratin layer of the papillae to desquamate
normally; brownish-black coloration may be due to staining by tobacco, food, or chromogenic organisms
"Strawberry" and Appearance of tongue during scarlet fever due to the hypertrophy of fungiform papillae plus changes in the filiformpapillae
"raspberry" tongue
"Bald" tongue Atrophy may be associated with xerostomia, pernicious anemia, iron-deficiency anemia, pellagra, or syphilis; may be accompanied
by painful burning sensation; may be an expression of erythematous candidiasis and respond to antifungals
Table 49- 1 Causes of Hirsutism
Gonadal hyperandrogenism
Table 5 3 - 4 causes of Alopecia
I
I. Nonscarring alopecia
Ovarian hyperandrogenism
A. Primary cutaneous disorders
Polycystic ovary syndrome/ functional ovarian hyperandrogenism
1. Telogen effluvium
Ovarian steroidogenic blocks
2. Androgenetic alopecia
Syndrome~ of extreme in:::ulin rc:::i:::tuncc
3. Alopecia areata
Ovarian neoplasms
4. Tinea capitis
Adrenal hyperandrogenism
Premature adrenarche 5. Traumatic alopecia"

Functional adrenal hyperandrogenism

8. Drugs
Congenital adrenal hyperplasia (nondassic and classic)
C. Systemic diseases
Abnormal cortisol action/ metabolism
1. Systemic lupus erythematosus
Adrenal neoplasms
2. Secondary syphilis
Other endocrine d isorders
3. Hypothyroidism
Cushing' s syndrome
4. Hyperthyroidism
Hyperprolactinemia
Acromegaly
5. Hypopituitarism

Peripher al androgen overproduction 6. Deficiencies of protein, iron, biotin, and zinc

Obesity II. Scarring alopecia
Idiopathic A. Primary cutaneous disorders
Pregnancy-r elated hyperandrogenism 1. Cutaneous lupus (chronic discoid lesions}b
Hyperr eactio luteinalis
Thecoma of pregnancy
2. lichen planus

Drugs 3. Central centrifugal cicatricial alopecia

Androgens 4. Folliculitis decalvans

Oral contraceptives containing androgenic progestins 5. Linear scleroderma (morphea)
Minoxidil 8. Systemic diseases
Phenytoin 1. Discoid lesions in the setting of systemic lupus erythematosusb
Diazoxide
Cyclosporine 2. Sarcoidosis

True hermaphroditism 3. Cutaneous metastases

Table 352-3 causes of Hyperphosphatemia
I. Impaired renal phosphate excretion
A. Renal insufficiency
B. Hypoparathyroidism
1. Developmental
2. Autoimmune
3. After neck surgery or radiation
4. Activating mutations of the calcium-sensing receptor
C. Parathyroid suppression
1. Parathyroid-independent hypercalcemia
a. Vitamin D or vitamin Aintoxication
b. Sarcoidosis, other granulomatous diseases
c. Immobilization, osteolytic metastases
d. Milk-alkali syndrome
2. Severe hypermagnesemia or hypomagnesemia
0. Pseudohypoparathyroidism
E. Acromegaly
F. Tumoral calcinosis
G. Heparin therapy
11. Massive extracellular fluid phosphate load s
A. Rapid administration of exogenous ph osph at e (intravenous, oral, rectal)
B. Extensive cellular injury or n ecrosis
1. Crush injuries
2. Rhabdomyolysis
3. Hyperthermia
4. Fulminant hepatitis
S. CYtotoxic therapy
6. Severe hemolytic anemia
C. Transceflular phosphate shifts
1. Metabolic acidosis
2. Respiratory acidosis
Table 47- 5 Causes of Non- Anion Gap Acidosis
I
I. Gast rointestinal bicarbon ate los s
' ~

A. Diarrhea
B. External pancreatic or smal l-bow el drainage Table 47-4 Causes of High Anlon-G ap Metabolic Acidosis
C. Ureterosigmoidostomy, jejunal loop, ileal loop
Lactic acidosis Toxins
D. Drugs
Ketoacidosis Ethylene glycol
1. Calcium chlo r ide (acid ifying agent)
Diabetic Methanol
2 . Magnesium sulfate ( d iarrhea)
3. Cholestyramine ( bile acid d iarrhea) Alcoho lic Salicylates

