Block 11

Front 1

What characterizes Neisseria meningitidis?

Back 1

Gram(-) diplococci, non-motile, non-hemolytic, non-spore forming, capsules, pili;
facultative anaerobes, grow on chocolate agar/Thayer-Martin media;
13 serotypes based on polysaccharide capsule (A, B, C, W-135, Y)

Front 2

What signs/symptoms are associated with N. meningitidis infection?

Back 2

Fever, stiff neck, sore throat, intense HA, photophobia, vomiting, seizures, petechial-purpuric rash – in neonates: temperature instability, listless, weak, v/d, changes in alertness

Front 3

What are the virulence factors of N. meningitidis?

Back 3

Pili (adherence), IgA1 protease (cleaves host IgA), capsule (resist phagocytosis and complement), meningobactin (iron binding protein), LPS (inflammation)

Front 4

What is the pathway of infection of N. meningitidis infection?

Back 4

Nasopharyngeal colonization --> invasion of the epithelium --> invasion of blood --> further dissemination (e.g. CSF)

Front 5

What describes the pathogenesis of N. meningitidis infection?

Back 5

Humans are the sole host, they can be normal flora/pathogen with 8-25% carrier rate (carriers have protective antibodies); Bacteria adhere and invade through the nasopharynx leading to bacteremia, endotoxemia, meningitis; The pathology is, in part, the result of the host inflammatory response

Front 6

What characterizes the transmission of N. meningitidis?

Back 6

Respiratory droplets, requires close contact

Front 7

What describes the epidemiology of N. meningitidis infection?

Back 7

>3000/year in US; major serogroups incl. B and C, secondary incl. Y and W-135; isolated cases or small outbreaks in day care centers or with college students; Predisposing factors: complement deficiency, immunocompromised, head trauma, neurodiagnostic procedures, surgery

Front 8

How does the anatomical location of a CNS infection determine the symptomatology?

Back 8

Frontal lobe abscess: frontal sinusitis, HA, memory defects, attention loss, diminished intellectual performance;
Temporal lobe encephalitis: personality changes, visual field defects, hemiparesis with large lesions, focal seizures;
Basilar meningitis: HA (suboccipital), neck stiffness, diplopia, cranial nerve palsies

Front 9

What are common causes of purulent meningitis?

Back 9

Newborns: GBS, E. coli, L. monocytogenes;
Infants/Children: S. pneumo, N. meningitidis, H. flu;
Adults: S. pneumo, N. meningitidis, H. flu (rarely)

Front 10

What are the various types of meningitis?

Back 10

Purulent: acute infections, rapid onset, bacterial origin;
Chronic: develop slowly, mycobacteria or fungal origin,
Aseptic: self-limiting, viral origin

Front 11

What are the complications of bacterial meningitis?

Back 11

In 10-20%: deafness, mental retardation, seizures, strokes, limb amputations;
10-30% mortality overall (10% mortality in treated patients)

Front 12

What virulence factors are seen with L. monocytogenes?

Back 12

Intracellular pathogen: cell-mediated immunity is protective, humoral response poor;
Hemolysin: pore-forming cytolysin, lyses phagosomal membrane to allow escape from the phagosome, necessary for virulence;
ActA: required for actin polymerization and motility

Front 13

What characterizes Listeria monocytogenes?

Back 13

Gram(+) rod, catalase-positive, hemolysin, motile, 13 serotypes (cell wall/flagellar antigens);
Epidemiology: contaminated food, non-pasteurized dairy products, can grow at cold temperatures, can have long incubation period (2-8 wks)

Front 14

What characterizes E. coli?

Back 14

Common cause of neonatal meningitis (resembles disease caused by GBS);
75% of cases are caused by strains with K1 capsular polysaccharide (contains sialic acid, identical to group B N. meningitidis);
infection occurs during childbirth from vaginal E. coli, infants are very susceptible –
treatment: 3rd generation cephalosporins

Front 15

Which populations most typically receive the MCV4 vaccine?

Back 15

US military recruits, people who might be affected during an outbreak, anyone traveling to commonly affected areas (e.g. W. Africa), anyone with a complement deficiency, college students, adolescents at 11-12yo, laboratory workers routinely exposed to N. meningitidis

Front 16

What vaccines are available against N. meningitidis?

Back 16

Meningococcal conjugate polysaccharide-protein vaccine (MCV4): for groups A, C, Y, W-135 (given between 11-55yrs, but especially at 11-12 years since this is when social activities start);
Meningococcal polysaccharide vaccine (MPSV4): for groups A, C, Y, W-135 (given >2yrs, for high risk groups like complement deficiencies and asplenia)

Front 17

What is the treatment for bacterial meningitis?

Back 17

Medical emergency: antibiotics that penetrate the meninges/enter CSF (β-lactams, like Cefotaxime), anti-inflammatory drugs (Dexamethasone); Prophylactic antibiotics in contacts of patients: Rifampin, quinolone antibiotics, Ceftriaxone; Antibiotic treatment of carriers

Front 18

What are the clinical findings with N. meningitidis infection?

Back 18

Acute bacterial meningitis: CSF analysis shows ↑PMNs, ↓glucose, ↑protein, Gram(-) diplococci;
Besides the CSF, organisms can be cultures from blood or a skin lesion; also PCR can be used

Front 19

What does the CSF show in subacute meningitis (mycobacterial/fungal)?

Back 19

↑ leukocytes/PMNs/protein (but even less so than with aseptic viral meningitis), ↓glucose

Front 20

What does the CSF show in aseptic viral meningitis?

Back 20

↑ leukocytes/PMNs/protein (but less than with bacterial meningitis), normal glucose

Front 21

What characterizes the symptomatology of L. monocytogenes infection?

Back 21

Normally asymptomatic; can see bacteremia, pneumonia, meningitis;
Pregnant women: miscarriage, granulomatosis infantiseptica; Elderly: more susceptible

Front 22

What describes the diagnosis and treatment of L. monocytogenes infection?

Back 22

Diagnosis: culture organism from blood/CSF/lesion;
Treatment: Penicillin G, Ampicillin, Erythromycin, Chloramphenicol

Front 23

What characterizes poliovirus?

Back 23

ssRNA, (+)sense, infects primates only, non-enveloped, 3 antigenic serotypes

Front 24

What characterizes the spread of enterovirus inside the body?

Back 24

Initial replication occurs in the intestinal tract in epithelial and lymphoid cells --> virus invades deeper tissues and enters the blood stream causing viremia --> virus may spread to the brain and spinal cord from the blood or by the retrograde axonal route in peripheral/cranial nerves

Front 25

What characterizes the transmission of enteroviruses?

Back 25

Excreted in large amounts in stool --> fecal-oral route of contamination; outbreaks in temperate climates mainly occur during the summer months, and all year-round in the tropics

Front 26

What happens when poliovirus particles are released from the host cell?

Back 26

They cause lysis (i.e. it’s a lytic virus)

Front 27

What characterizes translation and processing of poliovirus?

Back 27

Genome is translated into a single polypeptide (a “polyprotein”) --> polyprotein is processes sequentially by two viral proteases into its structural proteins (VP1-4) and non-structural proteins (e.g. VPg, RNA-dependent RNA polymerase, two proteases)

Front 28

Which step in the poliovirus life cycle determines the tropism of the virus?

Back 28

Not the receptor binding (since PVR is found in multiple regions, yet only has CNS effects), but some step downstream

Front 29

What characterizes the replication of poliovirus?

Back 29

Poliovirus attaches to a cellular receptor (PVR or CD155), which is a glycosylated protein at the “canyon” site --> RNA is released to the cytoplasm --> (+)sense RNA serves directly as an mRNA template for translation by host factors --> RNA is linked at the 5’ end to viral protein VPg that is a primer for RNA-dependent RNA polymerase

Front 30

What characterizes the various types of viral CNS infections?

Back 30

Encephalitis: infection of brain parenchyma;
Meningitis: infection of meninges;
Myelitis: infection of spinal cord

Front 31

Which Picornavirus genera are pathogenic to humans?

Back 31

Enterovirus: replicates in GI tract (e.g. polio);
Hepatovirus: cause viral hepatis (e.g. HAV);
Parechovirus: enteric cytopathic human orphan virus; Rhinovirus: common cause of cold

Front 32

What characterizes the Picornaviridae?

Back 32

Contain some of the smallest viruses known to infect man (thus pico); virions are icosahedral and about 30nm in diameter

Front 33

How is the diagnosis of polioviral infection made?

Back 33

Symptoms are non-specific; aseptic meningitis suggests enteroviral etiology; virus can be isolated and cultured from clinical samples (stool, throat, CSF); virus can be detected by ELISA and PCR

Front 34

What are Rhabdovirus features?

Back 34

They are bullet-shaped and relatively large, enveloped, contain (-)sense RNA

Front 35

What characterizes Rhabdoviruses?

Back 35

Consists of two genera:
Lyssavirus (e.g. rabies and rabies-related viruses),
Vesiculovirus (e.g. vesicular stomatitis virus) – rabies virus infects numerous mammalian species; it is an acute, progressive, incurable encephalitis

Front 36

What is the most frequent cause of enterovirus infection in the US?

Back 36

Coxsackieviruses

Front 37

Which vaccine should be administered to immune-deficient individuals?

Back 37

Salk vaccine, since it cannot cause poliomyelitis

Front 38

What two vaccines were made for poliovirus?

Back 38

Salk vaccine: killed vaccine, effective; Sabin vaccine: live, attenuated vaccine, more effective (since it infects the intestine and elicits IgA production, resembling the natural process)

Front 39

How is the diagnosis of polioviral infection made?

Back 39

Symptoms are non-specific; aseptic meningitis suggests enteroviral etiology; virus can be isolated and cultured from clinical samples (stool, throat, CSF); virus can be detected by ELISA and PCR

Front 40

What is the treatment for poliovirus infection?

Back 40

No drug therapy currently available; vaccination is the best method

Front 41

What are Rhabdovirus features?

Back 41

They are bullet-shaped and relatively large, enveloped, contain (-)sense RNA

Front 42

What describes the time course of poliovirus spread?

Back 42

Incubation period (1-3days): virus replicates in intestine with no or minor symptoms of fever/HA;
Abortive stage (2-6days): virus continues to replicate and initial Abs appear;
CNS invasion (5-10 days): virus spreads to CNS and causes paralysis

Front 43

What characterizes the epidemiology of rabies virus?

Back 43

In Africa, Asia, and Latin America, >90% of cases are caused by domestic dog bites, whereas in the US, Canada, and Europe, cases are caused by wild animals (bats, raccoons, foxes, skunks)

Front 44

What characterizes the post-exposure prophylaxis of humans?

Back 44

Passive administration of Abs: human rabies immune globulin (collected from immunized persons) – Vaccine is prepared from avian embryos or from various human/monkey cell lines (followed by inactivation)

Front 45

What characterizes the prevention of rabies infection?

Back 45

Since it is a zoonosis, vaccination of pets is mandatory; vaccination of wild animals is also used by spreading baited oral vaccine – pre-exposure prophylaxis is used among high-risk workers; post-exposure prophylaxis includes local wound treatment, administration of Abs, vaccination

Front 46

How is the diagnosis of rabies infection made?

Back 46

Through a direct fluorescent antibody test (dFA); test is performed on brain impressions (of an animal) with a FITC- conjugated anti-virus antibody; test can also be done with human skin biopsies from neck containing hair follicles surrounded by a nerve network

Front 47

What symptoms are associated with rabies infection?

Back 47

Early symptoms are non-specific; as the disease progresses, neurological symptoms appear (e.g. insomnia, anxiety, confusion, partial paralysis, excitation, hallucinations, agitation, hypersalivation, difficulty swallowing, and hydrophobia); eventually patients progress to coma and die within days of the onset of symptoms

Front 48

What characterizes the spread and pathology of rabies virus?

Back 48

Virus infects at the bite site and replicates --> incubation period is 1-3 months (can be a year or longer) --> moves to sensory neurons and travels towards the CNS --> within the CNS it causes encephalitis --> neurons die and demyelination occurs resulting in encephalopathy --> virus often returns to the periphery with preference to salivary glands

Front 49

What happens with rabies virus once it gains access to an animal (e.g. raccoons)?

Back 49

The virus moves along peripheral nerves to the CNS by retrograde flow --> it will incubate for 3-12 weeks (can be up to a year) --> the animal will show signs of the disease and dies as early as 7 days from the first signs of symptoms

Front 50

What characterizes the structure of rabies virus?

Back 50

Contains 5 genes which each code for one protein: G (envelope), M (matrix), N (nucleoprotein encapsulating RNA), L (RNA-dependent RNA polymerase), P (phosphoroprotein) – the ribonucleoprotein core (RNP) consists of RNA, N, L, and P proteins

Front 51

What do large amounts of accumulated nucleocapsids in neurons form?

Back 51

Inclusion bodies, called Negri bodies

Front 52

What are percutaneous absorption skin variables?

Back 52

Stratum corneum thickness, cutaneous vasculature, area of absorptive surfaces

Front 53

What are the topical retinoids?

Back 53

Natural: All-trans retinol, All-trans retinoic acid, Alitretinoin; Synthetic: Tazarotene, Adapalene

Front 54

What clinical effects are important regarding retinoids?

Back 54

Enhance keratinocyte differentiation leading to decreased follicular occlusion; Comedolysis; Epidermal thickening; Dermal regeneration/collagen formation

Front 55

What is an important pharmacological effect of retinoids?

Back 55

Decreased sebum production

Front 56

What is an important adverse effect of glucocorticoids?

Back 56

Atrophy and striae formation

Front 57

What are percutaneous absorption diseased skin variables?

Back 57

Inflamed skin, (ulceration)

Front 58

Which anatomic sites are the extremes of percutaneous absorptive capacity?

Back 58

Highest: mucous membranes; Lowest: palmar/plantar skin

Front 59

What concepts are related to the rate of diffusion of drugs across the skin?

Back 59

Movement through the epidermis, concentration, relative tenacity of the drug binding to the vehicle with which it is given, thickness of the stratum corneum/barrier, surface area to which applied

Front 60

What are percutaneous absorption vehicle variables?

Back 60

Ointment > solution, occlusive vehicle improves hydration, irritancy (alteration in skin barrier)

Front 61

What are percutaneous absorption drug variables?

Back 61

Concentration in vehicle (not volume), lipophilicity, molecular size

Front 62

What characterizes Doxycycline and Minocycline?

Back 62

Broad-spectrum antibiotics; At 20mg bid: inhibition of inflammatory cytokines, inhibition of collagenases/gelatinases; At 50-100 mg/day or bid: bacteriostatic and same actions as with 20mg

Front 63

What is Imiquimod used for?

Back 63

Genital/perianal warts, actinic keratosis, superficial basal cell carcinoma

Front 64

What is the mechanism of action of Imiquimod?

Back 64

Induces the production of TNF-α, IFN-α, IFN-γ, and other cytokines

Front 65

What is the use of 12% ammonium lactate?

Back 65

Moisturizer: detachment or keratinocytes, normalization of keratinization; used in xerosis and ichthyosis vulgaris

Front 66

What are the topical calcineurin inhibitors?

Back 66

Tacrolimus, Pimecrolimus – used for atopic dermatitis in patients >2yo; must monitor for decades to assure safety

Front 67

What is an important adverse effect of Minocycline?

Back 67

Blue-black pigmentation of nails, skin, scars, sclera, teeth

Front 68

What are important adverse effects of Doxycycline?

Back 68

Phototoxic effect, brown discoloration of teeth in children

Front 69

What are the systemic retinoids?

Back 69

Isotretinoin: acne vulgaris; Acitretin (don’t take alcohol): psoriasis; Bexarotene: mycosis fungoides – all are category X

Front 70

What characterizes Benzoyl peroxide?

Back 70

Broad-spectrum bactericidal agents, effective against P. acnes (no resistance seen)

Front 71

What adverse effects are seen with topical retinoids?

Back 71

Teratogenicity, (erythema, irritation, sun sensitivity, desquamation)

Front 72

What is the mechanism of action of Dapsone?

Back 72

Inhibition of neutrophil myeloperoxidase, neutrophil adhesion, neutrophil chemotaxis

Front 73

What adverse effects are associated with Thalidomide?

Back 73

100% teratogenicity if fetus exposed days 21-36 of gestation --> phocomelia (deformity of arms, legs)

Front 74

What are the uses of Thalidomide?

Back 74

Erythema nodosum leprosum

Front 75

What is the mechanism of action of Thalidomide?

Back 75

Potent inhibition of TNF-α and IL-12

Front 76

What adverse effects are associated with Dapsone?

Back 76

Hemolytic anemia (check for G6PD deficiency), peripheral neuropathy

Front 77

What is Dapsone used for?

Back 77

Systemic: leprosy, dermatitis herpetiformis; Topical: acne vulgaris

Front 78

How is the diagnosis of Botulism intoxication made?

Back 78

Link to ingestion of home-canned or exotic food; Clinical appearance: blurred/double vision, dilated pupils, dry mouth, difficulty swallowing/speaking, weakness/dizziness, eventual effects on respiration/heart; Laboratory diagnosis: detection of organism or toxin, mouse neutralization test, PCR (for neurotoxin genes) – this is a reportable disease

Front 79

What characterizes the epidemiology, treatment, and prevention of Botulism intoxication?

Back 79

Majority of outbreaks traced to home-cooked foods; Treatment: early use emetics/gastric lavage, treat with trivalent anti-ABE toxin horse serum and supportive therapy (respirator/nourishment);
Prevention: destroy C. botulinum spores (pressure cooker), in acid pH spores do not germinate

Front 80

What are the effects of Botulism intoxication on the body?

Back 80

Does not kill cells, but paralysis lasts for months (recovery requires formation of new nerve endings and connections at motor end-plates)

Front 81

What is the mechanism of botulinum toxin?

Back 81

Absorbed from intestine --> spreads by bloodstream --> binds to receptors on the presynaptic membrane of motor neurons of the PNS --> internalized by receptor-mediated endocytosis (RME) --> vesicle acidification causes release of LC into the motor neuron --> LC cleaves SNARE proteins (not the SNARE complex) resulting in inhibition of ACh release --> prevents muscle contraction --> flaccid paralysis

Front 82

What characterizes normal neurotransmitter release?

Back 82

Mediated by SNARE proteins: synaptobrevin interacts with syntaxin and SNAP 25 to cause fusion of the neurotransmitter vesicle with the pre-synaptic membrane (causing neurotransmitter release)

Front 83

What characterizes botulinum toxin?

Back 83

Most toxic substance in nature, heat-labile, AB-toxin; The B-subunit binds to ganglioside + protein receptors (synaptotagmin, found only on neural tissue), and forms the ion translocation channel; The A-subunit is a zinc metalloprotease (LC)

Front 84

What are the virulence factors for Clostridium botulinum?

Back 84

Neurotoxins (AB-toxins): there are 8 antigenic types (A-G, with A/B/E being most important); types A and B are chromosomal/plasmid encoded, whereas C and D are phage encoded

Front 85

What characterizes Clostridium Botulinum?

Back 85

Gram(+), long rods, spore-forming, obligate anaerobe

Front 86

What characterizes Botulism intoxication?

Back 86

Relates to ingestion of botulinum toxin (most deadly of food-borne illnesses); symptoms occur 12-36 hrs after ingestion, cranial nerves are affected first followed by respiratory paralysis;
25% mortality rate (if survive, frequently sustain neurological damage)

Front 87

What describes the transmission of Clostridium Botulinum?

Back 87

Found in soil and water; spores on fruits/vegetables – majority of outbreaks traced to home-produced foods

Front 88

By what route can wound botulism come about?

Back 88

Administration of black tar heroin (“skin popping”)

Front 89

What characterizes the disease caused by Clostridium tetani?

Back 89

Tetanus/lockjaw: toxin-mediated disease (produced during bacterial growth, released upon lysis); has an 8-day incubation period;
Symptoms: stiffening of jaw muscles, severe/painful spasms of voluntary muscles, difficulty swallowing, tightening of muscles of abdomen/limbs, fever, sweating, high BP, irregular heart beat, muscle spasms can last 3-4 weeks;
Complications: respiratory failure, spinal/long bone fractures; 10-78% mortality rate

Front 90

What characterizes Clostridium tetani?

Back 90

Gram(+), spore-producing, drumstick appearance, obligate anaerobe;
Transmission: found in soil/animal feces, bacteria enter through wounds, no person-person spread;
Diagnosis: isolate organism from wound, immunization history

Front 91

What is an additional use of botulinum toxin?

Back 91

Bioterrorism agent

Front 92

What complications are associated with Botox treatment?

Back 92

Ptosis, development of immunity to toxin

Front 93

What are therapeutic uses of botulinum toxin?

Back 93

Treatment of muscle disorders, hyperhidrosis, myofascial pain, migraine HA, cosmetic treatment

Front 94

What characterizes would botulism?

Back 94

Caused by deep wound contamination with C. botulinum spores --> germinate and produce toxin;
Symptoms: paralysis begins at wound, then become generalized;
Diagnosis: isolation of organism/ toxin from wound;
Treatment: Ampicillin/Penicillin, surgical drainage, anti-ABE toxin serum

Front 95

What characterizes infant botulism?

Back 95

Most common form of botulism in US; occurs in children < 9 months due to lack of development of normal flora; associated with ingestion of C. botulinum spores (mainly via honey); produce toxin which is transported to the blood stream

Front 96

What is the treatment for infant botulism?

Back 96

Supportive treatment (respiratory); BIG treatment: IV botulinum human immune globulin;
No antibiotics should be administered (!) – generally favorable outcome (mortality <2%)

Front 97

What are the symptoms of infant botulism?

Back 97

FTT, “floppy baby” (flaccid paralysis); implicated as a cause of SIDS

Front 98

What characterizes tetanus neonatorum?

Back 98

Major cause of death in developing countries; Disease: due to infection of umbilical stump in infants born to nonimmune mothers – related to lack of aseptic technique during childbirth

Front 99

What are the most common causes of tetanus?

Back 99

Puncture wounds, IDU, laceration

Front 100

What characterizes the prevention of tetanus?

Back 100

Toxoid vaccine: formalin, alum-treated toxin; included in DTaP; requires booster every 10 years

Front 101

What characterizes the treatment of tetanus?

Back 101

Clean wound, tetanus immune globulin, Penicillin, toxoid immunization (inject at different site to prevent formation of immune complexes), supportive measures (barbiturates, tracheostomy)

Front 102

What characterizes the epidemiology of tetanus?

Back 102

Rare in US, due to widespread use of tetanus toxoid vaccine; Common world-wide – up to 40% carrier rate in humans (transient member of flora)

Front 103

What are the differences between tetanus and botulinum toxin activity?

Back 103

Tetanus toxin: acts on CNS to inhibit release of glycine/GABA --> spastic paralysis;
Botulinum toxin: acts on PNS to inhibit release of ACh --> flaccid paralysis

Front 104

What are the virulence factors of Clostridium tetani?