II. Renal a cidosis Starvation Propylene glycol

A. Hypokalemia Pyrog lutamic acid
1. Proximal RTA (type 2 ) Renal failure (acute a nd chronic)
Drug-induced : acetazolamide, t opira mate
2. Distal (cl assic.) RTA (type 1)
nn l(J inrlJJr.Pd: ~n1 photP-ri r.in R .. ifo!=:f~midP

B . Hyperkalemia
1. Generalized distal nephron d ysfunction (type 4 RTA)
a. M ineral ocorticoid deficiency
b. M ineralocorticoid resistance ( autosomal dominant PHA I)
c. Vo lta ge defect (auto somal dominant PHA I and PHA II)
d. Tubulointerstitial disease
III. Drug-induced hyperkalemia (with renal insufficien cy)
A. Potassium -sparing d iu r etics ( a m iloride, triamt erene, spir onolactone)
B . Trimethoprim
c. P entamidine
D. ACE-Is and ARBs
E. Nonsteroidal anti-inflammatory drugs
F. Cyclosporine and tacrolimus

IV. Other
A. Acid loads ( a mmonium chloride , hypera limentation)
B. Loss of potential b icarbonate: ketosis with ketone excretion
C. Expansion acidosis ( rapid saline administration)
D . Hippurate
E . Cation exchanae r esins
Table 353-6 Classification of Pseudohypoparathyroidism (Php) and Pseudopseudohypoparathyroidism (Pphp)
I
Type Hypocalcemia, Response of Urinary cAMP to Serum Gsa Subunit AHO Resistance to Hormones in Addition to
Hyperphosphatemia PTH PTH Deficiency PTH
~ t
PHP- Yes Yes Yes Yes
Ia
~ t
PHP- Yes No No Yes (in some patients)
Ib
t
PHP-11 Yes Normal No No No
PPHP No Normal Normal Yes Yes No

Abbreviations: ~, decreased; t , increased; AHO, Albright's hereditary osteodystrophy; PTH, parathyroid hormone.

Table 333-2 Conditions Associated with Calcium Pyrophosphate Dihydrat e Disease

Aging

Disease-associated
Primary hyperparathyroidism

Hemochromatosis
Hypophosphatasia

Hypomagnesemia

Chronic gout
Postmeniscectomy

Gitelman's syndrome
Epiphyseal dysplasias
Table 143-2 Common causes of Petechial or Purpur ic Rash es
Enteroviruses
Influenza and other respiratory viruses
Measles virus
Epstein-Barr virus
Cytomegalovirus
Parvovirus
Deficiency of pro tein Cor S (including postvaricella proteinS deficiency)
Platelet disorders (e.g., idiopathic thrombocytopenic purpura, drug effects, bone marrow ih filt ration)
Henoch-Schonlein purpura, connective tissue disorders, t rauma ( including nonaccidental injuries in children)
Pneumococcal, streptococcal, staphylococcal, or gram-negative bacterial sepsis

Table 285-3 Maj or causes of Pafiillary Necrosis

Analgesic nephropathy
Sickle cell nephropathy
Diabetes w ith urinary tract infection
Prolonged NSAID use (rare)

Abbreviation: NSAID, nonsteroidal anti-inflammatory.

Table 33-3 Common Causes o f Noncardiogenic Pulmonary Ed ema
Direct injury to lung
Chest trauma, pulmonary contusion
Aspiration
Smoke inhalation
Pneumonia
Oxygen toxicity
Pulmonary embolism, reperfusion

Hematogenous injury to lung

Sepsis
Pancreatitis
Nonthoracic trauma
Leukoagglutination reactions
Multiple transfusions
Intravenous drug use, e.g., heroin
Cardiopulmonary bypass

Possible lung inj ury plus elevated hydrostatic pressures

High-altitude pulmonary edema
Neurogenic pulmonary edema
Reexpansion pulmonary edema
Recommendation
 Table 354~4 FDA-Approved lndicalions for Bmd Tests*
Es;rogen-de~cent won en at clin cal risk of osteoporosis
Vertebral ab1crmalites on x-ray suggestive of osteoporcsi; (osteopen a, ver.ebral fracture)
Glucocor.iooid trea:rrent equivalen: to ~ i ..: mg o' prednisone or duration of ther;;p~ >3 rronths
Primary hyJerpara:hyroidism
l~cnitoring response to an FDA-approveGmedica:icn for os:eJporosis
Repea: BMD evaluations at >23 -mon:h irterval; or more freqJently if medically ju;tWied

criteria ada~tec from the 1998 Bone Mass MeasurementJl.ct

Table 11-2 Painful Conditions that Respond to Tricyclic Antidepressants

Postherpebc neLJralgia

Diabetic neuropathy

Tension headache

~1i g rai ne headache

Rheumatoid arthritis, b

Chronic low back painb

Cancer Central post-stroke pain

Table 347-6 oral Contraceptives: Contraindications and Disease Risk

Contraindications
Absolute
Previous thromboembolic event or stroke
History of an estrogen-dependent tumor
Active liver disease
Pregnancy
Undiagnosed abnormal uterine bleeding
Hypertriglyceridemia
Women aged >35 years who smoke heavily
Relative
Hypertension
Women receiving anticonvulsant drug therapy
Women following bariatric surgery (malapsorptive procedure)
Disease Risks
Increased
Coronary heart disease-increased in smokers >35; no relation to progestin t ype
Hypertension- relative risk 1.8 (current Llsers) and 1.2 (previous users)
Venous thrombosis-relative risk ~4; may be higher with third -generation progestin, drosperinone, and patch; compounded by obesity (tenfold increased risk
compared with nonobese, no OCP); markedly increased with factor V Leiden or prothrombin-gene mutations (see Chap. 116)
Stroke-slight increase; unclear relation to migraine headache
Cerebral vein thrombosis- relative risk -13 - 15; synergistic with prothrombin-gene mutation
Cervical cancer-relative risk 2-4 Breast cancer-may increase risk in carriers of BRCA l and possible BRCA2
Decreased
Ovarian cancer- 50% reduction in risk
Endometrial cancer -40% reduction in risk
locus Repeat Triplet Length Gene Pmdoct
(Normai/Di!iease)
Narcolepsy
Receptors

TGF-B, MIS
Table 61-5 Selected Mitochondrial Diseases

Di sease/ Syndrome
ME LAS syndrome: mitochondrial myopathy with encephalopathy, lactacidosi s, and stroke
Leber's optic atrophy: hereditary optical neuropathy
Kearns-Sayre syndrome (KSS): ophthalmoplegia, pigmental degeneration of the retina, cardiomyopathy
MERRF syndrome: myoclonic epilepsy and ragged -red fibers
Neurogenic muscular weakness with ataxia and retinitis pigmentosa (NARP)
Chronic progressive external ophthalmoplegia (CEOP)
Pearson's syndrome (PEAR): bone marrow and pancreatic failure
Autosomal dominant inherited mitochondrial myopathy with mitochondrial deletion (ADMIMY)
Somatic mutations in cytochrome 1:> gene: exerci.se intolerance, lactic acidosis, complex Ill defici,ency, mus~Je pain, ragged-red fibE

Table 118-9 Comparison of the features of New Oral Anticoagulants in Advanced Stages of Developmen~
Featu~es Rivaroxaban Apixaban Oabigatran Etexilate
Target xa Xa IIa
Molecular weight 436 460 628
Prodrug No No Yes
Bioavailability (%) 80 so 6
Time to peak (h) 3 3 2
Half-life (h) 9 9- 14 12-17
Renal excretion (%) 65 25 80
Antidote None None None
Table 336- 3 Disorders Associated with Hypertrophic Osteoarthropathy
Pulmonary Cardiovascular
Bronchogenic carcinoma and other neoplasms Cyanotic congenital he art disease
Bronchogenic carcinoma and other neoplasms Subacute bacterial endocarditis
Lung abscesses, empyema, bronchiectasisChronic interstitial pneumonitisCystic fibrosis Infected arterial grafts
Chronic obstructive lung disease Aortic aneurysmb
Sarcoidosis Aneurysm of major extremity artery
Gastrointestinal Patent ductus arteriosusb
Inflammatory bowel disease Arteriovenous fistula of major extremity vessel
Sprue Thyroid (thyroid acropach y)
Neoplasms: esophagus, liver, Hyperthyroidism (Graves' disease)
bowel