Back 104

Tetanus toxin: heat-labile toxin, AB-toxin, similar to botulinum toxin – binds gangliosides on peripheral nerve endings at myoneural junctions, internalized by RME, transported to CNS; cleaves synaptobrevin in synaptic vesicles, preventing glycine/GABA release, causing muscle contraction --> spastic paralysis

Front 105

Which people are given bacterial meningitis prophylaxis?

Back 105

Those who have come in contact with a patient for 20hrs over 4-5 days; Medical personnel involved in intubation/resuscitation; Second case of H. flu in a day care within 60 days

Front 106

What characterizes perinatal HSV infection?

Back 106

Occurs at exposure to HSV secretions present in birth canal; risk of neonatal infection largely influenced by mother’s antibody status – maternal primary infection: 50% of neonates acquire; maternal secondary infection: 5% of neonates acquire

Front 107

What etiologic agent is thought to be responsible for 85-90% of cases of aseptic meningitis?

Back 107

Non-polio enterovirus

Front 108

What sequelae are associated with encephalitis?

Back 108

Mortality ranges from 0-80% depending on the agent; Morbidity is also dependent on the agent – many long-term sequelae are subtle: fine motor, discrete learning difficulties, partial hearing loss

Front 109

What are viral etiologies of meningitis?

Back 109

Enterovirus: by far the most common cause of meningoencephalitis and encephalitis;
HSV: common, treatable cause of encephalitis; Arbovirus

Front 110

What are etiologies of non-infectious encephalitis?

Back 110

Collagen-vascular disorders, neoplastic, malignant HTN, toxin ingestion, metabolic disease

Front 111

What sequelae are associated with bacterial meningitis?

Back 111

Sensorineural hearing loss (20-30% with S. pneumo, 5-10% with Hib/Neisseria, CSF glucose<20 has worst prognosis); Seizures; Developmental delay/static encephalopathy; Hydrocephalus -
5-10% mortality overall in developed countries

Front 112

What characterizes neurocysticercosis?

Back 112

Pork tapeworm cysts; cysts in brain cause seizures, behavioral disturbances, obstructive hydrocephalus, gait disturbances – leading cause of seizures in some parts of the world

Front 113

What is the treatment for neurocysticercosis?

Back 113

Avoid raw/undercooked beef/pork, treat those with adult GI tapeworm, sewage/hand hygiene;
Praziquantel, steroids, anticonvulsants

Front 114

What is ingested in order to get neurocysticercosis?

Back 114

Pork tapeworm eggs (i.e. another person in shedding eggs fecally, and they are ingested orally)

Front 115

How can perinatal HSV manifest itself?

Back 115

On skin, eyes, mucous membranes: 7-14 days; CNS infection: 14-21 days, 15% mortality/54% sequelae if treated; Disseminated infection: 54% mortality, 38% sequelae if treated

Front 116

What are the sequelae of TB meningitis?

Back 116

Long term: blindness, deafness, intracranial calcifications, diabetes insipidus, obesity, paraplegia, mental retardation – 41% if diagnosed early, 92% if diagnosed after altered mental status;
poor prognosis if <4yo and with seizures

Front 117

What characterizes the CNS involvement with a TB infection?

Back 117

95% meningitis, 2% tuberculomas, <1% abscess; 50% CNS involvement with miliary TB

Front 118

What characterizes TB meningitis?

Back 118

30% of children will have a positive PPD; Arises from lympho-hematogenous spread (2-6months after primary infection); Onset is gradual, over a period of 3 weeks; Most common in children less than 6yo (rare <4 months old, mean age 4yo)

Front 119

What is the treatment for perinatal HSV?

Back 119

Acyclovir – can cause crystallization in kidney, watch hydration

Front 120

What are the four factors of the epidemiology of zoonoses?

Back 120

Infective agent, host (vertebrate reservoir, human), transmission (vehicle, route), environment

Front 121

What is the usual role of humans in zoonoses?

Back 121

Usually a dead end in the chain of infection; person-person transmission can occur but is uncommon, examples include leishmaniasis, trypanosomiasis, viral encephalitides

Front 122

What characterizes the epidemiology of Yellow fever?

Back 122

Maintained in jungle: monkeys are primary reservoir hosts; forest species of mosquito acquire the virus and spread it to urban areas

Front 123

What characterizes the epidemiology of plague?

Back 123

200 different natural animal hosts; Primary reservoir hosts: rodents, transmission by fleas;
Secondary reservoir hosts (spread from sylvatic foci to urban foci): rats, mice, severe outbreaks

Front 124

What is the difference between transstadial and transovarial passage?

Back 124

Transstadial: passage of microbe from one developmental stage of the host to its subsequent stage;
Transovarial: passage of microbe from maternal body to eggs within ovaries

Front 125

What are examples of arthropod reservoirs?

Back 125

Rickettsia rickettsii: maintained for several years in tick, transstadial and transovarial passage;
Babesia microti: overwinters in tick vector, transmitted to rodents in spring

Front 126

What characterizes the primary and secondary reservoir hosts?

Back 126

Primary: permanent reservoir of infection; Secondary: involved in natural cycle of infection, important role in spread to humans, not necessary for survival of infectious agent

Front 127

What characterizes the Hantavirus Pulmonary Syndrome, 1993 outbreak?

Back 127

98 cases, 52% fatality rate; transmitted by deer mouse feces (aerosolized)

Front 128

What can be said about modern zoonoses?

Back 128

Viruses have a greater potential due to their ability to adapt changing ecologic condition, development of previously uninhabited areas, and increased contact between man and animals

Front 129

What defines zoonotic infections?

Back 129

Infections that are transmitted in nature between vertebrate animals and humans – criteria: vertebrate reservoir exclusive of humans, transmission, infectious disease syndrome in humans

Front 130

What are examples of diseases transmitted by animal contact?

Back 130

Rabies, viral hemorrhagic fevers, Hantavirus pulmonary syndrome, Q fever, leptospirosis, tularemia, etc.

Front 131

Which infections are considered occupational hazards?

Back 131

Leptospirosis: rice field workers;
Anthrax: carpet weavers;
Q fever: abattoir workers;
Cutaneous larva migrans: plumbers

Front 132

What are examples of geoclimatic conditions that affect epidemiology of infectious agents?

Back 132

Bacillus anthracis spores: alkaline soil containing calcium salts;
Vibrios of northern hemisphere: Winter in estuarine mud, significant numbers only at 20C;
RMSF/Lyme disease: excluded from Alaska by cold

Front 133

What are examples of common vehicle-borne infections?

Back 133

Food/milk: brucellosis, salmonellosis, tuberculosis; Water: leptospirosis

Front 134

What vector-borne infections are transmitted by fleas and lice?

Back 134

Fleas: plague, murine typhus; Lice: epidemic typhus, relapsing fever, trench fever

Front 135

What are the most common vector-borne viruses (indirect)?

Back 135

Arboviruses (stands for ARthropod-BOrne viruses): yellow fever, dengue fever, viral encephalitis

Front 136

What characterizes manners of airborne transmission?

Back 136

Droplet spread: direct spray onto conjunctiva, mucous membranes of mouth/nose, distance of up to 1 meter, droplet size > 5microns; Airborne transmission/droplet nuclei transmission: indirect, travel > 1 meter from source to host, droplet size < 5microns, animal or inanimate source of airborne droplet (e.g. Q fever, propagated by sheep/cattle, aerosolized particles)

Front 137

In which diseases are humans the reservoir?

Back 137

Plague and Yellow fever – promote rapid spread, responsible for fulminant outbreaks

Front 138

What are various routes of transmission?

Back 138

Contact, airborne, vector-borne, common vehicle (e.g. contaminated food)

Front 139

What complications can be seen with Pasteurella multocida infection?

Back 139

Osteomyelitis, tendonitis, bacteremia, can be life threatening

Front 140

What characterizes ulceroglandular tularemia?

Back 140

High fever, HA, prostration (loss of strength/exhaustion); Organisms gain entrance to host through lesion on skin, papule forms and ulcerates by 7th day, regional lymph nodes become painful and enlarge by 7th day (can suppurate)

Front 141

What virulence factors are associated with Francisella tularensis?

Back 141

Weak endotoxin; Able to survive and grow intracellularly in macrophages (major virulence factor)

Front 142

What characterizes Francisella tularensis?

Back 142

Small, Gram(-) rods, fastidious, facultative, require cysteine; cause Tularemia (rabbit fever)

Front 143

What is the treatment for a Pasteurella multocida infection?

Back 143

Penicillin

Front 144

Which animal is the most common cause of bites in humans?

Back 144

Dogs (followed by cats and other humans)

Front 145

Where can Pasteurella multocida be found?

Back 145

Oral flora of cats, dogs, pigs, horses, panthers, cougars – more prevalent in cat than dog

Front 146

What zoonoses are associated with direct contact?

Back 146

Pasteurella, Francisella, Bartonella

Front 147

What is the hallmark of Pasteurella multocida infection?

Back 147

Acute cellulitis: rapidly progressing, intense inflammation; can see regional lymphadenopathy and purulent discharge

Front 148

What characterizes Pasteurella multocida?

Back 148

Gram(-) coccobacillus; grows on blood agar with CO2; identified by biochemical tests; infection occurs after animal bites and scratches

Front 149

What characterizes pneumonic tularemia?

Back 149

Inhalation of organisms, highly fatal; can get cellular immunity with activated macrophages; live vaccine is available (not very good); diagnosis is made through fluorescent antibody of aspirate, PCR, serology, or culturing of aspirates (difficult and dangerous to grow)

Front 150

How is cat scratch disease diagnosed?

Back 150

History, PCR and serology (very high antibody titers!)

Front 151

What are complications of cat scratch disease?

Back 151

Encephalitis, oculoglandular syndrome, endocarditis

Front 152

What characterizes cat scratch disease?

Back 152

Fairly common; associated with kitten and cat scratches; self-limiting regional lymphadenopathy, often with fever; most common cause of chronic, benign adenopathy in young adults

Front 153

What characterizes Bartonella?

Back 153

Gram(-) rod; difficult to culture, very slow growing

Front 154

What characterizes Bartonella infection?

Back 154

Causes three disease: cat scratch disease (B. henselae), angiomatosis (B. henselae), trench fever (B. quintana)

Front 155

What is the treatment for tularemia infection?

Back 155

Ciprofloxacin, Streptomycin, or Gentamicin

Front 156

What are 50% of cases of tularemia associated with?

Back 156

Bite from deer fly or tick – similar to ulceroglandular tularemia, except that sometimes there is no local lesion

Front 157

What characterizes typhoidal tularemia?

Back 157

Drinking or eating contaminated food/water (eating undercooked rabbit, drinking water contaminated by beavers); causes a syndrome similar to typhoid fever

Front 158

What characterizes oculoglandular tularemia?

Back 158

Initial lesions near eye, with ulcer on eye-lid

Front 159

What is the most common arthropod-borne disease in the US?

Back 159

Lyme disease; caused by the spirochete Borrelia burgdorferi: multiplies in ticks and animals, it has a small linear chromosome with linear and circular plasmids

Front 160

What is the treatment for Lyme disease?

Back 160

Doxycycline early on; Ceftriaxone in later stages – Vaccine: recombinant OspA (OspA is expressed in ticks, but only transiently expressed in humans);
Prevention: Doxycycline 72hrs after tick bite

Front 161

How is the diagnosis of Lyme disease made?

Back 161

Clinical findings: erythema migrans, cardiac abnormalities, arthritis, neurologic manifestations;
Laboratory tests: ELISA using whole cell antigens, Western blot using whole cell antigens

Front 162

What are the virulence factors of Lyme disease?

Back 162

No endotoxin; Lipoproteins induce inflammation; VlsE lipoprotein: undergoes antigenic variation due to gene rearrangement; Differential gene expression allows it to grow in two different hosts (tick and animals); Motility

Front 163

What are the three stages of Lyme disease?

Back 163

Stage 1: bull’s eye rash (erythema migrans, 1-30 days after tick bite, seen in 60-80% of cases), fever, malaise, lymphadenopathy; Stage 2: neurological manifestations (cranial nerve palsies, arthritis, cardiac abnormalities, 2-8 weeks after bite); Stage 3: chronic disease (arthritis, often oligoarthritis, auto-immune disease), neurological (encephalopathy, peripherally neuropathy, chronic fatigue)

Front 164

What describes the Ixodes tick life cycle?

Back 164

Larvae (gets blood meal) --> nymph (responsible for most transmission)--> adult --> eggs

Front 165

What characterizes the transmission of Lyme disease?

Back 165

East: Ixodes scapularis, deer, mice; West: Ixodes pacificus, muskrat, deer, mice – infects host if tick bites at least for 48hrs

Front 166

What is the treatment for cat scratch disease?

Back 166

Azithromycin, Erythromycin

Front 167

What characterizes trench fever?

Back 167

Caused by B. quintana; transmitted by lice and animal contact (seen in crowded/homeless war-time condition); can see chills, fever, rash, splenomegaly, bacteremia, endocarditis; can be mild or severe with relapses; organisms replicate on surface of animal cells; treatment: Erythromycin

Front 168

What characterizes angiomatosis?

Back 168

Occurs in immunocompromised patients (e.g. AIDS); can see swelling of blood vessels, due to endothelial proliferation after engulfment; can also see fever, bacteremia, liver/spleen infection – transmitted by contact with cats; treatment: Erythromycin

Front 169

What drug is derived from Pacific Yew Bark?

Back 169

Paclitaxel (for breast/ovarian cancer) – 10-DAB from yew shrub needles can be synthesized into Paclitaxel and Docetaxel

Front 170

What characterizes biotin?

Back 170

It is the active group for a variety of carboxylation reactions (e.g. pyruvate carboxylase, acetyl carboxylase, propionyl-CoA carboxylase)

Front 171

What characterizes pantothenic acid?

Back 171

It is a portion of the coenzyme A (CoA) as well as a portion of fatty acid synthase; required for the metabolism of proteins, fats, carbohydrates – deficiency of pantothenic acid resembles the deficiency state of other B vitamins

Front 172

What characterizes vitamin B12 (cobalamin)?

Back 172

Vitamin B12 is the extrinsic factor important in pernicious anemia (whereas its endogenous counterpart is intrinsic factor, both are needed for B12 absorption); the methylated form of B12 converts homocysteine to methionine; the 5-deoxy adenosyl derivative causes methyl malonyl CoA to be converted to succinyl CoA

Front 173

What characterizes vitamin B3 (niacin)?

Back 173

It can be synthesized from tryptophan (though it is not produced in adequate amounts); it is a precursor of NAD and NADP; Nicotinic acid (i.e. niacin) causes flushing with taken orally and lowers lipids in the blood

Front 174

What does a cobalamin deficiency lead to?

Back 174

Degradation of the myelin sheath (due to defects in fatty acid metabolism) --> neurological s/s;
Hematological defects (require both B12 and intrinsic factor) --> pernicious anemia

Front 175

Who should be concerned about getting enough iron?

Back 175

Pre-adolescent children, and pre-menopausal women – supplemental iron intake in adult men or post-menopausal women can be a cardiovascular risk

Front 176

What characterizes copper?

Back 176

Important element in metalloenzymes; Deficiency lead to hypercholesterolemia, demineralization of bones, leukopenia, etc.; Excess seen in Wilson’s disease

Front 177

What characterizes zinc?

Back 177

Crucial substance in enzymes and gene factors, necessary for growth/maintenance of the body

Front 178

What are unsafe herbs and their reactions?

Back 178

****one exam question from this list!
Chaparral (cancer): hepatotoxicity; Comfrey (wounds): hepatotoxicity (!);
Ephedra (weight loss): high BP, arrhythmias; Lobelia (asthma): CNS over-stimulation;
Pennyroyal (abortion): CNS toxicity; Yohimbe (ED): CNS over-stimulation;
Germander (tonic): hepatotoxicity; Stephandra (tonic): bradycardia

Front 179

What characterizes Ephedra?

Back 179

Chinese stimulant “warming” herb, contains ephedrine/pseudoephedrine; long-used as a bronchodilator for asthma in China; Popular for weight loss, weight lifting; Removed from market by FDA due to the dangers of overdose: elevated BP, tachycardia, arrhythmias, stroke

Front 180

What does an iron deficiency lead to?

Back 180

Iron deficiency anemia (most prevalent dietary deficiency), causes a microcytic/hypochromic anemia

Front 181

Which herbs/supplements are not thought to have a benefit?

Back 181

Echinacea; Shark cartilage; Ephedra/Mah Huang (safety concerns!); Vitamin E; Dong quai;
Beta-carotene

Front 182

Which herbs/supplements are thought to have benefit?

Back 182

Green tea catechins; Flavonoid-rich juices: grape, pomegranate, acai; Omega 3 fatty acids;
St. John’s Wort (for mild depression); A healthy diet rich in fresh fruits and vegetables

Front 183

What cannot be done under DSHEA 1994?

Back 183

No claim can be made for a dietary supplement to treat, cure, or mitigate a disease; however, it can make claims that if affects or maintains the structure or function of the body

Front 184

What drug is derived from Goat’s Rue?

Back 184

Biguanides, a derivative of which includes Metformin (for DM)

Front 185

What is homeopathy?

Back 185

Diluted herbal/medicine essence (e.g. diluted poison ivy essence)

Front 186

What can star anise seeds be used for?

Back 186

Contain Shikimic acid, which is a vital precursor in the manufacture of Oseltamivir (for influenza treatment) – can also get Shikimic acid from Ginkgo biloba

Front 187

What is pharmacognosy?

Back 187

The scientific study of natural product medicines

Front 188

Which herb may improve symptoms of the common cold and acute bronchitis?

Back 188

Pelargonium sidoides root, from a South African geranium

Front 189

What characterizes Panax Ginseng?

Back 189

Root is used as an adaptagen (tonic herb) for decreased stamina and fatigue; Ginsenosides are the active component; Side effects: elevated BP, nervousness, insomnia, estrogenic effects, hypoglycemia; Caution: HTN, CV disease, avoid in pregnancy or with steroids, possible “ginseng abuse syndrome”; Status: may be useful for improved sense of well-being or energy

Front 190

What characterizes Kava?

Back 190

Used for anxiety (GABA receptor modifier) and stress reduction; contains methysticin and kavain; Side effects: decreased reflexes and judgement, kava dermatitis (flaking discolored skin), idiosyncratic liver toxicity; Caution: psychological dependence (avoid with alcohol, benzodiazepines, levodopa); Status: effective with some abuse and liver injury potential

Front 191

What characterizes St. John’s Wort?

Back 191

Contain hypericin/hyperforin which may inhibit neurotransmitter reuptake and activate GABA receptors to treat mild depression, it is not an MAOI at usual dose; SJW induces CYP3A4 (!);
Side effects: photosensitivity, nausea, dry mouth, restlessness, mania;
Caution: SSRI/MAOI (serotonin syndrome), pregnancy, alcohol, P450 drug interactions

Front 192

What characterizes Milk Thistle Seed?

Back 192

Used for hepatotoxic ingestions, and as a cytoprotectant/antioxidant/anti-inflammatory;
Side effects: loose stools; Status: liver protector used IV in Amanita mushroom poisoning in Europe, may shield liver from toxins but so far no evidence for chronic viral hepatitis or alcoholic cirrhosis

Front 193

What characterizes Saw Palmetto?

Back 193

Widely used for nocturia due to BPH; contains fatty acids thought to be anti-inflammatory and a weak 5-alpha reductase inhibitor; Very slow-acting but effective in the majority of studies;
Side effects: n/d/HA; No effect on PSA and doesn’t shrink prostate

Front 194

What characterizes Ginkgo biloba?

Back 194

Ginkgo extract contains flavonol glycosides and terpene lactones; should be taken at least 8 weeks before assessing efficacy; Ginkolic acid must be removed from Ginkgo lead before use to prevent seizures; It is used as a vasodilator for aged arteries and for mental alertness (though it probably doesn’t improve memory); Terpene lactone inhibits platelet activating factors and may increase bleeding risk if used with other anti-coagulants

Front 195

What is the difference between intrinsic and extrinsic adverse effects?

Back 195

Extrinsic: failure of good manufacturing practices leads to adverse effects;
Intrinsic: Type A (predictable toxicity, overdose, interaction with drugs), Type B (idiosyncratic reactions, like allergy/anaphylaxis)

Front 196

What characterizes Echinacea?

Back 196

Native American herb and garden flower, root extract and leaves of three related species;
Immune stimulant or “booster”; causes tongue to tingle if potent; No clinical benefit for cold prevention, mixed cold treatment results; appears safe but not effective

Front 197

What are infusions, decoctions, macerations, tinctures, and poultices?

Back 197

Infusion: near-boiling water poured on herb; Decoction: simmer herb and strain;
Maceration: steeping herb in room temp. water; Tincture: steeling herb in ethyl alcohol and water;
Poultice: herb paste application

Front 198

What characterizes Phytoestrogens?

Back 198

They are plant sterols that bind to estrogen receptors (SERMs, weak effect); used to control menopausal symptoms as an alternative to HRT; Soy/legumes contain isoflavones (genistein, daidzein), flax seed contains lignans, clover contains coumestans; May have favorable impact on lipids and cardiac risk

Front 199

What negative effect is associated with Green Tea?

Back 199

It interferes with the ability of Bortezomib to kill tumor cells (e.g. in the treatment of glioblastoma and multiple myeloma)

Front 200

What is Green Tea extract FDA approved for?

Back 200

Genital warts (HPV)

Front 201

What characterizes Green Tea (Camellia sinensis)?

Back 201

Contains catechin polyphenols (Epigallocatechin gallate – EGCG), which is a powerful antioxidant; Has an anticancer effect (EGCG inhibits growth of leukemia cells, reduces risk of esophageal cancer, and inhibits aryl hydrocarbon receptors), may help prevent Alzheimer’s disease, as well as cause enhanced weight loss, a reduction of tooth decay, contain anti-inflammatory properties, help against HPV, and reduce CV risk

Front 202

What characterizes Resveratrol (grape extractions)?

Back 202

It is a phytoalexin (found in Japanese knotweed roots and grape skin/red wines); Binds to and stimulates the Sir2 sirtuin enzyme, mimicking the effect of caloric restriction on longevity;
May reduce heat and cancer risk; research is mixed for mammalian longevity

Front 203

What describes the effectiveness of various antioxidants?

Back 203

Vitamin E: doesn’t seem to help prevent CAD or cancer, and may increase all cause mortality;
Beta-carotene: failed to prevent cancer in smokers and increased mortality;
Vitamin C: doesn’t reliably prevent colds but does help prevent post-fracture bone pain –
regular doses of anti-oxidants may actually increase mortality (except for vitamin C or selenium)

Front 204

What substances are thought to function as antioxidants?

Back 204

Green tea, vitamins E/C, grape seen extract, pycnogenol, turmeric, milk thistle, plant pigments (carotenoids, lycopene, flavonoids), statins (from red yeast rice)

Front 205

What characterizes Garlic?

Back 205

Used to improve lipid profiles, as an antibacterial, anti-thrombotic, anti-hypertensive, anti-inflammatory, and anti-cancer food; Active ingredient is Allicin; Only fresh Allicin is an effective anti-infective; Garlic increases NO synthesis, thus reducing the likelihood of blood clotting (should only be used as an adjunct for BP/cholesterol treatment); Excessive amounts cause gastritis or increase bleeding risk with Coumadin; Mixed results for decrease in cholesterol/BP

Front 206

What characterizes the functions vitamin A?

Back 206

Forms a dimer (beta carotene); essential for normal vision, prevention of night blindness, epithelial cell maintenance/differentiation, bone growth, body development, immune functioning

Front 207

What characterizes vitamin K?

Back 207

Consists of three different quinones (phylloquinone, menaquinone, menadione – vit. K1-3, resp.); Needed in the synthesis of four proteins involved in blood clotting: F2 (prothrombin), F7, F9 (plasma thromboplastin), F10 (Stuart factor); vitamin K causes gamma-decarboxylation of specific glutamic acid residues producing gamma carboxyglutamic acid, which is involved in chelation of ions (e.g. calcium, which allow prothrombin to become active) – vitamin K is also involved in bone healing/remodeling

Front 208

What characterizes vitamins E?

Back 208

A group of 8 substances called tocopherols and tocotrienols; they are fat-soluble antioxidants (Alpha D tocopherol is the most potent, but the others can prevent nitration damage);
they prevent red cell hemolysis and nerve damage

Front 209

What does a vitamin D deficiency result in and what about an excess?

Back 209

Deficiency: rickets; Excess: hypercalcemia --> muscle weakness, bone pain, anorexia, HTN, arrhythmias

Front 210

What characterizes the formation of vitamin D?

Back 210

Formed from ergocalciferol added to cow’s milk --> irradiated by UV light to vitamin D3 --> hydroxylated to 25-hydroxy-vitamin D by the liver --> hydroxylated to the active 1,25-dihydroxy-vitamin D by the kidney

Front 211

What vitamin A derivatives are used clinically?

Back 211

All-trans retinoic acid: acne, keratosis, pilaris, acute promyelocytic leukemia; Acitretin: psoriasis; Isotretinoin: acne; Adapalene: acne

Front 212

What do excessive amounts of vitamin A lead to?

Back 212

Toxicity to skin, spleen, kidneys, liver; bone thickening, pain

Front 213

What are the vitamins?

Back 213

Fat soluble: D, E, A, K (a deficiency state can occur when the patient has problems with the absorption of fats); Water soluble: B1-3, 6, 12, C, pantothenic acid, folic acid

Front 214

Which vitamins can act as antioxidants and how?

Back 214

C, E – they form a redox cycle with glutathione causing the oxidized form (R-SS) to become reduced (R-SH); reduced glutathione is a major cellular antioxidant

Front 215

Which vitamin is toxic in high doses?

Back 215

A

Front 216

What does a thiamine deficiency cause?

Back 216

Beriberi: mental confusion, ataxia (milder symptoms incl. depression, peripheral neuropathy, irritability, fatigue); seen in severe alcoholism

Front 217

What does a folate deficiency lead to?

Back 217

Decreased DNA synthesis --> cellular arrest (in S phase), produces a megaloblastic anemia;
since folate is used for the conversion of homocysteine to methionine, hyperhomocysteinemia can occur; Inadequate intake during pregnancy can lead to neural tube defects

Front 218

What characterizes folic acid?

Back 218

Free folic acid is reduced to tetrahydrofolate, which carries a methyl group on its N5 nitrogen; this methyl group is used in the biosynthesis of choline, serine, purines, and pyrimidines

Front 219

What does a deficiency of pyridoxines lead to?

Back 219

Depression, irritability, nervousness, microcytic anemia with high serum iron (since pyridoxal phosphate is needed to synthesize a precursor for heme biosynthesis), glucose intolerance, increased homocysteine (pyridoxines play a role in the conversion of homocysteine to cysteine)

Front 220

What characterizes vitamin B6-complex (pyridoxines)?

Back 220

Converted into pyridoxal phosphate, which is needed for the catabolism/interconversion of amino acids; also needed for the synthesis of neurotransmitters (5-HT/NE/sphingolipids for myelin prod.)

Front 221

What does a deficiency of riboflavin lead to?

Back 221

Angular cheilitis, glossitis, scaly dermatitis; seen in chronic alcoholism

Front 222

What characterizes vitamin B2 (riboflavin)?

Back 222

Structural component of the coenzymes FAD and FMN, which are necessary for energy production and respiration

Front 223

What does a deficiency of vitamin K result in?

Back 223

Increased prothrombin time (can happen in newborns and in adults using excessive anticoagulants), and possibly osteoporosis

Front 224

What characterizes vitamin B1 (thiamine)?

Back 224

Converted into active compounds that function in energy production via glycolysis and Krebs cycle

Front 225

Why is toxicity with water-soluble vitamins rarely found?

Back 225

They are excreted by the body

Front 226

What does a niacin deficiency lead to?

Back 226

Deficient DNA repair, since large amounts of NAD are required for the enzyme PARP, which is involved in nick-repair – give in time-release form for continuous supplies;
Deficiency leads to glossitis and pellagra (with severe deficiency): dermatitis, diarrhea, dementia

Front 227

What can magnesium deficiency lead to?

Back 227

Tetany

Front 228

What characterizes calcium?

Back 228

Most abundant of body minerals; essential part of bone formation, but also required for many enzymatic reactions incl. blood coagulation and muscle function; if calcium levels are insufficient, PTH causes bone dissolution which can lead to osteoporosis if calcium intake over time is low

Front 229

What does an ascorbic acid deficiency lead to?

Back 229

Mild: pinpoint hemorrhages under the skin (caused by increased capillary fragility);
Severe: scurvy (causes decreased wound healing, osteoporosis, hemorrhaging, anemia)

Front 230

What characterizes vitamin C (ascorbic acid)?

Back 230

Antioxidant; functions in hydroxylation of lysine/proline (collagen synthesis, maintenance of connective tissue, wound healing); concentrated in the adrenal gland where it may be linked to steroid hydroxylation reactions or in stabilizing DA/NE/Epi; aids in the absorption of iron by reducing it to the ferrous state in the stomach – vitamin C overdose is not significant, except for causing kidney stones in certain susceptible individuals

Front 231

What is the treatment for Lyme disease?

Back 231

Tetracycline (e.g. Doxycycline)

Front 232

What can be done once rabies symptoms appear in a human?

Back 232

Essentially nothing (almost 100% mortality rate)

Front 233

How long should a potentially rabid animal be observed?

Back 233

10 days; if they survive past 10 days, they probably do not have rabies

Front 234

What characterizes Congo-Crimean hemorrhagic fever?

Back 234

*****learning point
Tick-born viral hemorrhagic disease, spread from domestic animals (e.g. sheep) and wild animals; causes a capillary leak syndrome – treat with Ribavirin

Front 235

What is the treatment for rickettsial illness?

Back 235

Doxycycline

Front 236

What characterizes Typhus (African tick typhus)?

Back 236

*****learning point
A group of infectious diseases caused by rickettsiae, transmitted by arthropods (e.g. ticks) – will see a patient with an eschar, fever, and relative bradycardia

Front 237

What effect on the heart a lots of intracellular pathogens associated with?

Back 237

Bradycardia ( –will see a patient with a fever, but no tachycardia)

Front 238

What are the important families of spirochetes?

Back 238

Borrelia (Lyme disease), Treponema (Syphilis), Leptospira (Leptospirosis)

Front 239

Which spirochete can be seen on peripheral smear?

Back 239

*****learning point
Only Borrelia

Front 240

Which spirochete is associated with relapsing/remitting fever?

Back 240

Borrelia – due to antigenic variation

Front 241

Which disease is associated with a “break-bone fever”?

Back 241

Dengue fever – can also see a petechial rash

Front 242

What characterizes pneumonic plague?

Back 242

*****learning point
A rapidly progressive and often fatal form of plague which can be transmitted person-person

Front 243

In which disease do patients present with swollen lymph glands, called buboes?

Back 243

Bubonic plague – caused by Yersinia pestis

Front 244

What is the treatment for Dengue?

Back 244

Supportive treatment only

Front 245

What is the natural reservoir for Dengue?

Back 245

Monkeys – virus is transmitted by the Aedes mosquito

Front 246

What are the two types of Dengue?

Back 246

Dengue fever: hurts but doesn’t kill; Dengue hemorrhagic fever: hurts and kills

Front 247

What is the most widely distributes mosquito-borne infection?

Back 247

*****learning point
Dengue

Front 248

What should be done after someone has been bitten by a rabid animal?

Back 248

*****learning point
Prompt post-exposure prophylaxis: give Ig and vaccinate

Front 249

How is the diagnosis of rabies infection made?

Back 249

In animal: biopsy brain; In human: biopsy neck skin – look for Negri bodies

Front 250

What signs/symptoms are associated with rabies?

Back 250

Either agitation or depression

Front 251

What characterizes septicemic plague?

Back 251

Sepsis, DIC, high mortality rate

Front 252

What does the disease presentation of tularemia compare to?

Back 252

That of plague – ulcer at site of inoculation and swollen lymph nodes

Front 253

What disease is associated with open wounds and rabbits?

Back 253

Tularemia – caused by Francisella tularemia

Front 254

What is the treatment for plague?

Back 254

*****learning point
Aminoglycosides

Front 255

What organisms are involved in the transmission of Yersinia pestis?

Back 255

Rodents and fleas

Front 256

What are the potential side effects of herbal medicines?

Back 256

Allergic reactions, interaction with prescription drugs

Front 257

What are the adverse effects of particulates?

Back 257

Ultrafine particles (< 0.1 microns) are the most hazardous --> may cause pulmonary/systemic inflammation, arrhythmias due to autonomic effects, and increased blood viscosity (!)

Front 258

What are the adverse effects of SO2?

Back 258

In water releases acidic substances (H+, bisulfite, sulfite) --> upper/lower airways irritation

Front 259

What are the adverse effects of Ozone, NO, NO2?

Back 259

Forms hydrogen peroxide (and lipid aldehydes) on respiratory mucosa --> inflammation, bronchoconstriction (exacerbates asthma) – as little as 0.8 ppm during exercise can cause cough, chest discomfort, and lung inflammation; NO and NO2 release acidic substances in water causing upper respiratory irritation but are less reactive than ozone

Front 260

What are the 6 major pollutants EPA monitors regularly?

Back 260

Ozone, Nitrogen oxides, Sulfure oxides, Particulates, Carbon monoxide, Lead (!)

Front 261

What are the major sources of ambient air pollution?

Back 261

Fossil fuels, Photochemical reactions that make ozone, Power plants (create particulates, SO2/acid rain which irritates airways), Waste incinerators/smelters/industry (metals, mercury, acid aerosols)

Front 262

What group of volatile organic compounds is used widely in dry cleaning?

Back 262

Aliphatic hydrocarbons (e.g. chloroform, carbon tetrachloride, methylene chloride, perchloroethylene)
Perchloroethylene (used in dry cleaning): potential carcinogen, CNS depression/confusion, dermatitis

Front 263

Where does absorbed lead in children end up in?

Back 263

Bone and teeth (80%) with a half-life of 30 years in bone – Lead found in blood only indicates recent exposure to Lead as it is cleared rapidly from the blood

Front 264

What is the most important route of exposure to Lead?

Back 264

Occupational setting: inhalation (!) ***
Consumer setting: ingestion with greater absorption in infants/children and greater absorption with Ca, Fe, Zn deficiencies (Lead poisoning can begin in utero)

Front 265

What toxic chemicals are used in the rubber/plastic industry?

Back 265

Occupational: Vinyl chloride --> angiosarcoma of liver - 1,3 butadiene --> leukemia
Public: Phthlate --> testicular injury in rate – Bisphenol-A --> estrogenic proliferative effects

Front 266

How do polycyclic aromatic hydrocarbons (3 or more fused benzene rings) cause cancer?

Back 266

Their metabolites bind to DNA (e.g. scrotal cancer in chimney sweeps in 1700s)
Prototype carcinogen is benzo[a]pyrene --> present in cigarettes, can cause bladder and lung cancers

Front 267

What aromatic hydrocarbon is considered a carcinogen?

Back 267

Benzene: its CYP450 metabolites, benzoquinone and muconaldehyde, are toxic to the bone marrow --> aplastic anemia, acute leukemia

Front 268

What is caused by inhalation of vapors of petroleum products (gasoline, kerosene, turpentine)?

Back 268

Dizziness, incoordination, CNS depression

Front 269

What are the major effects of air pollutants?

Back 269

Major effect on lungs – children, asthmatics, and individuals with chronic lung/heart disease are esp. prone

Front 270

What are the adverse effects of Radon and Asbestos?

Back 270

Radon: lung cancer in as many as 10,000 per year in the US
Asbestos: lung cancer, mesothelioma
Fiberglass (replacement for asbestos): irritant but not a carcinogen

Front 271

What has been the trend in the levels of indoor air pollutants?

Back 271

Increasing levels due to more insulation and less ventilation of homes aimed at saving energy costs
Examples: CO, NO2, wood smoke (includes polycyclic aromatic hydrocarbons), formaldehyde, benzene, polycyclic aromatic hydrocarbons, radon (in basements), asbestos, fiberglass, bioaerosols (Legionella, allergens, sick building syndrome due to poor ventilation)

Front 272

What is the correlation between serum Lead levels in children and IQ levels?

Back 272

Inverse correlation (even at chronic levels <10 ug/dL can cause mental retardation)

Front 273

What characterizes dioxins?

Back 273

At low doses present in food, soil, water; at high doses may cause leukemia, lymphoma, sarcomas
Used in Agent Orange in the Vietnam war

Front 274

What are organophosphates?

Back 274

Irreversible cholinesterase inhibitors: cause abnormal transmission in CNS/PNS, absorbed via skin/GI/lungs, 40% of farm workers have inhibition of RBC or plasma cholinesterase activity
Carbamates: reversible cholinesterase inhibitors with similar effects (Carbaryl: potentially teratogenic)

Front 275

What are organochlorines?

Back 275

Insecticides that have low acute toxicity for humans; absorbed via GI, skin, lungs; examples include
DDT (metabolite DDE): persists in environment, accumulates in food chain/fat, found in human milk
Chlordane: possible lymphoma in farm workers; Lindane

Front 276

What characterizes pesticide toxicity to humans?

Back 276

Toxic to humans at high concentrations, herbicides have the lowest toxicity among pesticides; rodenticides possibly have the highest toxicity (death)

Front 277

What is an adverse effect of various metals besides Lead?

Back 277

Cobalt and Tungsten Carbide: Interstitial lung fibrosis (hard metal disease);
Cadmium: (acutely) lung edema and irritation, (chronically) kidney PCT damage;
Chromium: Cr3+ is carcinogenic by DNA damage and free-radicals;
Nickel: (mainly inhaled) carcinogenic by DNA damage, (if topical) contact dermatitis

Front 278

What is the correlation between serum Lead levels in females and puberty?

Back 278

As little as 3 ug/dL can delay puberty in females

Front 279

What is an early and characteristic finding in Lead poisoning?

Back 279

Hypochromic anemia: Lead inhibits enzymes that catalyze incorporation of Iron into heme, leading to reduced heme biosynthesis

Front 280

What is a blood test for (chronic) Lead poisoning?

Back 280

Elevated serum Zinc protoporphyrin, free RBC protoporphyrin (!)
Serum Lead is not measure as it only indicates acute exposure to Lead

Front 281

What are the various biochemical effects of Lead?

Back 281

Bone: competes with Ca --> stores in bone;
CNS: competes with Ca --> interferes with nerve transmission and brain development;
Hypochromic anemia: inhibits Iron incorporation into heme --? reduced heme synthesis
Inhibit membrane-associated enzymes --> decrease RBC survival, kidney damage, HTN
Impaired production of 1,25-diOH Vitamin D

Front 282

What natural toxins are produced by the nature?

Back 282

Fungi: mycotoxins (may contaminate food), e.g. Aflatoxin in peanuts --> carcinogen, liver cancer;
Plants: phytotoxins (may contaminate food);
Animals: dinoflagellate toxins ciguatoxin (paresis) and saxitoxin (paralysis) ingested by eating fish/snails/mollusks, e.g. paralytic shellfish poisoning (saxitoxin: neurotoxin, paralysis)

Front 283

How many drugs does the average geriatric patient take?

Back 283

3.2 drugs (women 3.5, men 2.8); 40% take more than three drugs;10% take more than five drugs’; 65% of total national usage of cardiovascular and diuretic drugs are consumed by the elderly

Front 284

When % of hospital admissions in the geriatric population is due to adverse drug effects or nonadherence?

Back 284

28%

Front 285

What describes the geriatric pharmacokinetics of absorption?

Back 285

Decreased gastric acid production (increased pH, usually due to comorbid illness); reduced splanchnic (intestinal) blood flow; decreased GI motility

Front 286

What describes the geriatric pharmacokinetics of Distribution and Metabolism?

Back 286

Lean body mass (vs. adipose tissue) declines w/ age as does plasma volume; Lipophilic drugs (benzodiazepines, lidocaine) are distributed more extensively, thereby prolonging half-life. Greater effect in F than M as F develop relatively less lean body mass w/ age; Water soluble drugs (acetaminophen) will not distribute as widely, therefore higher serum concs could occur; Decreased serum albumin (more likely in ill, frail, poorly nourished --> Protein-bound drugs (phenytoin, warfarin, thyroxine, NSAID) may be more available as free drugs, hence, toxic effects)

Front 287

How is Hepatic metabolism changed in Geriatric Pharmacokinetics?

Back 287

Phase 1 metabolism (oxidation, reduction, hydrolization): decreases w/ age; metabolites are as effective or more effective than the parent drug & are more water soluble; Phase 2 metabolism (conjugation to inactive metabolites) does not decrease w/ age (1st pass effect may yield more drug to the circulation as hepatic metabolism is diminished)

Front 288

What drugs have increased bioavailability in the elderly?

Back 288

Propranolol*, Labetalol, Levodopa*, nifedipine, Omeprazole, odansetron

Front 289

What describes the geriatric pharmacokinetics of Elimination?

Back 289

Renal metabolism declines with age and is worsened with disease, i.e., HTN (nephrosclerosis), CHF (decreased renal blood flow), diabetes (nephropathy); Renal function (creatinine clearance) over age 65 is about 1/2 that at age 20; Creatinine may not worsen as there is decreased lean body mass

Front 290

What important drugs must be used with caution in patients with renal impairment?

Back 290

Digoxin, aminoglycosides, cimetidine, lithium, penicillin

Front 291

What changes in the CNS are associated with normal aging?

Back 291

Decrease in muscarinic receptors; Increase in catechol O methyl transferase (COMT); Increase in Monamine oxidase ( MAO)

Front 292

What changes in the Cardiovascular system are associated with normal aging?

Back 292

Decreasing sensitivity of beta adrenergic receptors

Front 293

What changes in the Respiratory system are associated with normal aging?

Back 293

Decreased awareness of hypoxia and hypercapnia

Front 294

What changes in the GI system are associated with normal aging?

Back 294

Decrease in Vitamin D absorption, Slower transit times usually due to comorbid illness, medication and lifestyle.

Front 295

What changes in the eye are associated with normal aging?

Back 295

Ciliary atrophy, rigidity of lens and iris

Front 296

What changes in the skin are associated with normal aging?

Back 296

Decreased ability to sweat

Front 297

What changes in the urologic system are associated with normal aging?

Back 297

Decrease in contractility of bladder; Increase in size of prostate

Front 298

What changes in the GFR are associated with normal aging?

Back 298

Decrease in GFR --> Decrease in ability to excrete metabolites: Sodium and potassium

Front 299

What are predictors of therapeutic failure in the geriatric population?

Back 299

Multiple comorbid illness (i.e CHF, renal failure, Alzheimer’s); Poor functional ability (i.e. activities of daily living)

Front 300

What therapeutic considerations must be taken into account with geriatric patients?

Back 300

Diminished memory (complicated schedules, drug names, forgetting a dose or doubling); Costs; Psychiatric conditions commonly depression (subtle Sx, may mimic dementia, Overdose or refusal to take meds); impaired vision; Swallowing function (decreasing esophageal motility, worse GE reflux, achalasia, strictures, impaired salivation; i.e. Alendronate)

Front 301

What are some common pitfalls in geriatric therapy?

Back 301

OA (PT & acetaminophen best 1st choice, not NSAIDS); CA chemotherapy (Best predictor of success is severity of comorbid illnesses & functional ability- not age); Anxiety (Often coexists w/ depression, best 1st choice is SSRI, not benzodiazepine)

Front 302

What is “Beers list”?

Back 302

Some medications are statistically associated w/ ADE, Usually medications with anticholinergic effects, toxic metabolites, or long half lives and potential for significant side effects

Front 303

What medications are inappropriate medications in older people* (independent of diagnosis)?

Back 303

Propoxyphene; Indomethacin; Phenylbutazone; Pentazocine; Trimethobenzamide; Methocarbamol, carisoprodol, oxybutynin, chlorzoxazone, metaxalone, cyclobenzaprine; Flurazepam; Amitriptyline; Doxepin; Meprobamate; hlordiazepoxide, diazepam (long-half life benzo); Disopyramide; Dipyridamole; Methyldopa; Reserpine

Front 304

What herbal medications are inappropriate medications in older people?

Back 304

Dicyclomine, hyoscyamine, propantheline, belladonna alkaloids; Chlorpheniramine, diphenhydramine, hydroxyzine, cyproheptadine, promethazine, tripelennamine; dexchlorpheniramine; Ergot mesyloids; Ferrous sulfate supplements >325 mg/day

Front 305

If a geriatric pt is experiencing new symptoms, what should always be considered?

Back 305

That it is possibly being drug-related

Front 306

What is the treatment for S. aureus bacteremia/endocarditis/pneumonia?

Back 306

Nafcillin (if sensitive); if MRSA use Vancomycin – if sensitivities are unknown (i.e. initially) use Nafcillin plus Vancomycin

Front 307

What is the treatment for streptococcus pyogenes pharyngitis?

Back 307

Penicillin – if allergic use Azithromycin

Front 308

What is the treatment for streptococcus pyogenes TSS/necrotizing fasciitis?

Back 308

Clindamycin plus Penicillin G

Front 309

What is a good empiric therapy for endocarditis?

Back 309

Vancomycin plus Gentamicin

Front 310

What is the treatment for enterococcus endocarditis/bacteremia?

Back 310

IV Ampicillin plus Gentamicin (low dose) – if allergic to Ampicillin, give Vancomycin

Front 311

What is the treatment for streptococcal infective endocarditis?