Table 72- 3 Hormones that Decrease, Remain Stable, and Increase wit h Aging
Decrease No Change Incr ease
Growth hormone Prolactin Cholecyst okinin
Luteinizing hormone ( men} Thyrotropin Luteinizin g hormon e (women)
Insulin oro wth factor I Thyroid h ormones Follicle-stimu lat ino hormone
Testosteron e Epinephrin e Cortisol
Estradiol Glucao on -like p ep tide 1 Prolactin
DHEA and OHEAs Gastric in hib itory polypept ide Norepinephr ine
Pregnen olone Insu lin
25(0H) vitamin 0 Para thormone
Aldoster on e
vasoactive intest inal peptide
Melat onin
PGA II
r----:
Figure 247-3

Cholesterol

(17a hydroxylase)
I
Pregnenolone 17 OH Pregnenolone DHEA
I

Progesterone 17 OH Progesterone Androstenedione Testosterone

--- ---------
fleoxycorticosterone,
r

Deoxycbrtisol
(2 1 hydro>:ylase)

---- ----------- --
Corticosterone Cort,isol
(1 1~hydroxylase)

(
- --
Aldosterone ) Cortisone
(11 ~ hydroxysteroid dehydrogenase)

)
Mineralocorticoid Glucocorticoid Androgen
Source: Longo DL, Fauci AS, Kasper Dl , Hauser SL, Jameson Jl , Losca12o J : Harriso1l'S
Principles of lnterpal. Medlcitte, 18th Cdition: vJww.acces.smedicine.com
Copyright The f'.1cGrav/- Hi I Com,panles, I nc. All rights reserved.

Adrenal enzyma t ic d efects.

Table 356-6 Summary of the Maj or Drugs Used for the T reatmen t of Hyperlipidemia

Drug Major Indications Starting Maximal Mechanism Common Side Effects

Dose Dose
HMG-CoA reductase Elevated LDL-C Cholesterol synth esis, ~ hep atic Myalgias, arthralgias, elevated
inhibitors (stat ins) LDL receptors, VLDL pro duction t ransamin ases, dyspepsia
Lovastat in 20 mg 80 mg
daily daily
Pravastatin 40 mg qhs 80 mg qh s
Simvastat in 20 mg qhs 80 mg qh s
Fluvastatin 20 mg qhs 80 mg qh s
Atorvastatin 10 mg qhs 80 mg qh s
Rosuvastatin 10 mg qhs 40 mg qh s
Cholesterol absorpt ion Intestinal ch olesterol absorption Elevated transaminases
inhibitors
Ezetimibe Elevated LDL-C 10 mg 10 mg LDL receptors
daily daily
Bile acid sequestrants Elevated LDL-C t Bile acid excretion and ~ LDL Bloating, constipat ion, elevated
receptors t riglycerides
Cholestyramine 4 g d aily 32 g daily
Colestipol 5 g d aily 40 g daily
Colesevelam 3750 mg 43 75 mg
daily daily
Nicotinic acid Elevated LDL-C, low VLDL production Cutaneous flush ing, GI upset, elevated
HOl -C, elevated TG glucose, uric acid, and liver function tests
Immediate-release 100 mg tid 1 g tid
Sustained-release 250mg L 5g bid
bid
Exten ded-r elease 500mg 2 g q hs
qhs
Fibric acid derivatives Elevated TG, elevated t LPL, VLDL synthesis Dyspepsia , mya lgia, g allsto nes, elevated
remnants t ransaminases
Gemfibrozil 600mg 600 mg bid
bid
Fenofibrate 145 mg qd 145 mg qd
Omega 3 fatty acids Elevated TG 3 g d aily 6 g daily t TG catabolism Dysp epsia, diarrhea, fishy o dor to breath
Table 261-3 Diagnostic Value of Bronchoalveolar lavage in Interstitial lung Disease