Back 311

High dose Penicillin G – if allergic, give Vancomycin

Front 312

What is the treatment for an IV line infection with coagulase-negative staphylococci?

Back 312

Vancomycin

Front 313

What are causes of bacterial meningitis and what is their treatment?

Back 313

S. pneumo/N. meningitidis: Vancomycin plus Ceftriaxone; L. monocytogenes: Ampicillin

Front 314

What are causes of community-acquired pneumonia and what is the treatment?

Back 314

S. pneumo: Ceftriaxone; Mycoplasma pneumoniae/Legionella: Azithromycin

Front 315

What is the treatment for rickettsial infections (and ehrlichia)?

Back 315

Doxycycline – give right away when rickettsial infection is suspected (don’t wait for cultures)

Front 316

What is the treatment for intraabdominal/pelvic infections?

Back 316

Gentamicin (for Gram(-) rods) + Metronidazole (for anaerobes) + Ampicillin (for enterococcus) – alternatively, Metronidazole can be replaced by Ampicillin/Sulbactam or Clindamycin

Front 317

What is the treatment for inpatient cellulitis?

Back 317

IV Vancomycin (scale down therapy if possible) – In the case of a diabetic lower extremity or with a suspected mixed infection: Vancomycin plus Ceftriaxone plus Metronidazole

Front 318

What is the treatment for outpatient cellulitis?

Back 318

If known MSSA: Cephalexin; If unknown or MRSA: TMP/SMX, Doxycycline, Clindamycin (if sensitive); If GAS: Dicloxacillin, Clindamycin

Front 319

What is the treatment for otitis media and sinusitis (S. pneumo/H. flu)?

Back 319

1st line: Amoxicillin, TMP/SMX, Azithromycin; 2nd line: Amoxicillin/Clavulanate, Cefuroxime

Front 320

What is the treatment for Chlamydia trachomatis?

Back 320

Azithromycin (or Doxycycline)

Front 321

What is the treatment for Neisseria gonorrhea?

Back 321

Ceftriaxone

Front 322

What is the treatment for syphilis (T. pallidum)?

Back 322

Benzathine Penicillin IM (or aqueous Penicillin G, if neurosyphilis)

Front 323

What is the treatment for UTI in a young, otherwise healthy woman?

Back 323

Cystitis (E. coli): Trimethoprim/Sulfa (TMP/SMX) – if pregnant use Amoxicillin;
Pyelonephritis (Gram(-) rods, enterococcus): Ampicillin (enterococcus) + Gentamicin (E. coli)

Front 324

Who should not take Fluoroquinolones (e.g. Ciprofloxacin)?

Back 324

Children under 16, and in pregnancy

Front 325

What is the treatment for pseudomonas aeruginosa infection?

Back 325

Use 2 drugs: Aminoglycoside + Ceftazidime (or Piperacillin/Tazobactam, Cefepime or Imipenem) – if patient can’t take β-lactams use Aminoglycoside plus Ciprofloxacin

Front 326

What adverse effects are associated with Vancomycin?

Back 326

"Red man” syndrome”: immediate reaction, histamine release; Phlebitis, rash, bone marrow suppression, ototoxicity, nephrotoxicity

Front 327

What adverse effects are associated with Synercid (Quinupristin/Dalfopristin)?

Back 327

↑LFTs, myalgias, arthralgias

Front 328

What are Synercid, Linezolid, and Daptomycin used for?

Back 328

VRE and MRSA

Front 329

What adverse effects are associated with Doxycycline?

Back 329

Photosensitivity rash; ↑LFTs

Front 330

What adverse effects are associated with Trimethoprim/Sulfamethoxazole (TMP/SMX)?

Back 330

Rash, bone marrow suppression (esp. ↓WBC), ↑creatinine

Front 331

What adverse effects are associated with Metronidazole?

Back 331

Antabuse reaction, peripheral neuropathy, ataxia

Front 332

What adverse effects are associated with Macrolides (Erythro-/Azithro-/Clarithromycin)?

Back 332

May lead to QT prolongation; n/v/d, liver enzyme elevations – Clindamycin: diarrhea (including C. difficile), rash

Front 333

What adverse effects are associated with β-lactams (Penicillins, Cephalosporins)?

Back 333

Anaphylaxis; Rashes, n/v/d, interstitial nephritis; With high-dose, prolonged therapy: bone marrow suppression – Imipenem (less so Meropenem) may cause seizures, so avoid in patients with CNS pathology, seizure disorders, and renal failure

Front 334

What adverse effects are associated with Quinolones (Ciprofloxacin, Levofloxacin)?

Back 334

Nausea, CNS effects (hallucinations, confusion, seizures); May lead to QT prolongation;
Tendon rupture, arthropathy; Photosensitivity (esp. newer quinolones), hyper-/hypoglycemia

Front 335

What adverse effects are associated with Aminoglycosides?

Back 335

Renal toxicity; Ototoxicity (vest/aud); rarely, neuromuscular blockade

Front 336

What adverse effects are associated with Linezolid?

Back 336

Many drug interactions; Low WBC/platelets; Lactic acidosis; Retinopathy

Front 337

What antimicrobials are considered safe in pregnancy (category A/B)?

Back 337

β-lactams (Penicillin/Cephalosporins), Azithromycin/Erythromycin

Front 338

What antimicrobials should be avoided in pregnancy?

Back 338

Doxycycline/Tetracycline; Quinolones

Front 339

What adverse effects are associated with Daptomycin?

Back 339

↑creatinine kinase/LFTs, myopathy

Front 340

What are the toxic effects of Acetaldehyde and how are Asian effected?

Back 340

Nausea, flushing, tachycardia, hyperventilation, 50% of Asians have low ALDH activity and do not metabolize acetaldehyde well (low alcohol tolerance)

Front 341

Increased incidence of cancer of oral cavity, larynx, esophagus and liver are all associated with what toxicity?

Back 341

Increased incidence of cancer of oral cavity, larynx, esophagus and liver (hepatocellular carcinoma); May be related to acetaldehyde

Front 342

How does a baby with Fetal Alcohol Syndrome present at birth?

Back 342

Microcephaly, growth retardation, facial abnormalities, Reduction in mental functions, 0.1 to 0.5% of U.S. births

Front 343

How does chronic alcoholism cause malnutrition?

Back 343

Empty calories and Vitamin B1 deficiency (Peripheral neuropathies, Wernicke-Korsakoff syndrome)

Front 344

How does Chronic Alcoholism affect the Liver, Upper GI tract, Pancreas, CV system, & CNS?

Back 344

Liver (Fatty change, Alcoholic hepatitis, Cirrhosis, Hepatocellular carcinoma);
Upper GI Tract (Bleeding gastric ulcer, Esophageal varices);
Pancreas (Acute and chronic pancreatitis);
CV system (Dilated congestive cardiomyopathy, Hypertension);
CNS (Cerebral atrophy, Cerebellar degeneration)

Front 345

What are the acute & chronic effects of alcohol abuse?

Back 345

Acute (reversible: CNS depression, Gastritis and gastric ulcer, Fatty liver [hepatic steatosis]);
Chronic alcoholism (Morbidity, Shortened life span)

Front 346

What causes the accumulation of fat in the liver in of an alcoholic?

Back 346

Depletion of NAD which is required for fatty acid oxidation

Front 347

How is ethanol absorbed?

Back 347

Unaltered in stomach and small intestine, Evenly distributed to all tissues and fluids of body, 10% excreted intact in urine, sweat, and breath, Basis of breath test

Front 348

What effect does alcohol have on the CYP enzyme system?

Back 348

At high blood alcohol levels, the CYP system also converts ethanol to acetaldehyde, it is induced 5 to 10-fold in chronic alcoholics & may accelerate metabolism of other drug; Unless there is a high blood alcohol level, which competes for CYP, delays drug metabolism, and potentiates the depressant effects of narcotics, sedatives, etc.

Front 349

What describes the metabolism of alcohol?

Back 349

Most blood alcohol is converted to acetaldehyde in the liver, catalyzed by alcohol dehydrogenase (ADH), this rxn also converts NAD to NADH, Acetaldehyde is converted to acetic acid by acetaldehyde dehydrogenase (ALDH), Acetic acid is then used for energy source in the mitochondrial respiratory chain

Front 350

What was the significance of the Women’s Health Initiative study, 2002 about HRT?

Back 350

Increased risk of breast cancer and thromboembolism; No reduction in cardiovascular disease; Reduction in number of fractures

Front 351

What is the antidote for Acetaminophen toxicity in the first 12 hours?

Back 351

N-acetylcysteine, which restores GSH, tapering off the excess levels of NAPQ

Front 352

How does Acetaminophen use lead to hepatocellular injury and necrosis?

Back 352

Small proportion metabolized by CYP to NAPQI, a highly reactive & toxic metabolite, which is normally conjugated & detoxified with glutathione (GSH); In larger doses, GSH is depleted, & NAPQI accumulates & binds covalently to hepatic proteins causing injury

Front 353

What drug causes almost 50% of cases of acute liver failure, has a mortality rate 30%, & may require liver transplant for survival?

Back 353

Acetaminophen

Front 354

What is the major adverse effect of Acetaminophen and Aspirin?

Back 354

Acetaminophen: Hepatic necrosis (at large doses) (!); Aspirin overdose: respiratory alkalosis, metabolic acidosis; Aspiring chronic toxicity (3 grams/day): tinnitus, erosive gastritis, bleeding, analgesic nephropathy

Front 355

What are the ADR in Anabolic Steroids?

Back 355

Males: Testicular atrophy, gynecomastia, acne;
Females: Facial hair, menstrual changes;
also: Premature MI, hepatic cholestasis, psychiatric problems

Front 356

What are the adverse effects from use of Oral Contraceptives?

Back 356

Thromboembolism (Overall, a 3-fold increased risk, Increased synthesis of coagulation factors (seems to be induced by OC));
Cardiovascular disease (Smokers have increased risk of MI, Nonsmokers have increased risk of MI after age 35):
Cancers (Reduced incidence of endometrial & ovarian CA (not an ADR!), Small increased risk of breast CA in 1st 5 yrs);
Increased risk of Hepatic Adenoma (benign)

Front 357

What are the beneficial effects caused by moderate consumption of alcohol and red wine?

Back 357

Increased HDL levels, decreased platelet aggregation, Red wine contains resveratrol, may promote longevity

Front 358

What is the consequence of using Estrogen only Hormonal Replacement Therapy?

Back 358

Increased risk of endometrial cancer, so used only post-hysterectomy

Front 359

How many hospitalized pts are affected by Adverse Drug Reactions & how many of them die?

Back 359

Affect 10% of hospitalized patients, Of whom 10% die (implies that 1% of all hospitalized pt will die of an ADR)

Front 360

What are the symptoms of toxicity with Acetaminophen?

Back 360

Pretty non-specific, Nausea, vomiting, diarrhea, sometimes shock, Jaundice in a few days

Front 361

What drug can cause Analgesic Nephropathy?

Back 361

Tubulointerstitial nephritis with renal papillary necrosis caused by long-term use of combinations of aspirin and phenacetin (acetaminophen) in large quantities

Front 362

What are the morphological changes associated with chronic aspirin toxicity?

Back 362

Acute erosive gastritis;
Gastric ulcer;
Petechiae in skin and viscera;
Bleeding tendency

Front 363

How does Acute salicylate overdose present?

Back 363

Early respiratory alkalosis (Hyperventilation from stimulation of respiratory center);
Metabolic acidosis later (Uncoupling of oxidative phosphorylation, Accumulation of pyruvate and lactate);
In larger doses there are CNS effects (range from nausea to coma)

Front 364

What can cause Inadvertent poisoning when combined w/ Aspirin?

Back 364

Excess use of ointment with oil of wintergreen (methyl salicylate) (otherwise overdose is usually suicidal)

Front 365

What are examples of particulate radiation?

Back 365

Alpha: 2 neutrons + 2 protons (e.g. Radon gas) --> strongly ioninzing, low penetration;
Beta: electrons --> less ionizing, more penetrating than alpha

Front 366

How does oxygen level of tissue become a factor in the damage caused by radiation?

Back 366

Hyperbaric oxygen increases cell injury by gamma and x-rays as ionizing radiation produces oxygen-radicals (may be counteracted by antioxidants)

Front 367

What is the most significant subcellular target of radiation?

Back 367

DNA: rapidly dividing cells are more radiosensitive (e.g. hematopoietic, GI, squamous epithelia, endothelial, lymphocytes), whereas quiescent cells are not as sensitive (bone, cartilage, muscle, peripheral nerve)

Front 368

What are the most significant factor in the biological effect of radiation?

Back 368

Dose rate: single dose of 40 is more damaging than 10 doses of 4 (less time for cellular repair)
Whole body radiation: more damaging than regional doses with shielding
Cell cycle and cell type: G2 and mitotic phases are most sensitive

Front 369

How do gamma and alpha rays differ in their radiation energy transferred?

Back 369

Alpha: produce heavy damage in a restricted area by interacting with many molecules over a short distance
Gamma: penetrate deeply, dissipating energy more gradually over a longer distance, while producing less damage per unit of tissue

Front 370

What units are commonly used in radiation?

Back 370

Gray: measures energy absorbed by target tissue per unit mass, expressed as ergs/gram ; Sievert: unit of dose that measures biologic effect ; Different types of radiation differ in the degree of tissue damage they produce, even at the same physical dose (Gray); The equivalent dose (Sievert) corresponds to the absorbed dose (Gray) multiplied by relative biologic effectiveness of the radiation; For X-rays, 1 Sievert=1 Gray

Front 371

What is radiation?

Back 371

Electromagnetic energy which at short wavelengths (high frequency) acts as particles and at long wavelengths (low frequency) acts as waves; radiation exposure is 80% from natural sources (cosmic, UV, natural radioisotopes such as Radon gas), 20% from manufactured sources (medical imaging, radio waves, microwaves)

Front 372

What is ionizing radiation?

Back 372

Short wavelength (high frequency), high-energy radiation that may be unsafe and ionize/eject electrons from molecules; examples include X-rays, gamma rays, cosmic radiation

Front 373

What is non-ionizing radiation?

Back 373

Long wavelength (low frequency), low-energy radiation that is safe and produces only vibration/rotation of atoms; examples include electric, radio, microwaves, IR, UV (!)

Front 374

What is the most important delayed effects of radiation?

Back 374

Blood vessels are among tissues most vulnerable to delayed radiation injury
Inflammation of blood vessels --> endothelial cell necrosis --> luminal narrowing by fibrosis -->occlusion --> ischemic changes to organs supplied (fibrosis, atrophy); this may occur at doses used for cancer treatment

Front 375

What are the delayed or chronic effects of radiation to the following organs?

Back 375

Skin: epidermal atrophy, dermal fibrosis, dilation of SC vessels --> poor healing, ulceration, SCC, BCC;
Heart: fibrosis of heart/pericardium --> MI, CHF, constrictive pericarditis due to fibrosis;
Lung (acute: 1-6 months post-treatment): edema, inflammation, dyspnea;
Lung (delayed radiation pneumonitis: months to years post-treatment): dyspnea, chronic cough, decreased lung function, fibrosis, increased incidence of lung cancer;
Kidneys: tumors of kidney; fibrosis of vessels/glomeruli --> HTN, atrophy;
Bladder: tumors of bladder; epithelial cell necrosis, submucosal fibrosis --> ulcers, bleeding from bladder;
GI (acute): exfoliation of mucosa --> loss fluids/electrolytes, inflammation;
GI (chronic): small vessel injury --> ischemia (ischemia of bowel shown on slide 48);
Breast: diagnostic doses during adolescence increase breast cancer incidence in 15-20 years;
Breast: radiation therapy for breast cancer --> dense fibrosis, pleomorphism of epithelial cells, radiation-induced sarcoma;
Ovary and Testis: spermatogonia extremely sensitive, acute degeneration of ovarian follicles;
Eyes: cataracts (lens is sensitive) (!) *****;
Brain: focal necrosis, demyelination of white matter;
Spinal cord: transverse myelitis with paraplegia below the level of injury (!) ******

Front 376

In what manner is radiation used for therapy?

Back 376

Doses given in fractions while shielding adjacent normal structures
Used to shrink tumor, relieve pain, or alleviate compression of adjacent structures
Side effects include: radiation sickness, decreased PMNs/platelets, sterility, 2’ cancers, fibrosis (delayed radiation injury), fatigue/n/v

Front 377

What is caused by acute whole-body radiation?

Back 377

Radiation sickness (acute radiation syndrome), potentially lethal, causes four clinical syndromes depending on severity of radiation: subclinical (prodormal: nausea, vomiting) --> hematopoietic --> GI --> CNS

Front 378

Which cancers are most commonly seen as a result of radiation injury?

Back 378

Population at large: skin cancer, osteogenic sarcoma, leukemia, lung cancer
Children: breast, thyroid, GI, urinary tract

Front 379

What is the latent period for cancer development following radiation?

Back 379

10-20 years: due to accumulation of mutations from genomic instability caused by radiation

Front 380

What is the most important acute effect of radiation?

Back 380

DNA damage (cross-links, breaks) directly from radiation or indirectly via oxygen-radicals

Front 381

What are the effects of radiation on cells?

Back 381

High doses: necrosis;
Intermediate doses: killing of proliferating cells; Low doses: no histopathologic effects, but subcellular damage occurs to DNA, some undergo apoptosis --> surviving cells may have delayed effects (mutations, malignancy, delayed organ dysfunction by vascular damage or atrophy)

Front 382

What characterizes damage due to UV radiation?

Back 382

Acute effects (low dose): erythema, pigmentation (UVA oxidizes melanin --> transient darkening);
Acute effects (high dose): erythema, edema, acute inflammation from histamine release;
Chronic effects: tanning (UVA and UVB --> increased # of melanocytes, transfer of melanin to keratinocytes); UVB tanning is more protective for subsequent UV exposure than UVA tanning

Front 383

What can repeated UV exposure lead to? *******

Back 383

Degeneration of collagen and elastin (irreversible), solar elastosis, irregular pigmentation --> premature sking aging; Triggers UV response pathways, which may be protective via inducing DNA repair, cell cycle arrest, and apoptosis (!)

Front 384

What are the causes of injury from the physical environment?

Back 384

Mechanical force, heat/cold, electric injuries, high altitude

Front 385

What factors determine the character of a gunshot wounds?

Back 385

Type of gun (rifle, handgun, shotgun: the longer the barrel, the more bullet energy), ammunition (caliber), distance from body, location of injury, trajectory of bullet (right angle or oblique), gyroscopic stability of bullet (tumbling bullets cause more injury)

Front 386

What characterizes incisions?

Back 386

Incision: sharp cutting object (knife) causing tear in skin, with clean margins and no bridging strands, margins readily approximated by suture, leaves little scarring

Front 387

What characterizes lacerations?

Back 387

Laceration: blunt force causing irregular tear in skin due to over-stretching, can involve deep tissue organs without involving the skin (e.g. spleen laceration), can be stellate or linear, shows bridiging blood vessels, and fibrous tissue strands, hemorrhagic margins (look at slide 9)

Front 388

Which age group is especially prone to large hematomas from contusions?

Back 388

Elderly due to small vessel fragility

Front 389

What characterizes contusions?

Back 389

Contusion: blunt force causing bruising without skin disruption, bruise caused by small vessel damage and interstitial bleeding; usually seen right away if superficial, but may not be evident if deep (swelling and tenderness may be only signs)

Front 390

What are the various types of injuries from mechanical forces?

Back 390

Abrasion, contusion, laceration, incision, gunshot wounds

Front 391

In what age category is trauma a major cause of death?

Back 391

Up to age 44 – includes accidental injuries, homicides, suicides

Front 392

What are the biggest disparities in adult mortality rate of blacks compared to whites and Hispanics?

Back 392

Death from HIV and homicide are almost 10-fold higher

Front 393

What characterizes abrasions?

Back 393

Abrasion: scrape, superficial epidermis torn off by friction or force, regenerates w/o scarring

Front 394

What characterizes exit injuries from gunshot wounds?

Back 394

Larger and more irregular than entrance wounds

Front 395

What complications occur with large burns?

Back 395

Greater than 50%: potentially fatal
Greater than 20%: release of osmotically active materials from dying cells --> fluid shift to interstitium --> increased interstitial osmotic pressure --> hypovolemic shock, generalized edema, pulmonary edema

Front 396

What is the hypermetabolic state that is caused by large burns?

Back 396

Excess heat loss and increased need for nutrition --> increase in resting BMR --> breakdown of tissues to meet caloric needs if insufficient nutrition --> protein breakdown --> starvation (to preven, keep room temperate elevated, provide aggressive nutritional support)

Front 397

What is the leading cause of death from in burn patients?

Back 397

Organi failure from sepsis due to secondary infection of burns (main organisms: Pseudomonas aeruginosa, Candida, antibiotic-resistant S. aureus) (!)

Front 398

What are the possible complications of thermal burn?

Back 398

% body surface involved, airway/lung injury, 2ndary infection (leading cause of death), hypermetabolic state

Front 399

What are the grading criteria for thermal burns?

Back 399

Partial thickness (pink or mottled, blistered or painful);
1st: epidermis only;
2nd: superficial dermis (dermal appendages intact, can regenerate);
Full thickness (white or charred, dry and anesthetic);
3rd degree: full thickness skin;
4th degree: subcutaneous

Front 400

What factors determine the clinical significance of thermal burns?

Back 400

Depth, % body surface involved, internal injuries from inhaling hot/toxic fumes

Front 401

How are close gunshot wounds different from long-range gunshot wounds?

Back 401

Within 1 foot: shows fouling (gray discoloration of skin from burned powder), stippling (unburned powder);
1 to 3 feet: shows stippling without fouling;
Greater than 3 feet: no fouling or stippling

Front 402

What characterizes internal injuries from gunshot wounds?

Back 402

Low velocity bullets: burrowing, through and through (i.e. bullet goes through, no other damage in its path);
High velocity bullets: laceration of viscera (i.e. bullet causes much more damage in viscera in addition to going through)

Front 403

What characterizes entrance injuries from gunshot wounds?

Back 403

Entrance is slightly smaller than bullet, may have narrow rim of abrasion, if shot at angle may be asymmetric, at close range may have lacerations of skin due to entering gas elevating the skin

Front 404

What characterizes heat cramps?

Back 404

Loss of electrolytes from sweating --> cramping of voluntary muscles with exercise – body has normal core temperate

Front 405

What factors determine the type of injury caused by electrical injury?

Back 405

Current intensity;
Electrical resistance of tissues (greater resistance --> greater heat): Dry skin (high resistance) -->
surface burn;
Wet skin (low resistance) --> ventricular fibrillation or respiratory paralysis current intensity

Front 406

What are hypothermias direct and indirect effects on body?

Back 406

Direct: physical disruption of organelles, high salt concentration due to crystallization of ICF/ECF water;
Indirect (circulatory changes): if slowly developing, will get vasoconstriction, increased permeability, edema, “trench foot”; if rapidly developing, will get more rapid vasoconstriction, ischemia of toes and feet (frost bite), peripheral nerve damage, edema evident only after rewarming

Front 407

What occurs with severe hypothermia (90°F)?

Back 407

Loss of consciousness, bradycardia, atrial fibrillation (arrhythmia is cause of death)

Front 408

What temperature in heat stroke is associated with >50% mortality?

Back 408

≥ 106°F

Front 409

What characterizes heat stroke?

Back 409

High ambient temp and humidity --> stopped sweating --> core body temperature rises --> marked peripheral vasodilation, peripheral pooling of blood, hypovolemia --> muscle/myocardium necrosis, arrhythmia, DIC

Front 410

What characterizes heat exhaustion?

Back 410

Hypovolemia from water loss --> sudden weakness and collapse --> quick recovery of equilibrium

Front 411

What fluids should be used to reverse the hypovolemic shock caused from large burns?

Back 411

Osmotically active fluids: albumin, plasma (not normal saline)

Front 412

What is caused by hyperthermia?

Back 412

Heat cramps --> heat exhaustion (most common) --> heat stroke (most dangerous)

Front 413

How do lungs/airways get injured in thermal burns?

Back 413

Direct effect of heat, toxic components in smoke (water soluble (chlorine, sulfur oxides) --> upper respiratory, bronchial injury;
lipid soluble (nitrous oxides) --> lower respiratory, lung injury)

Front 414

What is an example of a high intensity current that can cause electrical injury?

Back 414

Lightning – injury is characterized by lightning marks (linear arborizing burns)

Front 415

What is the treatment for decompression disease?

Back 415

Repressurize --> depressurize gradually

Front 416

What symptoms develop within hours of rapid decompression?

Back 416

Respiratory difficulty, Substernal pain due to gas emboli in lungs (“the chokes”)
Headache, visual problems, disorientation, vertigo due to inner ear involvment (“the staggers”)
Periarticular gas bubbles, joint pain (“the bends”)
Delayed aseptic necrosis of femoral/humeral head due to embolic occlusion of blood supply, may cause degenerative joint disease eventually

Front 417

What characterizes decompression (caisson) disease?

Back 417

O2 and N2 dissolved in blood at high pressure come out of solution as tiny gas bubbles if decompression is too rapid (O2 redissolves quickly) --> N2 and Helium bubbles can form emboli

Front 418

What are injuries related to changes in atmospheric pressure?

Back 418

High-altitude illness: low O2 tension --> confusion, increased capillary permeability, pulmonary edema
Blast injury (air blast, immersion/water blast): violent increase in pressure --> thorax collapse, abdominal compression, visceral rupture, alveoli damage, decompression wave with sudden expansion of abdomen and thoax may rupture intestines/lungs
Decompression (caisson) disease (aka barotraumas): occurs in deep sea waters, underwater workers with rapid ascent

Front 419

How is Rickettsia rickettsii transmitted?

Back 419

Eastern US: dog tick (Dermacentor variabilis); Western US: wood tick (Dermacentor andersoni) – most cases occur outside of the Rocky Mountains

Front 420

How is Rickettsia prowazekii transmitted (Epidemic typhus fever)?

Back 420

By the human louse Pediculus humanus; lives on human blood; Louse bites infected human --> louse becomes infected --> louse bites another human and defecates (feces contain Rickettsia) --> human scratches and becomes infected – once the human dies, the lice leave the host

Front 421

What is the treatment for RMSF?

Back 421

Initiate antibiotic treatment as soon as possible (within 5 days of illness); Tick removal with forceps

Front 422

How is the diagnosis of RMSF made?

Back 422

Clinical diagnosis is most important: history of tick bite, spring/early summer; can also do an agglutination tests of the patient’s serum, as well as fluorescent antibody testing of biopsied tissue

Front 423

What characterizes the symptomatology of RMSF?

Back 423

Incubation period: 2-6 days; Signs/symptoms: intense HA, rash (palms), fever, irritable, eventual coma and death; The severe vasculitis it causes starts on the wrists/ankles --> palms/soles --> up the extremities (some pts have no rash); can also see thrombocytopenia and hyponatremia

Front 424

When does transmission of Rickettsia rickettsii occur once the tick latches on?

Back 424

Within 4-6 hours as the tick becomes engorged

Front 425

How does Rickettsia rickettsii from the tick to the human?

Back 425

Either via transovarial transmission (to offspring and then into the human) or via an intermediate infected animal (to another tick and then into the human)

Front 426

What are the obligate intracellular parasites and how are they transmitted?

Back 426

Rickettsia: Dermacentor ticks; Coxiella: aerosol-inhalation; Ehrlichia: Amblyomma ticks; Anaplasma: Ixodes, Dermacentor ticks; (and Chlamydia: STD)

Front 427

What are the two groups of Rickettsia?

Back 427

Spotted fever group: always produces rash, affect endothelial and smooth muscle cells, includes Rickettsia rickettsii (causative agent of Rocky Mountain Spotted Fever – RMSF);
Typhus fever group: sometimes produce rash, affect endothelial cells, includes Rickettsia prowazekii (Epidemic typhus fever) and Rickettsia typhi/prowazekii (Endemic typhus fever)

Front 428

What characterizes Rickettsia?

Back 428

Gram(-), non-motile, slow-growing; Parasitize animal for ATP

Front 429

What characterizes Q fever?

Back 429

Caused by Coxiella burnetii; Transmission occurs via aerosolized particles (cells are resistant to desiccation) which can come from contaminated milk, hides, dried feces, amniotic fluid, and placental tissues (!); High numbers are associated with birthing of infected cattle, sheep, goats

Front 430

What characterizes Human granulocytic ehrlichiosis (HGE)?

Back 430

Caused by Anaplasma phagocytophilia; Transmitted by the Deer tick (Ixodes scapularis) and Dog tick (Dermacentor variabilis); Diagnosis: inclusion in granulocytes, IFA, serology (at later stage); Treatment: Doxycycline

Front 431

What characterizes Human monocytic ehrlichiosis (HME)?

Back 431

Caused by Ehrlichia chaffeensis; Transmitted by the Lone star tick (Amblyomma), seen in the South (esp. with golfer); Causes leukopenia and thrombocytopenia; Diagnosis: IFA, serology (at a later stage); Treatment: Doxycycline

Front 432

What signs/symptoms are associated with Ehrlichia and Anaplasma?

Back 432

Fever, HA, ↑liver enzymes, myalgia, leukopenia, thrombocytopenia

Front 433

How does Coxiella burnetii multiply in the human host?

Back 433

After being endocytosed, fusion with the lysosome activates Coxiella and allows it to multiply inside of the phagolysosome

Front 434

How is Q fever diagnosed, and what is the treatment?

Back 434

Diagnosis: serology, PCR; Treatment: Tetracycline

Front 435

What are the signs/symptoms of Q fever?

Back 435

Fever, intense HA, malaise, chills, pneumonitis; can lead to endocarditis and death

Front 436

How is the diagnosis of Epidemic typhus fever made?

Back 436

Rash on trunk, stupor; Seen in Africa and S. America – Prevention: sanitary conditions; Treatment: Tetracycline

Front 437

What is Endemic typhus fever associated with?

Back 437

Rat flea, flying squirrels

Front 438

Why is aspirin contraindicated with hemorrhagic fever?

Back 438

It prevents clotting, leading to increased bleeding

Front 439

What is the treatment for Dengue?

Back 439

Hydration, avoid aspirin

Front 440

What are preventative measures for Dengue?

Back 440

Wear DEET; wear clothes that cover arms, legs, feet; close unscreened doors/windows; No good vaccine available

Front 441

How is the laboratory diagnosis of Dengue made?

Back 441

Leukopenia, thrombocytopenia, elevated serum transaminases; ELISA, RT-PCR (during acute phase), test for viral antigen in blood, test for virus in growth culture; measure an increase in antibody titer over acute vs. convalescent serum

Front 442

Which Dengue infection is most severe?

Back 442

Reinfection with a second serotype: due to the production of some non-protective antibodies during the initial infection causing greater uptake of viruses into monocytes/macrophages during the second infection (this gives the virus greater access to macrophages, where they reproduce) –
also occurs in concurrent infection with two serotypes

Front 443

What describes the signs/symptoms of Dengue?

Back 443

Incubation period: 3-14 days; May be asymptomatic; s/s: fever, chills, severe HA, myalgias, bone and joints of very painful (breakbone fever), rash with severe itching, leukopenia, thrombocytopenia, elevated serum transaminases; Severe manifestations: Dengue hemorrhagic fever, Dengue shock syndrome

Front 444

What characterizes Dengue?

Back 444

Replicates in the cytoplasm of monocytes/macrophages; Transmitted by the mosquito Aedes aegypti (feeds on humans and primates); can also undergo transovarial transmission; It is the most prevalent arboviral disease; there are 4 serotypes (protection against one serotype does not mean protection against the others)

Front 445

What three manifestations are seen with arboviral infections?

Back 445

Hemorrhagic fever (small vessels  petechiae and intestinal hemorrhage); CNS involvement (meningitis, meningoencephalitis); Liver damage

Front 446

What describes the replications of Flaviviruses?

Back 446

Viral RNA is translated into a large polyprotein --> the first protein is cleaved and acts as a protease --> the protease cleaves the polyprotein to generate capsid proteins and polymerase --> polymerase makes the (-)RNA strand which serves as the template for viral nucleic acids

Front 447

What characterizes Flaviviruses?

Back 447

(+) ssRNA, enveloped, no polyA tails; Includes Dengue, Yellow Fever virus, West Nile virus, Tick-borne Encephalitis virus, St. Louis Encephalitis virus

Front 448

What describes the symptomatology of WNV?

Back 448

Incubation period: 3-14 days; ~80% are asymptomatic; ~20% get “West Nile Fever”; <1% will develop CNS disease (10% of which is fatal); West Nile Fever consists of fever, chills, HA, fatigue (can be severe), n/v, rash (usually not itchy, lasting a few days, mainly on chest/back/ abdomen/arms) – persistent fatigue is common and may continue for months

Front 449

What is the treatment for WNV?

Back 449

None available (α-IFN being tested)

Front 450

How is the diagnosis of WNV made?

Back 450

Suspect in meningitis, encephalitis, flaccid paralysis from summer through fall (or December in the South); should also consider other arboviral diseases (St. Louis/La Crosse); History of recent travel; Test serum of CSF for WNV IgM/IgG

Front 451

What characterizes WNV-associated flaccid paralysis?

Back 451

Affects relatively healthy young people; may not have fever/HA before paralysis; Clinical hallmarks: onset early in infection, weakness can often be in only one limb, absence of numbness, pain sometimes present

Front 452

What age group is WNV more so seen in?

Back 452

Elderly

Front 453

What characterizes WNV encephalitis?

Back 453

More likely than meningitis patients to have memory problems, dysarthria, dysphagia, focal motor abnormalities (incl. cranial nerve palsies); severity ranges from mild confusion to coma/death

Front 454

What characterizes WNV meningitis?

Back 454

More likely than encephalitis patients to have myalgias, arthralgias, n/v, rash , back pain; can see WBC in CSF; HA may be quite severe; Most people improve though persistent symptoms may include fatigue, weakness, and memory/concentration problems

Front 455

What characterizes West Nile virus?

Back 455

Has only recently made its way to the US; Transmission occurs through the mosquito;
birds (crows and blue jays) are considered amplifying hosts (i.e. they allow for massive viral reproduction), after which mosquitoes become more likely to infect humans; Most cases occur late summer and in the fall

Front 456

Besides mosquito bites, what other modes of transmission exist for WNV?

Back 456

Blood transfusions (now tested for viral nucleic acid), organ transplantation, intrauterine infection, breast milk (probable)

Front 457

How does transmission of Dengue and West Nile virus (WNV) differ?

Back 457

The mosquitoes associated with Dengue bite mostly early during the day, whereas those associated with WNV bite more commonly during dusk and in the evening

Front 458

What characterizes Yellow Fever?

Back 458

Also known as black vomit fever; Transmitted by Aedes species (incl. A. aegypti); very common disease; Undergoes two cycles: monkey --> human (jungle fever), human --> human (most common); can also see transovarial transmission

Front 459

What is the symptomatology associated with La Crosse encephalitis?

Back 459

Fever, HA, n/v, lethargy; severe disease incl. seizures, coma, paralysis, disorientation, increase in cranial nerve pressure, meningitis; in some pts, long-term behavior and cognitive deficits persist

Front 460

What describes the epidemiology and transmission of La Crosse encephalitis?

Back 460

WV is among states where it is most common (50% of US cases); seen in heavily wooded areas where Aedes triseriatus and rodents live together; Chipmunks and squirrels serve as amplifying vectors; can be transmitted transovarially

Front 461

What characterizes La Crosse encephalitis (a Bunyavirus) and its replication cycle?

Back 461

(-) ssRNA virus, 3 segments, enveloped; one segment codes for the replicase; Enter cell by RME --> virus ribonucleoprotein escapes into the cytoplasm, then into the nucleus --> (-) strand of RNA transcribed into (+) strands --> viral encoded RNA polymerase generates (-) strand viral genomes --> assembled viruses escape cell by budding, with plasma membrane lipids

Front 462

What are prevention measures regarding Yellow Fever?

Back 462

Eliminate sites where Aedes mosquitoes grow; Vaccination (live attenuated vaccine) – treatment is supportive only

Front 463

How is the diagnosis of Yellow Fever made?

Back 463

Patient history; ELISA, RT-PCR, FA, culture

Front 464

What describes the symptomatology of Yellow Fever?

Back 464

Incubation period: 3-6 days; Acute phase: fever, HA, muscle aches (back, knees), n/v, loss of appetite, dizziness, red eyes/face/tongue; Toxic phase (15% of cases): jaundice, abdominal pain, vomiting (sometime blood), decreased urination, bleeding from nose/mouth/eyes, arrhythmias, liver/kidney failure, brain dysfunction (incl. delirium, seizures, coma), death (20-50% of toxic cases)

Front 465

What are the outcomes for WNV?

Back 465

Younger age is more predictive of full recovery than is initial illness severity; WN meningitis mortality is almost none, while WN encephalitis mortality is 15-25%; With WN flaccid paralysis some people have almost complete recovery, others continued weakness

Front 466

What characterizes Tick-borne encephalitis?

Back 466

Transmitted by the Deer tick; not endemic in the US, prevalent in Europe and Asia

Front 467

What characterizes St. Louis encephalitis?

Back 467

Transmitted by the Culex mosquito throughout the US; transmission is from infected birds to humans; most have a mild case, few develop encephalitis; rare disease

Front 468

What are the alphaviruses?

Back 468

Eastern equine encephalitis (EEE), Western equine encephalitis (WEE), Venezuelan equine encephalitis (VEE)

Front 469

What characterizes WEE?

Back 469

Most cases are unapparent; natural cycle involves birds/mosquitoes; inactivated vaccine available

Front 470

What characterizes EEE?

Back 470

Rare but deadly disease (if disease progresses to encephalitis, mortality is 90%); there is a vaccine available for horses and laboratory workers

Front 471

What can cause impairment of the CMI (Cell-Mediated Immunity)?

Back 471

Certain medications (immunosuppressives, corticosteroids); AIDS; extremes of age; lymphomas; malnutrition

Front 472

What infections are associated with asplenia?

Back 472

Certain encapsulated bacteria: *Streptococcus pneumoniae (MOST IMPORTANT), Haemophilus influenzae
Other bacteria: Neisseria meningitidis, Salmonella species, C. canimorsus (dog contact)
Other infections worse after splenectomy: Babesiosis; Ehrlichiosis

Front 473

What are examples of common humoral deficiencies? What is the common presentation?

Back 473

Primary Immunoglobulin deficiencies
Genetic, X-linked agammaglobulinemia (rare; severe)
Acquired: Selective IgA deficiency - most common humoral defect in population at large
Common Variable Immunodeficiency – decreased levels of IgG, IgM, IgA
*Both acquired disorders may present with recurrent sinus and pulmonary infections

Front 474

Why do bacteria produce a capsule?

Back 474

Protection from PMNs (granulocytes)

Front 475

What type of organisms does humoral immunity provide protection?

Back 475

Important in protection against infection w/ bacteria, esp. encapsulated ones; Strep. pneumoniae, H. influenzae

Front 476

What is a common manifestation of a Listeria (g + rod) infection?

Back 476

Meningitis

Front 477

What infections are associated with defects in the CMI?

Back 477

Bacteria (esp. intracellular pathogens): Mycobacteria, Legionellae, Listeria, Nocardia, Salmonella;
Fungi: Cryptococcus, Histoplasma, Pneumocystis jirovecii
Viruses: Cytomegalovirus, Herpes simplex, Varicella-zoster virus
Parasites: Toxoplasma gondii (found in brain, pathology exclusive to CMI defect)

Front 478

What is the most common defect of neutrophils?

Back 478

Neutropenia (absolute count <1000)

Front 479

What infection is associated with complement deficiencies (esp. C5-C9)?

Back 479

Neisseria meningitidis (!) (possibly Neisseria gonorrhea)

Front 480

What infections are associated with neutropenia?

Back 480

Mainly organisms of natural flora - Gram negative enteric rods, Pseudomonas aeruginosa, Staph & Strep species, Candida (esp. retina, liver/spleen), Aspergillus

Front 481

What other disease states are associated with lower immunoglobulin levels or function?

Back 481

CLL; multiple myeloma; nephrotic syndrome; splenectomized patients; AIDS

Front 482

What diagnostic test is used to ID Cryptococcus neoformans?

Back 482

India ink, Crypto Antigen test

Front 483

Which causes of meningitis present chronically w/ low CSF glucose?

Back 483

Cryptococcus neoformans, other fungi, Mycobacterium tuberculosis,
Less likely:
Listeria monocytogenes (but course is probably too long)
Viruses such as CMV, HSV, VZV etc, (CSF glucose usually only slightly depressed in viral CNS infection)

Front 484

What diagnostic test should be used in a patient w/ recurrent sinus/pulmonary infections? Which organisms involved? Possible diagnosis? Tx?

Back 484

CBC, differential and platelet count, PPD and controls (screening test for cell-mediated immunity), quantitative serum immunoglobulin levels, HIV antibody test, CD4 count.
Pyogenic bacteria especially encapsulated species (ex. Streptococcus pneumoniae, Haemophilus influenzae)
Dx - Common Variable Immunodeficiency - they won’t respond to vaccines
Tx - IV Ig

Front 485

Does undernutrition occur solely in poor populations?

Back 485

No – it occurs in affluent as well as poor populations

Front 486

What are two examples of PEM?

Back 486

Marasmus, Kwashiorkor

Front 487

What tests are used to assess PEM in each of the two functional protein compartments?

Back 487

Somatic compartment: body weight and height vs. standard, loss of fat (reduced thickness of skin folds), loss of muscle (reduced mid-arm circumference)
Visceral compartment: measure of visceral proteins (albumin, prealbumin, transferin)

Front 488

What are the two functional protein compartments and what diseases are associated with PEM in each?

Back 488

Somatic compartment (skeletal muscles): more affected by calorie deficiency --> marasmus
Visceral compartment (liver): more affected by protein deficiency --> kwashiorkor

Front 489

What are some common causes of malnutrition?

Back 489

Ignorance/poverty: PEM in elderly/homeless/poor, unrecognized increased nutritional needs in infants/adolescents/pregnant women
Chronic alcoholism: PEM, more risk for vitamin deficiencies (thiamine, pyridoxine, folate, vitamin A), multifactorial causes (poor diet, absorption, high loss, etc)
Acute/chronic illnesses: elevated BMR (e.g. burn patients), increased requirement for all nutrients
Self-imposed dietary restriction: anorexia, bulimia, body-image-concerned, fearful of CV disease

Front 490

What are some uncommon causes of malnutrition?

Back 490

Malabsorption syndromes, genetic diseases, drug therapies that interfere with uptake of a specific nutrients, total IV nutrition

Front 491

Where in the world is protein-energy malnutrition (PEM) most common?

Back 491

In 3rd world (affects up to 25% of children) and developing countries, whereas overnutrition is prevalent in industrialized nations

Front 492

What body in the US is responsible for setting the daily allowances for proteins, vitamin, and minerals for healthy adults?

Back 492

National Research Council

Front 493

What is secondary malnutrition?

Back 493

Malnutrition despite nutrient supply deemed to be adequate for a normal person – this can be due to various reasons: malabsorption, impaired use/storage of nutrients, excess loss of nutrients, increased need for nutrients (burn patients)

Front 494

What is an adequate diet?

Back 494

One that provide energy in form of carbohydrates/fat/proteins, essential AA, essential fatty acids, vitamins, and minerals – any diet missing one or more of these components in adequate amounts is called “primary malnutrition”

Front 495

What clinical findings are associated with Kwashiorkor?

Back 495

Enlarged and fatty liver due to lack of lipoprotein production in liver to mobilize fats
“Flaky paint” appearance of skin with alternating areas of hypo/hyperpigmentation and desquamation

Front 496

What characterizes Anorexia nervosa and Bulimia nervos?

Back 496

Anorexia nervosa: Self-induced starvation, marked weight loss
Builima nervosa: binge-eating followed by self-induced vomiting

Front 497

What changes occur similarly in both Kwashiorkor and Marasmus?

Back 497

Hypoplastic bone marrow --> reduced RBCs --> anemia (hypochromic microcytic, mixed micro/macrocytic with folate deficiency)

Front 498

What changes occur mostly in Kwashiorkor and rarely in Marasmus?

Back 498

Reversible small bowel mucosal atrophy, loss of villi and digestive enzymes (e.g. disaccaridase deficiency --> leading to milk intolerance in babies), Liver enlargement due to fatty liver

Front 499

How does BMR change in chronic starvation and cachexia?

Back 499

Decreases in chronic starvation, increases in cachexia due to cytokines produced during sepsis or by tumors (e.g. TNF)

Front 500

What is cachexia?

Back 500

Severe form of Marasmus seen in chronic illnesses (lung/GI, cancer) – associated with loss of SC fat, wasting of quadriceps/deltoid muscles, and ankle and sacral edema

Front 501

What is a clinical setting in which Kwashiorkor is seen?

Back 501

Acute, catabolic illness (severe trauma, burn, sepsis), develops over weeks, leads to low serum albumin (<2.8 gm/dL), edema, easy pluckable hair (normal fat and muscle)

Front 502

What characterizes Marasmus?

Back 502

Reduced caloric intake, >60% reduction in body weight with extremities emaciated, head appearing too large, and deficiency in immune system – associated with loss of somatic protein, muscle mass, SC fat; visceral protein depletion is slight (serum albumin normal or slightly reduced)

Front 503

What characterizes Kwashiorkor?

Back 503

More severe than Marasmus, caloric intake is reduced and consists of carbs, protein intake is severely reduced --> hypoalbuminemia --> edema, depletion of visceral protein, 60-80% of normal weight, relative sparing of SC fat and muscle mass

Front 504

What is a clinical setting in which Marasmus is seen?