Condition Bronchoalveolar lavage Finding

Sarcoidosis Lymphocytosis; CD4 :CD8 ratio >3.5 most specific of diagnosis
Hypersensitivity pneumonitis Marked lymphocytosis ( >50%)
Organizing pneumonia Foamy .macrophages; ,mixed patterr of increased cells characteristic; decreased CD4 :CD8 ratio
Eosinop hilic lung disease Eosinophils >25%
Diffuse alveolar bleeding Hemosiderin-laden macrophages, red blood cells
Diffuse alveolar damage, drug toxicity Atypical hyperplastic type II pneumocytes
Opportunistic infections Pneumocystis carinii, fungi, cytomegalovirus-transformed cells
Lymphangitic carcinomatosis, alveolar cell Malignant cells
carcinoma, pulmonary lymphoma
Alveolar proteinosis r~ il ky effluent, f oamy macrophages and lipoproteinaceous intraalveolar material (periodic acid-
Schiff stain-positive)
Lipoid pneumonia Fat globules in macrophages
Pulmonary Langerhans cell histiocytosis Increased CDl+ Langerhans cells, electron microscopy demonstrat ing Birbeck granule in lavaged
macrophage (expensive and difficult t o perform)
Asbestos-related pulmonary disease Dust particles, ferruginous bodies
Berylliosis Posit ive lymphocyte transformation test to beryllium
Silicosis Dust particles b y polarized light microscopy
Lipoidosis Accumulation of specific lipopigment in alveolar macrophages
Table 58- 3 Ri.sk Factors for Thrombosis

Venous Venous and Arterial

Inherited Inherited
Factor V Leiden Homocystinuria

Prothrombin G20210A Dysfi brinogenemia

Antithrombin deficiency Mixed ( inherited and acquired)
Protein c deficiency Hyperhomocysteinemia
Protein 5 deficiency Acquired
Elevated FVIII Malignancy
Acquired Antiphospholipid antibody syndrome
Age Hormonal therapy

Previous thrombosis Polycythemia vera

Immobilization Essential thrombocythemia
.M ajor surgery Paroxysmal nocturnal hemog lobinuria
Pregnancy and puerperium Thrombotic thrombocytopenic purpura
Hospitalization Heparin -induced thrombocytopenia
Obesity Disseminated intravascular coagu lat ion
Infection

APC resistance, nongenetic

Smoking

Unknown*
Elevated factor II, I X, XI
Elevated TAFI levels
Low levels of TFPI
 Table 234-7 Etiology o f Chron ic Cor Pulmon ale
Diseases Leading to Hypoxemic Vasoconstriction
Chronic bronchitis
T~ble 359-1 fltedications with Uricosuric Adivity Chronic obstructive pulmonary disease
Cystic fibrosis
Acetohexamide Gly,:ery guaiacolate
Chronic hypoventilation
ACTH Gly:opyrrolate
Obesity
Asccrbic acid f-aloferate
Neuromuscular di.s ease
Azauridine L.osartan Chest wall dy sfunction
3enzb'o11arone ~leclcfenarrate Living at high altitude;

: aIctcn1n
' Phenolsu fonphrh31ein Diseases that Cause Occlusion of the Pulmonary Vascular Bed
Thromboembolic di.sease, acute or chronic
: hlorprothixene Phen(lbu:azone
Pulmonary arterial hypertension
: itrate Probenecid
Pulmonary veno-occlusive disease
)'icu11arol Rad.icgraphic contrast agents Diseases that Lead to Parenchymal Disease
) iflunisal Sal cylates (>2 g/d) Chronic bronchitis
::strogens Sul7inpyrazone Chronic obstructive pulmonary disease

i'enofibrate Tetracycli1e that is outdated Bronchiectasis

Cystic fibrosis
3lucooorticoids Zoxazolan1be
Pneumoconiosis
. . " .
Sarcoidosis
Interstitial lung disease
Table 35- 1 Causes of cyanosis
Central Cyanosis
Table 53- 2 Causes of Erythro d erma
l
1. Primary cut aneous disorders
Decreased arterial oxygen saturation
a . Psoriasis"
Decreased atmospheric pressure - high altitude
Impaired pulmonary function
b. Dermatitis iatopic, contact >> stasis (with autosen sitization) or seborrheic_r
Alveolar hypoventilation
Uneven relationships between pulmonary ventilation and c. Pityriasis rubra p ilaris
perfusion (perfusion of hypovent ilated alveoli) 2. Drugs
Impaired oxygen diffusion 3. Systemic diseases
Anatomic shunts a . Cutaneous T cell lymphoma
Certain types of congenital heart disease b. Lymphoma
Pulmonary arteriovenous fistulas 4. I diopathic
Multiple small intra pulmonary shunts
Hemoglobin with low affinity for oxygen
Hemoglobin abnormalities
Methemoglobinemia- hereditary, acqui red
Sulfhemoglobinema-acquired
Carboxyhemoglobinemia (not t rue cyanosis)
Peripher al Cy anosi s
Reduced cardiac output
Cold exposure
Redistribution of blood flow from extremities
Arterial obstruction
Venous obstruction