Back 504

Chronic illness (chronic lung/GI disease, cancer), develops over months, leads to loss of weight/muscle/SC fat with normal or mildly reduced serum proteins

Front 505

What are measures of fat accumulation?

Back 505

BMI (kg per square meter): underweight: < 18.5, normal: 18.5-24.9, overweight: 25.0-29.9, obese: ≥ 30
Skin fold measurements, body circumferences (ratio of waist to hip)

Front 506

What are effects of diet on systemic diseases?

Back 506

Low sodium intake: reduces HTN – dietary fiber: reduces colon diverticulosis
Omege-3 fatty acids in diet: significantly reduces fatal MI
Caloric restriction: increases lifespan in experimental animals

Front 507

What are some obesity-related conditions?

Back 507

Insulin resistance/hyperinsulinemia: type II diabetes, improves with weight loss
HTN: risk increases with weight in previously normotensive individuals, may be due to hyperinsulinemia
Non-alcoholic steatohepatitis, cholelithiasis (gallstones), osteoarthritis, venous thrombosis, ischemic stroke
Hypoventilation syndrome (Pickwick syndrome): day and night hypersomnolence, sleep apnea, polycythemia, right-sided heart failure
Metabolic syndrome (syndrome X): abdominal obesity, insulin resistance, hyperTAGemia, low serum HDL, HTN, increased risk of CAD (!)

Front 508

What system in the body regulates energy intake and expenditure?

Back 508

Lipostat or internal set point: keeps body weight in narrow range for years, regulation is done by hormones
Ghrelin (short term control): secreted by stomach, increases before meals, decreases when full
Leptin (long term control): produced by fat cells, inhibits anabolism, triggers catabolism, net effect is reduce food intake and increase energy expenditure (!) ***

Front 509

What shape of central obesity is associated with higher risk of high BMI morbidities?

Back 509

Apple-shape with abdominal and chest fat confers higher risk morbidities (pear –shape with fat in thighs/hips confers lower risk)

Front 510

What are two general positions of fat accumulation in people with high BMI?

Back 510

Central (visceral), subcutaneous

Front 511

What morbidities are associated with high BMI?

Back 511

Beginning at BMI of 25, there is increased prevalence of diabetes, HTN, CAD, osteoarthritis

Front 512

What are the clinical findings in Anorexia nervosa?

Back 512

Similar to severe REM plus endocrine effects: amenorrhea (low GRH), low thyroid hormone (cold intolerance, bradycardia, constipation, dry skin, fine/pale hair), decreased bone density (low estrogen, mimicking post-menopausal osteoporosis), lymphopenia, anemia, hypoalbuminemia

Front 513

What are the clinical findings in Bulimia nervosa?

Back 513

Less amenorrhea (<50%), normal weight, major complications due to vomiting (electrolyte imbalance, hypokalemia, arrhythmias – aspiration – rupture of esophagus)

Front 514

What is leading cause of death in Anorexia nervosa?

Back 514

Cardiac arrhythmia and sudden death due to hypokalemia

Front 515

What is the consensus on the effect of diet on carcinogenesis?

Back 515

There is no definite proof that diet can cause or protect against cancer (!) ***

Front 516

What aspects of a clinical history suggest pesticide illness?

Back 516

Multiple cases with similar symptoms and an exposure history; History of chemical application (home or office); Accidental ingestion (esp. children); Suicide/homicide attempts

Front 517

What characterizes rodenticides?

Back 517

In general, they have no target selectivity (except for behavioral differences between various animas), some include emetics so that cats/dogs/babies will vomit, but rodents won’t (lack reflex)

Front 518

What are examples of fungicides that are toxic to humans?

Back 518

Thiocarbamates (e.g. Zineb): sensitizer in skin patch test, dermatitis, Antabuse-like reaction;
Phtalimide derivatives (e.g. Captan): sensitizes, dermatitis;
Substituted aromatics (e.g. Chlorothalonil, Hexachlorobenzene): sensitizes, dermatitis;
Inorganic (e.g. elemental sulfur): skin irritant

Front 519

What characterizes the bipyridyl herbicides?

Back 519

Broad-spectrum herbicides; Paraquat: highly toxic, use restricted to registered pesticide applicators, overexposure results in lung toxicity (active transport into the lung --> produces ROS); Diquat: overexposure results in GI/renal toxicity

Front 520

What characterizes the chlorophenoxyacetic acids?

Back 520

Used for broadleaf plants; Key compound is 2,4-dichlorophenoxyacetic acid (2,4-D); Overexposure causes muscle weakness, aching and tenderness, renal failure

Front 521

What characterizes herbicides?

Back 521

Chemicals that kill plants; in general, they have low toxicity (except for some dermal irritation); Examples that do affect humans incl. chlorophenoxyacetic acids and bipyridyl herbicides

Front 522

What are the signs/symptoms of pesticide illness?

Back 522

Non-specific s/s: rash, flu-like symptoms (dizziness, malaise, respiratory tract irritation), GI symptoms, seizures, odor-related effects (not toxicological effects of active ingredient)

Front 523

What pesticides or metabolites can be detected in the general population due to exposure?

Back 523

Organophosphates: parathion, chlorpyrifos; Organochlorines: DDT-related compounds;
Pyrethrin; Herbicides: 2,4-D; Pest repellents: DEET

Front 524

What substances are found in pesticide formulations?

Back 524

Technical grade chemical (the active ingredient); Adjuvants/synergists; “Inert” ingredients (does not mean biologically inactive, just means that they are not the active ingredient)

Front 525

What is the US EPA toxicity classification?

Back 525

Class I: danger, fatal if ingested, corneal opacity, corrosive to skin;
Class II: warning, may be fatal if ingested, reversible corneal opacity, severe skin irritation;
Class III: caution, harmful if ingested, no corneal opacity, moderate skin irritation;
Class IV: caution, may be harmful if ingested, no eye irritation, mild/no skin irritation

Front 526

What are examples of other rodenticides?

Back 526

Coumarins/Indandiones: decrease synthesis of clotting factors, increase capillary permeability, these incl. warfarin, brodifacoum/difenacoum (“superwarfarins”), chlorphacinone (Indandione);
Zinc phosphide: causes pulmonary edema in dust form, when ingested a phosphine is formed and absorbed in the gut leading to n/v, hepatic failure, hypoglycemia, renal tubular damage, cardiomyopathy, ventricular arrhythmias

Front 527

What characterizes the pyrethrin and pyrethroids?

Back 527

Products of chrysanthemums, natural products (contact allergies, asthma, anaphylactic reactions); Frequent cause of pesticide-induced symptomatic illness (generally not fatal in the US);
Examples: pyrethrin, fenvalerate, permethrin; MoA: alters ion flux across neutral membranes;
Overexposure: neuronal hyperactivity, incoordination, tremors with hyperthermia, seizures;
Treatment: Diazepam

Front 528

What are the signs/symptoms of overexposure to organochlorine insecticides and what is the treatment?

Back 528

Overexposure: paresthesias (esp. of tongue/face/lips), apprehension, irritability (highly responsive to stimuli), tremors, convulsion; Treatment: Diazepam, Phenobarbital

Front 529

What is the mechanism of action of organochlorine insecticides?

Back 529

Interfere with ion movements across neutral tissue membranes (GABA related)

Front 530

What characterizes the organochlorine insecticides?

Back 530

Examples incl. dichlorodiphenylethanes (DDT, dicofol [Kelthane]) and chlorinated benzenes (lindane); Most are banned because of environmental problems (resistant to degradation in environment, bioaccumulation, DDT has estrogenic effects/impaired fertility/eggshell thinning)

Front 531

What characterizes the insecticides?

Back 531

Highly lipid soluble, metabolism via bioactivation/inactivation, generally neurotoxic;
Classes: organochlorines, pyrethrins/pyrethroids, cholinesterase inhibitors (carbamates, organophosphates)

Front 532

What characterizes DEET (diethyltoluamide)?

Back 532

Common pesticide implicated in symptomatic illness; Causes skin irritation to blistering and erosion (esp. in occluded areas); When systemically absorbed, causes toxic encephalopathy (HA, restlessness, irritability, incoherent speech, ataxia, loss of consciousness, seizures) – children should use DEET concentrations below 10% (discontinue with emotional/behavioral change)

Front 533

What are examples of rodenticides that function as convulsants?

Back 533

Compound 1080: blocks energy metabolism, induces metabolic acidosis, shock, arrhythmias, neurotoxicity (violent tonic-clonic convulsions); Strychnine: direct convulsant

Front 534

What signs/symptoms are seen in agricultural workers exposed to cholinesterase inhibitors?

Back 534

GI distress (n/v), miosis, urinary frequency, sweating, weakness, bradycardia

Front 535

By what mechanism does irreversible inhibition of AChE come about?

Back 535

The serine residue on AChE attacks phosphate on the organophosphate molecule --> the OP becomes attached to the serine residue and does not undergo hydrolysis to return to the original state (i.e. AChE is stuck with the OP and cannot perform any more reactions)

Front 536

What is the mechanism of ACh hydrolysis by acetylcholinesterase?

Back 536

ACh docks inside AChE --> a serine residue on AChE attacks the acetyl portion of ACh, causing it to become attached to the serine residue --> water then attacks the acetyl molecule on serine, causing it to be released, and returning AChE to its original state

Front 537

What long-term effects are seen in patients exposed to high levels of organophosphates?

Back 537

Long-term effects: fasciculations, weakness, impaired memory/concentration, emotional lability;
Intermediate syndrome (1-4 days after acute): muscle weakness, respiratory distress;
Chronic toxicity (OP-induced delayed neuropathy, OPIDN): axonal/myelin degeneration, occurs with some non-pesticide organophosphates, is due to neurotoxic esterase inhibition

Front 538

What is the treatment for cholinesterase inhibitor overexposure?

Back 538

Atropine: competes with ACh at the receptor, dose must be repeated every 10-30 minutes;
2-PAM: reactivates enzyme (for organophosphates only), adverse effects incl. arrhythmias/HTN

Front 539

What can be done for a lab diagnosis of exposure to cholinesterase inhibitors?

Back 539

Blood tests for “true”/acetylcholinesterase (RBC) or “pseudo”/butyrylcholinesterase (plasma);
Urine metabolites; Foliage and clothing pesticide residues – diagnosis is primarily clinical

Front 540

What signs/symptoms are seen in children exposed to cholinesterase inhibitors?

Back 540

Cholinergic signs less pronounced; Can see seizures, mental status changes, flaccid muscle weakness

Front 541

What characterizes the carbamate insecticides?

Back 541

Examples incl. carbaryl (Sevin); MoA: reversible inhibition of acetylcholinesterase; Overexposure: same symptoms as organophosphates; Overexposure treatment: Atropine

Front 542

What are the signs/symptoms of cholinesterase inhibition?

Back 542

All are due to excess acetylcholine (parasympathetic, somatic, CNS stimulation) –
Eyes: miosis, blurred vision; Glands: tearing, salivation, sweating, pulmonary edema;
Heart: bradycardia, tachycardia; Smooth muscle: bronchoconstriction, vomiting, diarrhea, urination; Skeletal muscle: fasciculations, twitching, cramps, weakness, paralysis;
CNS: HA, malaise, anxiety, confusion, impaired memory, convulsions, coma

Front 543

What characterizes the organophosphate (OP) insecticides?

Back 543

Number one pesticide implicated in fatal poisonings; Examples incl. parathion, malathion;
MoA: inhibition of acetylcholinesterase (can be become irreversible)

Front 544

What is meant by the “aging” of AChE?

Back 544

The irreversible inhibition of AChE (the pace at which “aging” occurs depends on the chemistry of the AChE inhibitor)

Front 545

What are the signs/symptoms for skin exposure to a nerve agent?

Back 545

Skin sweating at the site, muscle fasciculation in the area, systemic GI effects (30min-18hrs later)

Front 546

What is the treatment for exposure to nerve agents (Sarin, Soman, or VX)?

Back 546

Atropine, 2-PAM, Diazepam, Atropine (topical for eye pain from miosis)

Front 547

What are common effects that occur with exposure to Sarin, Soman, or VX?

Back 547

Runny nose, watery eyes, miosis, eye pain, blurred vision, drooling, excessive sweating, cough, chest tightness, tachypnea, d/n/v, increased urination, confusion, drowsiness, weakness, HA, slow or fast HR, abnormally low or high BP – with vapor exposure, effects can appear within seconds; with liquid exposure, effects can appear within minutes to up to 18hrs; latex/polyvinyl gloves are not a good barrier for handling these agents (use nitrile/neoprene gloves)

Front 548

What characterizes VX?

Back 548

It is an oily liquid, amber in color; it evaporates very slowly, but contact is considered lethal; it is odorless and tasteless

Front 549

What characterizes Sarin nerve gas?

Back 549

The most volatile of the nerve agents; clear, colorless, and tasteless liquid that has no odor –
Soman is a nerve gas of the same class that causes “aging” within 2 minutes of exposure

Front 550

How does 2-PAM work?

Back 550

It attacks the phosphate group that is bound to the inactivated serine residue on AChE, and causes AChE to return to its original state, thus restoring its functionality – treatment must be given before the “aging” reaction takes place

Front 551

What is the role of metabolism with solvent toxicity?

Back 551

Acute effects on CNS are due to parent compound; Delayed toxicities are associated with metabolites formed in affected tissue

Front 552

What characterizes hexacarbon neuropathy?

Back 552

Caused by the metabolite of hexane and methyl-N-butyl ketone: 2,5-hexanedione; this compound forms a pyrrole with lysine, which then causes cross-linking of neurofibrils, thus inhibiting neurofibril transport; this leads to swelling of axons as proteins accumulate

Front 553

What are the aromatic hydrocarbons that cause solvent toxicity?

Back 553

Benzene: used for high-speed printing/latex rubber coating/anti-knock, causes bone marrow toxicity (aplastic anemia/leukemia), metabolites incl phenol/catechol/hydroquinone/benzoquinone, hydroquinone and benzoquinone are involved in a redox cycle and generate ROS;
Toluene: causes CNS depression, atrophy (with high exposure), ototoxicity, liver/kidney toxicity, reproductive toxicity (possible) – both are metabolized by CYP2E1

Front 554

What other signs/symptoms are seen with solvent toxicity?

Back 554

Toxic peripheral neuropathy (axonopathy), hearing loss, hematological effects (leukemia, aplastic anemia), renal effects (tubular toxicity, cancer), asthma

Front 555

What characterizes the chronic symptomatology of solvent-related diseases?

Back 555

Chronic toxic encephalopathy – Mild/type 1: fatigue, memory impairment, irritability, difficulty concentrating, mild mood disturbance; Mild chronic/type 2: sustained personality changes, impaired intellectual function/learning capacity); Severe chronic/type 3 (Painter’s syndrome/ psycho-organic syndrome): global deterioration, cerebellar/cerebral atrophy in abusers

Front 556

What characterizes the acute symptomatology of solvent-related diseases?

Back 556

Acute intoxication: CNS depression (sedation, narcosis, anesthesia);

Front 557

Which CYP enzyme is involved in the formation of toxic metabolites from solvents?

Back 557

CYP2E1 (induced by alcohol, poorly controlled diabetes, and fasting)

Front 558

What are important properties of the various solvents?

Back 558

Polar vs nonpolar, hydrophilic vs lipophilic, volatility, flammability – in terms of toxicity, nonpolar, lipophilic solvents have the greatest concern

Front 559

What aspects of solvent exposure are regulated?

Back 559

Time weighted average (TWA) of solvent exposure (i.e. the total amount over a period of time);
Acceptable ceiling concentration/short-term exposure limit (i.e. the maximum peak concentration)

Front 560

What are solvents used for?

Back 560

Degreasing agents, vehicle for coatings, chemical manufacturing, (also with manicures)

Front 561

What characterizes carbon disulfide (CS2)?

Back 561

Used for the production of rayon/cellophane; Exposure effects: organic brain damage (memory loss, mood changes), hearing loss, visual disturbances, distal neuropathy/axonopathy (neurofilament cross-linking), atherosclerosis

Front 562

What characterizes the glycols (e.g. ethylene glycol, propylene glycol)?

Back 562

Ethylene glycol: used as antifreeze, metabolized to oxalic acid, causes renal toxicity (oxalate stones), treatment is fomepizole; Propylene glycol: used as a drug vehicle, metabolized to lactate

Front 563

What characterizes the aliphatic alcohols (ethanol, methanol)?

Back 563

Ethanol: anesthetic (poor therapeutic index), induces CYP2E1, metabolized to acetaldehyde and acetic acid; Methanol: causes CNS depression, blindness, acidosis, metabolized to formaldehyde and formic acid (builds up), treated by inhibiting its metabolism (i.e. via ethanol or fomepizole – fomepizole does not have the CNS depressant effects of ethanol)

Front 564

What characterizes the chlorinated ethane/ethylene derivatives (e.g. trichloroethylene)?

Back 564

Used as a degreasing agent (dry cleaning) and anesthetic (formerly); Exposure effects: myocardial sensitization, increases sensitivity to ethanol, renal cancer, impaired intrauterine growth, cardiac teratogenesis; Metabolized by CYP enzymes and alcohol dehydrogenase (competitive inhibition); toxic metabolites are formed through CYP enzymes and through glutathione conjugation (in the kidney)

Front 565

What characterizes the halomethanes: chloroform, carbon tetrachloride, methylene chloride?

Back 565

CHCl3, CCl4: water disinfection by-products, used in pharmaceutical industry, causes centrilobular necrosis, both undergo bioactivation by P450, toxicity increased by fasting/alcohol/poorly controlled DM (i.e. induction of CYP2E1), they sensitize heart muscle to arrhythmogenic effects of endogenous epinephrine; CH2Cl2: paint stripper/degreasing agent/former fire extinguisher/ decaffeinating agent (not anymore), metabolized to CO, previous exposure standard was based on minimizing carboxyhemoglobin formation but currently based on carcinogenicity

Front 566

What characterizes dimethylformamide – HCON(CH3)2?

Back 566

Used for acrylic fiber spinning, chemical manufacture, coatings/adhesives, textile dyes, printing;
Exposure effects: easily absorbed across skin/lungs, HA, dizziness, abd. pain, n/v, constipation, liver damage, alcohol intolerance, possibly carcinogenic

Front 567

What are the most common side effects associated with the use of NSAIDs?

Back 567

GI upset (can cause ulcers, most common); Renal problems (due to effects on PG’s then can change intrarenal blood flow & lead into kidney failure); Lung problems (causes exacerbation of asthma)

Front 568

Beyond steroids and NSAIDs, What is the most commonly prescribed drug for the treatment of RA in the US?

Back 568

Methotrexate

Front 569

How many people with RA take steroids for treatment?

Back 569

About 50% of pts take a small dose of prednisone every day

Front 570

What is the most severe side effect of steroids?

Back 570

Really lowers resistance to infections (also weight gain, diabetes, osteoporosis, cataracts)

Front 571

What is the safest drug known for the treatment of RA?

Back 571

Hydroxychloroquine

Front 572

What antimalarial agent is used as a treatment of RA?

Back 572

Hydroxychloroquine, MOA is unknown

Front 573

What Gold historically used in treating?

Back 573

RA, given as shots; Example of the 1st controlled trial of a drug in the treatment of a disease that showed efficacy, done in England before WWII

Front 574

What are the symptoms of Rheumatoid Arthritis?

Back 574

Morning stiffness (most prominent), Joint swelling in wrists, MCP & PIP joints, & Joint Pain

Front 575

What do all NSAIDs how in common?

Back 575

They are all prostaglandin synthetase inhibitors, they work by interfering w/ the synthesis of intermediaries of metabolism that are all prostaglandin or prostaglandin-related, they all have the same efficacy & very similar side effect profiles

Front 576

How does essentially everyone with RA begin treatment?

Back 576

NSAIDs (Aspirin, Ibuprofen, Naprosyn, Naproxen,, Tolmine Sodium, Indomethacin)

Front 577

What is the Theoretical advantage of giving Etanercept & Adalimumab over Infliximab?

Back 577

You do not having this crossing species line issues because they are all human vs Infliximab which is part human part mouse chimeric antibody, Theoretically the immunological rxn in the pts body to receiving these injections will be less with Etanercept & Adalimumab than with Infliximab

Front 578

What drugs can cause reactivation of TB?

Back 578

Biologics, particularly Infliximab, you need to check the pt’s PPD before starting treatment

Front 579

What are the two main side effects apart from the immunologic factors of biologics?

Back 579

Site reaction where the shot is given (most common)May be an increased incidence of cancers (lymphomas, adenocarcinomas), Increased Incidence of infections, demyelination of the CNS

Front 580

What receptor fusion protein is used for the treatment RA?

Back 580

Etanercept (Enbrel), It is a receptor for TNF- α that you give by injections and it circulates in their circulation, & soaks up the TNF-α

Front 581

What Human-mouse chimera antibody is used for the treatment RA?

Back 581

Human-mouse chimera antibody to TNF- α, Anti-TNF- α antibody

Front 582

What Human Monoclonal Antibody is used for the treatment RA?

Back 582

Adalimumab (Humira), it is a circulating antibody to TNF- α

Front 583

What are the biologics used for the treatment of RA?

Back 583

Etanercept, Adalimumab, Infliximab

Front 584

What describes the MOA & side effects of MTX?

Back 584

MOA: It is a folic acid inhibitor, it inhibits an enzyme called Dihydrofolate Reductase; Side Effects: mouth sores, lowered blood counts, can make your hair fall out, cirrhosis

Front 585

What are the antimetabolites used in the treatment of RA?

Back 585

Methotrexate (MTX), Azathioprine (AZA)

Front 586

What is the rare side effect of MTX that indicates a CI for what?

Back 586

Can cause micronodular cirrhosis of the liver (looks like the type of cirrhosis seen in ppl who drink), Alcohol is CI

Front 587

How many adults in the US have metabolic syndrome?

Back 587

1 out of 5 adults, 40% of ppl over 60 yo

Front 588

What is the 1st step in the Metabolic Syndrome Treatment Algorithm?

Back 588

Lifestyle Intervention (diet, exercise, smoking cessation) for at least 3-6 months

Front 589

What elements are involved in Metabolic Syndrome (a.k.a. Insulin resistant state)?

Back 589

Glucose intolerance, Dyslipidemia, HTN, Hypercoagulability, Hyperinsulinemia; they can all lead to cardiovascular disease (intervene to prevent)

Front 590

What are the associated abnormalities of Metabolic Syndrome?

Back 590

NASH; Obstructive sleep apnea; PCOS; Increased inflammatory markers/cytokines (IL-6, CRP, PAI-1)

Front 591

What defines Metabolic Syndrome in Children (IDF)?

Back 591

Criteria for children aged 10-16
(1) Obesity - > 90th percentile
(2) TG > 150mg/dl;
(3) HDL-C < 40mg/dl;
(4) BP > 130/85;
(5) Glucose > 100mg/dl or T2DM (OGTT)

Front 592

What defines the metabolic syndrome in Adults?

Back 592

Need 3 out of 5 to meet criteria:
(1) Abdominal obesity, waist circumference in M >102 cm (40 in) & in F >88 cm (35 in);
(2) Serum triglycerides ≥150 mg/dL (1.7 mmol/L) or drug treatment for elevated triglycerides;
(3) Serum HDL cholesterol <40 mg/dL (1 mmol/L) in M <50 mg/dL (1.3 mmol/L) in F or drug treatment for low HDL-C;
(4) BP ≥130/85 mmHg or drug treatment for elevated BP;
(5) Fasting plasma glucose (FPG) ≥100 mg/dL (5.6 mmol/L) or drug treatment for elevated blood gl

Front 593

What A1C level is considered to be diagnostic of diabetes and prediabetes?

Back 593

Diabetic: A1C > 6.5;
Prediabetic: A1C 5.7-6.5

Front 594

What are the treatment goals of metabolic syndrome after lifestyle modifications alone have failed?

Back 594

In addition to lifestyle modification:
(1) Achieve target A1C goal (< 7%);
(2) Avoid hypoglycemia;
(3) Avoid weight gain;
(4) Improve BP and lipid control;
(5) Optimize patient adherence*

Front 595

What are the triad of defects seen in type 2 DM?

Back 595

(1) Defective insulin secretion (beta-cell dysfunction); (2) Insulin resistance (fat and muscle); (3) Increased hepatic glucose output

Front 596

What is the drug of choice at time of Dx of DM-2?

Back 596

Lifestyle modification and Metformin (target is to decrease hepatic glucose output) unless there is an indication not to give it

Front 597

What is the best drug to start for HTN in a patient with DM?

Back 597

Angiotensin converting enzyme inhibitors or Angiotensin converting enzyme blockers

Front 598

What classifies the Critical Biological Agents: Category A (CDC) and what pathogens are included?

Back 598

Pathogens that pose greatest risk to national security:
(1) Can be easily disseminated OR transmitted person-to-person;
(2) Cause high mortality with potential for major public health impact;
Bacillus anthracis (anthrax);
Variola major (smallpox);
Clostridium botulinum (botulism);
Yersinia pestis (plague);
Francisella tularensis (tularemia);
Hemorrhagic fever viruses

Front 599

What are the virulence factors of B. anthracis that cause disease?

Back 599

Organism produces antiphagocytic capsule & edema factor (EF), lethal factor (LF) & protective antigen (PA) --> produce Edema Toxin & Lethal toxin --> necrosis of lymphatic tissues ---> causes release of large numbers of B. anthracis into bloodstream --> Overwhelming septicemia rapidly occurs

Front 600

How does Inhalation Anthrax replicate within the human host?

Back 600

Exposure to necessary inoculum, LD50 estimated to be 8,000-10,000 inhaled spores, Uptake of spores by pulmonary macrophages which carry spores to tracheobronchial or mediastinal lymph nodes, Spores vegetate --> replicating bacteria

Front 601

What are the 3 types of Clinical Manifestations of Anthrax?

Back 601

Inhalational (most serious);
Cutaneous (most common in natural form);
Gastrointestinal (least likely)

Front 602

What is Bacillus anthracic and how does it cause disease?

Back 602

Aerobic, gram positive spore-forming, non-motile, non-hemolytic species, it is acquired usually by contact with infected animals or their hides, Spores can survive for decades and they germinate when enter environment rich in nutrients

Front 603

What organisms are Critical Biological Agents in Category C (potentially a threat) of bioterrorism?

Back 603

Hantavirus;
Yellow Fever;
Multi-drug resistant TB;
Genetically-altered microbes

Front 604

What organisms are Critical Biological Agents in Category B (Moderate Risk) of bioterrorism?

Back 604

Coxiella burnetti (Q fever);
Brucella species (brucellosis);
Burkholderia mallei (glanders);
Alphaviruses (VEE, others);
Toxins: ricin, Staph. Enterotoxin B;
Food and waterborne pathogens

Front 605

What is the definition of bioterrorism?

Back 605

“Those occurrences, (deliberate), that result in human suffering and damage from exposure to biological agents”

Front 606

What are the Epidemiological Features of Possible Bioterrorism Attacks?

Back 606

Clusters of pts from single locale; Rapidly increasing disease incidence; Endemic disease rapidly emerging at unusual time or pattern; Any pt presenting w/ a disease that is uncommon and has bioterrorism potential

Front 607

What is the incubation period of Inhalational Anthrax & what develops after incubation?

Back 607

Incubation period of 1-16 days, but cases may arise later, up to 60 days; After incubation a nonspecific flu-like illness develops (Fever, myalgia, HA, nonproductive cough, mild chest discomfort, n/v)

Front 608

What organisms are Critical Biological Agents in Category C (potentially a threat) of bioterrorism?

Back 608

Hantavirus;
Yellow Fever;
Multi-drug resistant TB;
Genetically-altered microbes

Front 609

What is the definition of bioterrorism?

Back 609

“Those occurrences, (deliberate), that result in human suffering and damage from exposure to biological agents”

Front 610

What are the clinical features of Inhalational Anthrax?

Back 610

High fever, dyspnea, stridor, then rapid respiratory failure, shock; Hemorrhagic meningitis (in 50% cases) may occur late; Mortality > 90% (historically)

Front 611

What is the emperic and prophylactic ABX treatment?

Back 611

Emperic: Ciprofloxacin IV or Doxycycline IV for 60 days, in adults AND children; Prophylactic: PO Doxycycline or Ciprofloxacin

Front 612

How is Gastrointestinal Anthrax?

Back 612

Follows ingestion of insufficiently cooked contaminated meat, presents severe abdominal distress, followed by fever, signs of septicemia, Case-fatality rate 25-60%

Front 613

What pathognomic of cutaneous anthrax lesion?

Back 613

Starts as papule, then vesicle, then depressed black eschar

Front 614

What infection disease is of major concern due to a 30% case fatality rate, physically disfiguring, no treatment available, very communicable from person-to-person, & many susceptible people today?

Back 614

Smallpox, an acute viral illness caused by the variola virus

Front 615

What are characterized the transmission and clinical manifestations of Smallpox?

Back 615

Spreads by aerosol or droplet nuclei from oropharynx (Contaminated clothing, linen could also spread virus; Incubation period 7-17 d; high fever, malaise, prostration with headache, backache, Severe abdominal pain, delirium)

Front 616

What other rashes can mimic smallpox and what should you do?

Back 616

Chicken pox, monkey pox, disseminated cutaneous herpes simplex; Then send specimens to State lab, CDC: PCR of tissue available; Observing typical virions by electron microscopy, Viral antigens, culture

Front 617

How do the lesions of smallpox differ than those of chickenpox?

Back 617

Smallpox: Maculopapular rash appears 1st on mucosa of mouth, pharynx, face & forearms, spreading to trunk & legs; W/in 1-2 days, rash becomes *vesicular*then pustular (tense, deep in dermis), Crusts form d 8-9, separate, then scar, *Lesions develop synchronously**
(vs Chickenpox which have lesions in different stages of development on the same pt)

Front 618

Why is the smallpox vaccine contraindication in pre-exposure setting to pts who are immunocompromised, have certain skin diseases, or are pregnant?

Back 618

Vaccinia can spread through out the skin & cause disseminated Vaccinia

Front 619

What is the unique feature of the post-exposure smallpox vaccine that is not seen in other infectious diseases?

Back 619

if vaccinated them w/in 3 days after exposure, you can prevent smallpox disease

Front 620

What toxin inhibits release of acetylcholine resulting in flaccid paralysis?

Back 620

Botulinum toxin, potent neurotoxin produced by Clostridium botulinum (anaerobic gram positive bacillus), Spores present in soil and marine sediment worldwide

Front 621

What is suspected in a pt that presents as Responsive w/ absence of fever, Symmetrical cranial neuropathies, Blurred vision, diplopia, symmetrical descending weakness in a proximal to distal pattern & has no sensory deficits?

Back 621

Botulism

Front 622

What is the incubation period for Botulism and how is it managed?

Back 622

Foodborne: 12-36 hrs after exposure;
Inhalational: 24-72 hrs exposure;
Supportive therapy & Trivalent botulinum antitoxin in the inhalational bioterrorism form

Front 623

What is organisms is a gram negative bacillus, often bipolar staining and what does it cause?

Back 623

Yersinia pestis and it causes plague

Front 624

What three syndromes can Yersinia pestis cause depending on its route of transmission?

Back 624

Bubonic (regional lymphadenopathy);
Septicemic;
Pneumonic (would be most likely form in bioterrorism event, and resulting from aerosol exposure)

Front 625

What bioterrorism diseases use doxycycline or ciprofloxacin for post-exposure prophylaxis?

Back 625

Plague, Anthrax, and Tuleremia

Front 626

How is Plague diagnosed and what is the treatment?

Back 626

Cultures of sputum and blood

Front 627

What bioterrorism diseases use Streptomycin or gentamicin as treatment?

Back 627

Plague, Tuleremia

Front 628

What is the Differential Dx of Respiratory Syndrome?

Back 628

Inhalational anthrax;
Pandemic Influenza;
Plague;
Tularemia;
Q fever;
Other atypical pneumonia (e.g. Hantavirus, SARS, Legionnaire’s Disease);
Strep. pneumoniae, S. aureus, etc.

Front 629

What are the etiologies of Viral Hemorrhagic Fever (VHF) and how does it present?

Back 629

Etiologies: Arenaviruses, Filoviruses, Bunyaviruses, Flaviviruses;
Clinical signs: high fever, headache, myalgias, bleeding; shock, Low platelet count common; also decreased WBC

Front 630

What is the differential diagnosis for Viral Hemorrhagic Fever, how is it diagnosed, & how is it treated?

Back 630

Dx: use serologies rapid EIA; viral culture; DDx: meningococcemia, plague, Rickettsial illness (Rocky mountain fever), DIC from other causes; Treatment: ribavirin may be helpful in select cases (eg Lassa fever)

Front 631

What features of disease would suggest bioterrorism?

Back 631

Unusual disease or number of cases, location, or fatalities

Front 632

What is the medical response when dealing with bioterrorism agents and disease?

Back 632

Patient directed-isolation, treatment; Public heath directed-contact authorities at once

Front 633

What bioterrorism diseases do NOT have person-to-person transmission?

Back 633

Anthrax, Botulism

Front 634

What bioterrorism disease does NOT have any available treatments?

Back 634

Smallpox, Viral Hemorrhagic Fever (exception is Lassa fever, use Ribavirin)

Front 635

What bioterrorism diseases have person-to-person transmission?

Back 635

Smallpox, Pneumonic Plague, Viral Hemorrhagic Fever

Front 636

What describes the absorption and distribution of inorganic lead (e.g. salts, oxides)?

Back 636

30% absorbed with inhalation of dusts; 10-15% absorbed orally; 90% distributes to bone – blood levels are a poor indicator of body burden but are useful in assessing recent/ongoing exposure

Front 637

What are the reproductive/developmental effects of lead poisoning?

Back 637

Reduced sperm counts/motility, implicated in miscarriages/stillbirths, reduced birth weight and premature birth

Front 638

What are the renal effects of lead poisoning?
x

Back 638

What are the renal effects of lead poisoning?
Impairs proximal tubular function, aminoaciduria, glucosuria, hyperphosphaturia

Front 639

What are the recommended actions regarding lead poisoning in children?

Back 639

With low levels of exposure: retesting after some time period, education, and case management;
With higher levels of exposure (20-44): clinical evaluation, education, environ. investigation;
With high levels of exposure: clinical evaluation/hospitalization, chelation therapy, education, environmental investigation

Front 640

What are the signs/symptoms of lead poisoning in children?

Back 640

Lowered intelligence, diminished school performance, growth retardation, hearing loss, impaired bone growth and shortened stature, hyperactivity, sleeping problems, GI problems (stomachache)

Front 641

How does anemia come about with lead poisoning?

Back 641

Lead inhibits δ-ALA dehydratase, thus affecting the conversion of ALA to porphobilinogen;
It also inhibits mitochondrial ferrochelatase, decreasing conversion of protoporphyrin IX to heme–
Overall these effects lead to increased ALA in plasma, excess coproporphyrinogen III in urine, and accumulation of protoporphyrin IX in erythrocytes

Front 642

What signs/symptoms are associated with lead poisoning in adults?

Back 642

Mild (>40): CNS involvement (tiredness, somnolence), also reproductive effects and HTN;
Moderate (>80): CNS effects (more severe), GI effects (metallic taste, abd. pain), nephropathy;
Severe (>100): CNS effects (severe: encephalopathy, coma, seizures), PNS effects (foot/wrist drop), GI effects, pallor due to anemia, nephropathy

Front 643

What are the two categories of metal that cause toxicity?

Back 643

Essential metals: low intrinsic toxicity, examples incl. zinc, copper, selenium;
Nonessential metals: higher intrinsic toxicity, for ex. lead, mercury, cadmium, beryllium, arsenic

Front 644

What characterizes lead poisoning?

Back 644

One of the most common exposures; inorganic and elemental forms are of toxicological concern

Front 645

By what general mechanisms do metals cause toxicity?

Back 645

Binding of sulfhydryl groups, inhibiting enzyme activity, disrupting cellular transport, precipitating proteins

Front 646

What characterizes organic mercury toxicity?

Back 646

With chronic toxicity, can see CNS effects (sensory defects, paresthesias, constriction of visual fields, loss of hearing/taste/smell), PNS effects (motor dysfunction, tremors, muscle incoordination), reproductive toxicity (fetus will have CNS damage at levels not toxic to mother) – the kidney is not a target organ

Front 647

What is the biomarker for arsenic poisoning?

Back 647

Mees lines on fingernails (transverse white lines) – also seen in other disease states

Front 648

What characterizes arsenic poisoning?

Back 648

People most at risk are those working the in manufacture of insecticides, weed killers, wood preservatives, and metal refining; the burning of arsenic-treated wood poses a health hazard;
The major mechanism of toxicity is to disrupt energy metabolism in the cell;
Acute toxicity: affects GI, heart, neuro, hematological, liver, kidneys, will see many s/s;
Chronic toxicity: skin lesions (hyperpigmentation, hyperkeratosis, allergic contact dermatitis), peripheral neuropathy, obliterative arterial disease of extremities (with groundwater contamination), anemia – antidotes incl. BAL and Succimer

Front 649

What characterizes cadmium poisoning?

Back 649

Exists only in the inorganic form (salts/oxides), those at risk are workers in industries;
With oral ingestion 5% is absorbed, whereas with inhalation 30-60% is absorbed;
Chronic toxicity leads to kidney damage (major target organ, proximal tubular damage), bone damage (osteomalacia due to disruption of calcium/phosphate homeostasis);
Acute toxicity leads to lung damage (pneumonitis, emphysema) – there are no effective antidotes, chelators will cause release of cadmium in the kidneys (and thus lead to kidney damage)

Front 650

What antidotes are available for mercury poisoning?

Back 650

Chelating agents: BAL/Succimer/DMPS for inorganic forms; elemental and organic forms are more resistant to chelation

Front 651

What characterizes inorganic mercury toxicity?

Back 651

Mercury salts, exposure occurs mainly by oral ingestions; Chronic toxicity can lead to GI effects (irritation of oral cavity, abd. pain, intestinal bleeding), kidney damage (major target organ, proximal tubular damage, increased excretion of amino acids, glucose, phosphate), CNS toxicity (not a major concern); Acute toxicity can lead predominantly to oral/GI toxicities (gingivitis, stomatitis, abd. pain) as well as cardiovascular collapse with severe intoxication

Front 652

What are Minamata disease and Iraqi food exposure examples of?

Back 652

Organic mercury poisoning from food, leading to fetal toxicity

Front 653

What is the antidotal therapy for lead poisoning?

Back 653

Succimer (DMSA): used for mild adult symptoms and asymptomatic children;
CaNa2EDTA, BAL: moderate/severe adult symptoms and asymptomatic/symptomatic children

Front 654

What characterizes elemental mercury toxicity?

Back 654

Risk from inhalation of vapors (oral ingestions poses little risk due to poor absorption); Chronic toxicity is associated with CNS effects (irritability, insomnia, depression, emotional instability), PNS effects (motor dysfunction, tremors, muscle incoordination), renal toxicity (damage to proximal tubules) – acute toxicity is rare, s/s incl. GI complaints, HA, visual disturbances, and lung damage (cough, chest pain, pneumonitis at very high concentrations)

Front 655

What characterizes mercury?

Back 655

Toxic in elemental, organic, and inorganic forms; Exposure is primary found in a variety of occupations, combustion effluents of coal, and in food (fish/seafood)

Front 656

What characterizes beryllium poisoning?

Back 656

Used in many high-tech products; Acute toxicity: irritant dermatitis, eye irritation, pneumonitis, anorexia, fatigue; Chronic toxicity: berylliosis (chronic granulomatous disease in the lung, delayed hypersensitivity), allergic contact dermatitis – no antidotes available

Front 657

What characterizes metal fume fever?

Back 657

Seen in the welding profession, very common; Occurs within 3-12 hours of exposure to metal oxide dusts (zinc oxide, magnesium oxide, aluminum oxide, cadmium oxide, etc.);
Signs/symptoms: HA, fever, chills, muscle aches, thirst, n/v, chest soreness, fatigue, GI pain, weakness, tiredness (symptoms may last 6-24hrs, complete recovery within 24-48hrs, long-term consequences unknown)

Front 658

What metals are considered carcinogens?

Back 658

Arsenic: skin, lungs; Chromium (hexavalent): lungs; Nickel: nose; Beryllium: lungs;
Cadmium: prostate; Lead (probable carcinogen): kidney

Front 659

What is the most common form of metal toxicity?

Back 659

Allergic contact dermatitis: delayed hypersensitivity reaction (they are haptens); seen with beryllium, nickel, chromium, arsenic, platinum, and gold

Front 660

What characterizes manganese poisoning?

Back 660

Associated with Parkinson-like symptoms; seen in welding profession

Front 661

What characterizes iron poisoning?

Back 661

Children are at the greatest risk; Acute toxicity in children (with iron-containing supplements): irritation of GI tract/hemorrhage, liver damage (within days), renal failure, with severe exposure can see convulsions/coma/death – antidote: Deferoxamine

Front 662

What describes the developmental period of fertilization/implantation?

Back 662

Conception – day 17 of gestation: mitotic activity in all cells, cells are functionally equivalent in terms of totipotentiality, injury resulting in cell death can be overcome except in the case of a lethal dose (leads to spontaneous abortion/resorption of the developing organism); if recovery follows, no structural deformity in the fetus is seen

Front 663

What aspects of the fetal-placental-maternal unit can cause fetal toxicity?

Back 663

Direct toxicity to the fetus, damage to the placenta, indirect fetal toxicity through maternal factors (e.g. nutrition [excess vit. A], disease [DM, HTN, AIDS, thyroid dysfunction], infections [HSV, CMV, syphilis])

Front 664

What characterizes the placental transfer of chemicals?

Back 664

Not a very effective barrier for many chemicals; diffusion dependent on size, pKa, and lipid solubility of the chemical

Front 665

What characterizes the susceptibility to tumor induction during gestation?

Back 665

Seen with DES (diethylstilbestrol, used to prevent miscarriages/premature deliveries), ionizing radiation, and >50 chemicals

Front 666

What are reasons for the CNS sensitivity during the embryonic period?

Back 666

Proportionally high blood flow to the brain; Proportionally high lipid content relative to later in life; Poorly developed BBB

Front 667

What describes the fetal period of development?

Back 667

Day 56 – parturition: time of growth and development, fetus shows relative resistance to teratogens, primary malady from exposure to chemicals is reduction in cell size/number, can see growth retardation/functional deficits, developing brain is particularly prone to injury since its development (e.g. myelination) is incomplete even at birth, most common outcomes are learning disorders/behavioral problems/retardation

Front 668

What describes the embryonic period of development?

Back 668

18 – 55 days, organogenesis: period of extreme sensitivity to teratogenic agents (will cause structural malformations, most frequent time period involved in teratogenicity), frequently the mother will not know she is pregnant during this period; sensitivity is due to rapid cell turnover, immature biological barriers, and immature detoxicification processes (P450 system)

Front 669

What percent of causes of developmental defect in humans can be attributed to drugs and environmental chemicals?

Back 669

4-5% (65-70% is unknown)

Front 670

What are the FDA pregnancy risk categories?

Back 670

A: fetal harm appears remote;
B-D: intermediate concern;
X: high risk of fetal abnormalities

Front 671

What are the final outcomes of exposure to a developmental toxicant?

Back 671

Lethality, malformation, functional disorder, growth retardation

Front 672

What characterizes methyl mercury?

Back 672

Fetal exposures can result in neurological defects (mental retardation, speech disturbances) without maternal toxicity – seen in accidental mass exposures in Japan and Iraq

Front 673

What characterizes male reproductive toxicity?

Back 673

Chemical whose toxicity is through disruption of cell division will be more detrimental to male reproductive status than with females; Testicular damage/infertility is seen with dibromochloropropane; Decreased libido/impotence can be seen with lead, vinyl chloride, TDI; Spermatotoxicity is seen with cytotoxic drugs, dibromochloropropane, and lead

Front 674

What characterizes retinoid embryopathy?

Back 674

Caused by Isotretinoin use; associated with a high risk of birth defects (even with small amount for short period); birth defects incl. hydrocephaly, microcephaly, mental retardation, ear/eye abnormalities, cleft palate and other facial abnormalities, heart defects

Front 675

What characterizes fetal effects of cocaine use?

Back 675

Premature detachment of the placenta (vasoconstriction), increased spontaneous abortions, intrauterine growth retardation, disruption of CNS development

Front 676

What characterizes fetal alcohol syndrome (FAS)?

Back 676

Leading preventable cause of mental retardation and birth defects, characterized by abnormal facial features (short palpebral fissures, epicanthal folds, short/upturned nose, thin upper lips, small jaw), growth deficiencies, and CNS problems (mild/moderate mental retardation, learning disabilities, poor motor coordination, irritability during infancy, hyperactivity in childhood), urinary tract defects – native Americans have a greater incidence of FAS than other ethnic groups

Front 677

What does fetal exposure to ethyl alcohol (i.e. ethanol) cause?

Back 677

Fetal alcohol spectrum disorders (FASDs): umbrella term for range of effects caused by maternal ingestion of alcohol, incl. physical/mental/behavioral/learning problems with lifelong implications – most severe effects of drinking during pregnancy is fetal alcohol syndrome

Front 678

What does fetal lead exposure cause?

Back 678

Impaired CNS development (intelligence/cognitive development)

Front 679

Which common drugs were initially thought to be teratogenic, but were subsequently proven to be safe?

Back 679

Diazepam, OCs, spermicides, salicylates, Bendectin (Doxylamine plus pyridoxine)

Front 680

What characterizes Thalidomide?

Back 680

Fetal exposure results in amelia (congenital absence of a limb/limbs), hemimelia (congenital absence of part of an extremity), or phocomelia (defective development of arms/legs);
Critical period of exposure is between days 20-36 – Thalidomide is currently used for leprosy (Hanson’s disease) and appears promising for the treatment of multiple myeloma and SLE

Front 681

What defines neonatal and infant periods?

Back 681

Neonate: first month of life post-partum; Infant: first year of life post-partum

Front 682

What are the TORCH organism?

Back 682

Organisms that can cauase transplacental infections of fetus: TOxoplasma, Rubella, CMV, Herpesvirus, and other bacterial/viral agents

Front 683

What characterizes transplacental infections of the infant/fetus?

Back 683

Acquired via the “hematological route” from mother to fetus: most viral/parasitic, few bacterial (Listeria, Treponema), gain access to fetal bloodstream via chorionic villi either at anytime thru delivery or at delivery via maternal-to-fetal transfusion – examples include TORCH organisms

Front 684

What is caused by the ascending infection of candida?

Back 684

White opacification of umbilical vessels (barber pole) and small granules – detected by GMS stain

Front 685

What characterizes transcervical infections of the infant/fetus?

Back 685

Acquired via the “ascending route” from cervix into uterus: most bacterial, few viral, infection can occur by either inhalation of infected amniotic fluid (resulting in congenital pneumonia) or by passage through infected cervical canal – common diseases include pneumonia, sepsis, meningitis

Front 686

What can cervical cone biopsy to detect HPV-related cervical cancer lead to?

Back 686

Prematurity

Front 687

What is the 2nd most common lethal condition of neonatal period?

Back 687

Prematurity – risk factors for prematury include preterm premature rupture of membranes, intrauterine infections, structural abnormalities of uterus/cervix/placenta, multiple gestation

Front 688

What is a systemic way of categorizing pathological findings?

Back 688

SNOMED: organizes pathology by T-M matrix, includes comprehensive list of systems for patient history and physical diagnosis, organizes reprint files

Front 689

What are various perinatal pathological conditions?

Back 689

M1: trauma: obstructed labor, fetal malpresentation
M2: congenital: 1% neural tube defects (folate deficiency), cretinism (maternal hypothyroidism), congenital syphilis
M4: infections: rotavirus, syphilis, HIV, Group B strep, tetanus (shows up in infant in 7-10 days, due to lack of maternal immunity)

Front 690

What is the definition of live birth in the US?

Back 690

All births that show any sign of life, regardless of prematurity (many countries report this as stillbirth)

Front 691

What is placental previa?

Back 691

Placenta attached to uterine wall close to or covering the cervix – may lead to infant death due to hypoxia during delivery

Front 692

What is a complication of neonatal RDS?

Back 692

Hemorrhage in germinal matrix with secondary hemorrhage into brain ventricles because blood vessels are susceptible to hypoxic damage in subependymal germinal matrix

Front 693

What is the treatment for neonatal RDS?

Back 693

Surfactant replacement, oxygen administered via ventilation

Front 694

What is neonatal respiratory distress syndrome (RDS)?

Back 694

Aka “hyaline membrane disease”, main cause is prematurity and low gestational age, is due to deficiency of pulmonary surfactant (normally decrease surface tension, production of surfactant can be stimulated by cortisol) (!) (many points from powerpoint omitted per instructor’s advice to “not worry” about them)

Front 695

What is the mortality rate based on APGAR scores?

Back 695

Score 0-1: 50% mortality; Score > 7: 0% mortality
Score at 1 minute assesses the need for resuscitation, score at 5 minute determines long-term prognosis of newborn

Front 696

What is the APGAR scoring system?

Back 696

Measure of physiological condition and responsiveness of newborn: scores range from 0 to 2 for the following factors: HR, respiration, muscle tone, color, response to catheter in nostril – maximum score is 10 – scores are measured at 1 minutes and 5 minutes

Front 697

What is twin-twin transfusion syndrome?

Back 697

Disproportionate distribution of blood from one fetus to another when two or more fetuses share a chorion and hence a single placenta, but have separate amniotic sacs

Front 698

What can occur with Listeria infection of pregnant mothers?

Back 698

Can infect placenta via blood, causing abscess and massive gram (+) growth --> termination

Front 699

What is placental abruption?

Back 699

Premature detachment of placenta from the uterine wall

Front 700

What conditions can cause fetal growth restriction?

Back 700

Uteroplacental deficiency: vascular anomalies, placental abruption/previa/thrombosis/infarct or infection

Front 701

What is necrotizing enterocolitis?

Back 701

Ischemic colitis due to prematurity - presents with blood stools, abdominal distention, and/or circulatory collapse

Front 702

In what conditions is Rhogam use recommended?

Back 702

All Rh(-) women who want to become pregnant: timed at 28 weeks and delivery – rhogam is safe, single exposure may result in natural sensitization, sensitization may be life-long, after natural sensitization to Rh-antigen Rhogam is not effective (!)

Front 703

What characterizes Rh disease of the newborn?

Back 703

Fetus Rh(+) blood can be reacted against by maternal defense system in a mother with Rh(-) blood type who has antibodies against Rh-antigen (due to exposure of mother’s defense system to Rh(+) blood from current or previous pregnancies, etc)

Front 704

What are findings in SIDS autopsy cases?

Back 704

Subtle findings, mostly petechial hemorrhages (e.g. found in viscera including thymus, lungs)

Front 705

What has occurred to the rate of SIDS over the years?

Back 705

Declined – improvement is mainly associated with having babies sleep on their back instead of in a prone position (lying face downward)

Front 706

Mandatory child abuse and neglect laws that require that which certain professionals and institutes are report suspected abuse to child protective services?

Back 706

Health care providers, Teachers, School staff, Social workers, Police, Foster care providers, Daycare providers

Front 707

What is the consequences of failure to immediately report child abuse?

Back 707

Misdemeanor in most states, and physician can be liable for civil damages

Front 708

What age group of children had the highest rate of victimization?

Back 708

Birth to 3 years old

Front 709

What is the race has the highest incidence of child abuse?

Back 709

White (49.7%); ¼ (23.1%) were African American; and 17.4% were Hispanic (it is currently increasing in Hispanics)

Front 710

What kind of child abuse is the most cause of death?

Back 710

42.2% of the fatalities were attributed to neglect (76.6% of the fatalities were younger than 4 years)

Front 711

Who is the most common perpetrators of child abuse?

Back 711

Parents (79.4%), Relatives (6.8%), <10.1% of perpetrators were unrelated (foster parents, daycare providers and legal guardians); 57.8% of perpetrators were female

Front 712

What are the different types of abuse?

Back 712

Physical, Nutritional deprivation, Sexual abuse, Intentional drugging or poisoning, Neglect of medical care or safety, Emotional abuse

Front 713

What classifies death precipitated by injury to the mother?

Back 713

Feticide (Death can be result of premature birth)

Front 714

What is classification of death within the first 30 days and death within 1 month to 1 year?

Back 714

Neonaticide; Infanticide

Front 715

In neonaticide who is most likely the responsible party if death occurs within the 1st 24, and if death occurs > 24 hours, and what is the usual cause of death?

Back 715

First 24 hours almost always the mother; >24 hours father slightly more likely to be guilty party; COD: Asphyxia

Front 716

Minor scalp hemorrhage, Small cephalohematoma with no evidence of skull fractures or significant intracranial injuries is classified as what?

Back 716

Neonaticide: Delivery Injuries

Front 717

What is the most common type of child abuse?

Back 717

70% physical abuse, 25% sexual abuse, 5% underfeeding or neglect

Front 718

What types of face trauma are indicative of child abuse?

Back 718

Frenulum tears, Dislodged teeth

Front 719

Why is full body x-rays done on all infant and pediatric death?

Back 719

Evidence present in 1/3 of abused children, Epiphyseal-metaphyseal fractures of long bones of the arms and legs and rib fractures, Extremities 77%; Skull 34%; Rib cage 19%

Front 720

What type extremity fracture is most often associated with child abuse?

Back 720

Spiral Fracture

Front 721

How does death from child abuse usually result?

Back 721

Die as a result of head trauma: Subdural hemorrhage, Subarachnoid hemorrhage, +/- skull fractures, Brain injury; followed by abdominal injury

Front 722

What are the signs of Elder Neglect?

Back 722

Contractures, Malnutrition, Dehydration, Decubitus ulcers

Front 723

What are Risk Factors for Elder Abuse?

Back 723

Shared living situation, Dementia, Social isolation, Pathologic characteristics of perpetrators

Front 724

What are the different stages of Decubitus ulcers and what stages are considered abuse?

Back 724

Stage 1: reddening of the skin;
Stage 2: ulceration of the skin but it does not go past the subcutaneous tissue (needs to be clean and dry);
Stage 3: through the skin & fascia, sign of abuse, must be reported
Stage 4: to the bone, sign of abuse, must be reported

Front 725

What are some examples of chemicals that are poorly or not adsorbed by charcoal?

Back 725

Alkali, DDT, organic mercury, water-insoluble compounds, etc.

Front 726

What characterizes the use of activated charcoal?

Back 726

Place into stomach to adsorb poison; has been reported that charcoal not only removes unabsorbed poison but also increases the clearance of systemically absorbed poison; charcoal can also interrupt the entero-hepatic cycle and increase the excretion of the poison
What characterizes the use of activated charcoal?
Place into stomach to adsorb poison; has been reported that charcoal not only removes unabsorbed poison but also increases the clearance of systemically absorbed poison; charcoal can also interrupt the entero-hepatic cycle and increase the excretion of the poison

Front 727

What factors determine the effectiveness of gastric lavage?

Back 727

Physical characteristics of the toxic agents (e.g. plants, tables, capsules, liquids), rate of absorption of toxic agents, diameter of lavage tube, volume/rate of installation of lavage solution

Front 728

What are complications/hazards of gastric lavage?

Back 728

Aspiration pneumonia secondary to emesis with unprotected airway, laryngospasm with cyanosis

Front 729

What are contraindications of gastric lavage?

Back 729

Corrosives, petroleum distillates, seizures

Front 730

What are some reasons for the pediatric population not to take Ipecac?

Back 730

It sometimes causes prolonged vomiting and lethargy similar to drowsiness that might be caused by an overdose of sedative drugs (symptoms may complicate diagnosis and treatment); It may also not totally empty the stomach of poison or may linger and cause the child to vomit up other antidotes; some studies have found that Ipecac did not improve outcomes

Front 731

What are contraindications for emetic drugs?

Back 731

When the poison ingested is a convulsant, hydrocarbon, or corrosive acid/alkali;
When the patient is unconscious/comatose, does not have a gag reflex, has severe CV disease/emphysema/extremely weakened blood vessels, is under 6 months of age

Front 732

What characterizes Apomorphine?

Back 732

More reliable than Ipecac (in professional setting); Stimulates CTZ; does not store well (made fresh); it is a narcotic drug that causes emesis in 3-5min.; never to be used unless a narcotic antagonist (e.g. naloxone) is available to reverse the effects after emesis; should be followed with large amounts of fluid – be careful of repeating since it has mild CNS depressant effects that may act synergistically with depressants responsible for the intoxicant being treated

Front 733

In what cases is hemodialysis effective with toxin ingestions?

Back 733

Toxic manifestations are related to the concentration of the poison, poison is distributed in the vascular component, poison is diffusible, poison is not tightly bound to tissue/plasma proteins

Front 734

Why are nitrites used cyanide poisoning?

Back 734

They convert some of the hemoglobin to methemoglobin, which preferentially binds cyanide rather than having it bind cytochrome oxidase (thus negating some of its toxicity)

Front 735

What is the antidote dimercaprol (BAL) used for?

Back 735

Arsenic poisoning (as well as mercury poisoning)

Front 736

In what situations are cathartics not recommended?

Back 736

Following caustic ingestion (chemically exerting an effect resembling a burn); Bowel sounds are absent; History of recent bowel surgery; Caution with Na-containing cathartics (HTN, CHF) and Mg-containing cathartics (renal disease)

Front 737

What characterizes the use of cathartics?

Back 737

Used following activated charcoal to aid in evacuation of the bowels; can be given together with activated charcoal; caution with potential fluid loss and electrolyte imbalance –
examples incl. magnesium sulfate/citrate, sodium sulfate, sorbitol

Front 738

What are common substances removed by hemoperfusion?

Back 738

Barbiturates, non-barbiturate sedatives (e.g. glutethimide, diazepam), analgesics (aspirin, methyl salicylate, acetaminophen), antidepressants, alcohols, CV drugs (not digoxin since it is tightly bound to plasma proteins), amanita phalloides, carbon tetrachloride, OPs, methotrexate

Front 739

What are indications for hemoperfusion?

Back 739

Deep coma or hyperactivity (caused by dialyzable drug which cannot be treated with conservative means), hypotension (threatening renal/hepatic function which cannot be corrected by adjusting circulating volume), marked hyperosmolality (which is not due to easily corrected fluid problems), severe acid/base disturbances (unresponsive to therapy), severe electrolyte disturbance (unresponsive to therapy)

Front 740

What can be used to alkalinize the urine?

Back 740

IV NaHCO3/Na-lactate/CA inhibitors (e.g. acetazolamide) – helpful for excretion of phenobarbital and aspirin

Front 741

Which substances are not affected by forced diuresis?

Back 741

Acetaminophen, glutethimide, TCAs

Front 742

What can be used to acidify the urine?

Back 742

IV NH4Cl/ascorbic acid – helpful for the excretion of amphetamines, quinidine, and strychnine

Front 743

What is used to treat digitalis poisoning?

Back 743

A steroid-binding resin (since it is tightly protein-bound)

Front 744

What is the use of potassium salts and BB in digitalis poisoning?

Back 744

Potassium salts and BB restore normal function by repairing or by-passing the effect of digitalis – also goes for methylene blue/agents that produce methemoglobinemia (!), guanidine/botulinum toxin, folinic acid/methotrexate, thymidine/5-FU, purines/6-MP

Front 745

What is the use of atropine in cholinesterase inhibitor poisoning?

Back 745

Atropine blocks receptors responsible for the toxic effects caused by the cholinesterase inhibitor

Front 746

What is the use of oxygen in carbon monoxide poisoning?

Back 746

Oxygen competes with carbon monoxide for essential receptors – same goes for neostigmine/curare, vitamin K/coumarins, naloxone/morphine

Front 747

What is the use of chloride in bromide poisoning?

Back 747

Chloride specifically accelerates excretion of bromide – same goes for calcium salts/strontium

Front 748

What is the use of cysteine in selenocystathione poisoning?

Back 748

Cysteine blocks metabolic formation of poison from a less toxic precursor – also goes for ethanol/methanol

Front 749

What is the use of thiosulfate in cyanide poisoning?

Back 749

Thiosulfate accelerates metabolic conversion of cyanide to a non-toxic product

Front 750

What characterizes the impact of injury from conception to 17 days of gestation?

Back 750

All-or-none response: either spontaneous abortion or resoprtion of developing organism from damage, or no structural deformity if totipotential cells recover

Front 751

What characterizes the placental transfer of material?

Back 751

Placenta is not a good barrier – small size, lipid-soluble, uncharged compounds pass more easily by passive diffusion

Front 752

What are examples of compounds that increase susceptibility to tumor induction during gestation?

Back 752

Diethylstilbestrol (DES): linked to vaginal cancer in children; ionizing radiation

Front 753

What is the reason behind CNS sensitivity in the embryonic and fetal period?

Back 753

High blood flow to brain, high lipid content of brain relative to later in life, poor BBB (!)

Front 754

Which organ is especially prone to developmental toxicity during the fetal period (day 56 to birth)?

Back 754

Brain (e.g. demyelination) because its development is incomplete even at birth – most common outcomes are learning disorders, behavioral problems, mental retardation

Front 755

What toxicities are most seen in the fetal period (day 56 to birth)?

Back 755

Growth retardation and functional deficits (e.g. CNS injury, retarded development) since growth in size is the primary process in this stage

Front 756

What developmental period is associated with the highest frequence of structural defects?

Back 756

Days 18-55 (organogenesis, embryonic period) during which pregnancy may be unknown to the mother High sensitivity in this period is due to rapid cell turnover, immature biological barriers, and immature detox processes (!)

Front 757

What percent of developmental defects are linked to drugs and environmental chemicals?

Back 757

5% - however, 70% of causes of developmental defects are unknown and may be due to drug and chemical

Front 758

What are the developmental periods of fetus?

Back 758

Conception to 17 days gestation: fertilization and implantation
Days 18-55: organogenesis, embryonic period; Day 56 to birth: fetal period

Front 759

What are possible outcomes of developmental toxicity?

Back 759

Lethality, malformation, functional disorder, growth retardation

Front 760

What can fetal exposure to Lead cause?

Back 760

Impaired CNS development as measure by IQ test and cognitive development

Front 761

Why is male reproductive system is more prone to damage from compounds that disrupt cell cycle?

Back 761

Because male germ cell population is continually replicating
Testicular damage: Lead, dibromochloropropane, Kepone
Decreased libido and impotence: Lead, vinyl chloride, TDI, Mn
Spermatotoxicity: Lead, dibromochloropropane, cytotoxic drugs, carbon disulfide, radiation thermal stress

Front 762

What compounds can cause Retinoid Embryopathy?

Back 762

Isotretinoin (even at small amounts for short periods), excess Vitamin A

Front 763

What race has the highest risk for Fetal Alcohol Syndrome in US?

Back 763

Native Americans

Front 764

What characterizes Fetal Alcohol Syndrome?

Back 764

Permanent condition: growth deficiency (prenatal, postnatal), abnormal facial features (short eye slits, short and upturned nose, thin upper lips, small jaw), CNS problems (MR, learning problems, poor motor coordination, irritable infant, hyperactive child), urinary tract defects

Front 765

What can fetal exposure to Ethyl Alcohol cause?

Back 765

Fetal Alcohol Spectrum Disorders (FASDs), which include Fetal Alcohol Syndrome: leading known preventable cause of MR

Front 766

What can fetal exposure to Cocaine cause?

Back 766

Premature detachment of placenta (due to vasoconstriction), risk for spontaneous abortion, intrauterine growth retardation, disruption of CNS development

Front 767

What changes can lead to developmental problems?

Back 767

Direct toxicity to fetus, damage to placenta, indirect fetal toxicity thru maternal factors (nutrition: excess vitamin A; disease: diabetes, HTN, AIDS, hypo/hyper-thyroidism; infections: herpes, CMV, syphilis)

Front 768

What can fetal exposure to Methyl Mercury cause?

Back 768

Neurological defects (MR, speech problems) without maternal toxicity

Front 769

What can fetal exposure to Thalidomide cause?

Back 769

Amelia, hemimelia, phocamelia in upper and lower limbs – critical period of exposure is days 20 to 36

Front 770

What should be addressed in a clinical history regarding acute poisoning?

Back 770

Who: age, weight, gender, relationship to others; What: name, dose, amount, co-ingestants;
When: time, date of ingestion;
Where: route of administration, location of ingestion (e.g. at home);
Why: accidental, intentional, associated details

Front 771

What characterizes Ipecac?

Back 771

Emetic drug, must be taken with large amounts of fluid to induce emesis, takes 15-30 min.;
can be used as a home remedy; Active compounds incl. Cephaline and Emetine (active alkaloids);
Produce GI irritation; Stimulated vomiting center in the medulla; Cardiotoxic if no vomited, CNS depression at high doses – not to be confused with fluid extract of Ipecac (14x more potent); not to be mixed with charcoal because it is adsorbed by charcoal and thus inactivated

Front 772

What are some important aspects of absorption following drug poisoning?

Back 772

With the exception of aspirin and some anticholinergics, little drug remains in the gut after 4 hrs; however, delayed gastric emptying associated with pylorospasm/shock can cause retention of the drug for longer than 4 hrs (e.g. with ingestion of salicylate)

Front 773

What is the first step in management if drug poisoning appears likely?

Back 773

Prevent further absorption of the unabsorbed drug in the gut lumen: emesis/gastric lavage followed by activated charcoal, castor oil for highly lipid soluble drugs, efficacy of procedures depends on time interval between ingestion and removal attempt, as well as absorption of the drug

Front 774

What should be considered regarding the differential diagnosis of a comatose patient?

Back 774

AEIO/TIPS – Alcohol; Encephalopathy: epilepsy, encephalitis, hypertensive encephalopathy;
Insulin: hyper-/hypoglycemia; Opiates: and other CNS active drugs in high doses;
Trauma: to head; Infection: meningitis, bacteremia, pneumonia; Psychiatric: hysteria, catatonia;
Syncope: vasovagal attack

Front 775

What should be given to every comatose patient in whom the initial diagnosis is not evident?

Back 775

IV hypertonic glucose (because of the real and treatable possibility of hypoglycemia) – also, save urine and vomitus for possible toxicologic assays, if needed

Front 776

What are the initial steps in coma care during an emergency?

Back 776

ABCDs – Airway: blocked, make patent; Breathing: chest wall/air moving, artificial respiration;
Circulation: need good gas exchange first, effective pulse beat, reasonable rhythm, no blood loss;
Definitive diagnosis/treatment: need good circulation first, get IV line, draw blood for analysis, start IV drip, determine hematocrit/acetone/glucose immediately, and serum urea nitrogen/Na/Ca

Front 777

Which toxic substances are most commonly involved in child poisonings?

Back 777

Commonly: cough/cold/pain relievers, antihistamines, antidepressants, sedatives, CV drugs;
Spring time: pesticides, herbicides, fertilizers – 2yo child represents peak age for poisoning risk

Front 778

What toxic substances are most commonly associated with death after ingestion?

Back 778

Antidepressants, analgesics, stimulant/street drugs, CV drugs, alcohols/glycols, chemicals, etc.

Front 779

What are the most common substances involved in human poisonings (all ages)?

Back 779

Cleaning substances, analgesics, cosmetics, cough/cold medicines, plants, bites (insect/snake), etc.

Front 780

What are indications for gastric lavage?

Back 780

Risk/benefit ratio (risk of aspiration with unconscious patient is reduced by using cuffed endotracheal tube), semiconscious, unconscious child/adult, loss of gag reflex, Ipecac-induced emesis is ineffective or contraindicated, conscious patient ingesting large quantity of highly toxic substance – continue until all particulate material is removed (clear fluid)

Front 781

What are mechanisms by which the metabolism and elimination of toxins can be hastened?

Back 781

Metabolism to inactive compounds by the liver microsomes, binding of active drug to protein or lipid-binding sites, excretion of active drug by the kidney, maintenance of proper oxygenation/ temperature/perfusion of vital organs, maintenance of brisk urinary output, acidification/ alkalinization of urine (in amphetamine and phenobarbital intoxication, respectively)