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Disease & Defense > Unit 3 > Flashcards

Unit 3 Flashcards

1
Q

What is the genetic composition of the herpes viruses?

A

dsDNA

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2
Q

What are the cells targeted for primary infection/latency by HSV1 and HSV2?

A

Sensory neural ganglia

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3
Q

What are the cells targeted for primary infection/latency by varicella zoster virus?

A

Sensory neural ganglia

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4
Q

What are the cells targeted for primary infection/latency by cytomegalovirus?

A

Monocytes, lymphocytes, and possibly others

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5
Q

How is HSV transmitted?

A

Close contact with a person who is shedding active virus at a mucosal surface, or in genital/oral secretions

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6
Q

What is the incubation period of HSV?

A

2-12 days (average is 4 days)

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7
Q

What is the incubation period of VZV?

A

10-21 days after exposure

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8
Q

What is the incubation period of cytomegalovirus?

A

2 weeks to 2 months

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9
Q

Describe the virion structure of herpesviruses

A

Innermost: A dsDNA genome that is protected by an icosahedral capsid.

Next layer: tegument, composed of fully-formed and active proteins

Outermost: envelope derived from host membrane + glycoproteins important for binding

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10
Q

Explain latency and reactivation

A

Latency: silent infection during which no virus particles are produced

Reactivation: (in sensory neuron infections) virus particles travel down the axon and reestablish an infection on skin or mucus membrane in area supplied by nerve

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11
Q

What are some clinical manifestations of HSV infection?

A

Gingivostomatitis –> most common symptomatic infection)

Herpetic whitlow –> on fingers

Encephalitis –> HSV most common cause; predilection for temporal lobes

Herpes keratitis –> inflammation of the cornea; fluorescein staining reveals distinctive dendritic pattern

Genital herpes –> lesions last 10-14 days, very painful

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12
Q

What are the 3 forms of neonatal HSV?

A

(1) Skin, eye, and mucous membrane disease (SEM)
Commonly seen at sites of trauma (forceps site). Eye lesions can lead to corneal ulcers & blindness

(2) CNS
Encephalitis, usually severe. Mortality with acyclovir 5%

(3) Disseminated
Pneumonitis, hepatitis, DIC +/- encephalitis, skin rash, eye involvement. Mortality with acyclovir 30%

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13
Q

Are reactivated lesions in HSV infectious?

A

YES. People often continue to shed virus for a period of time after the lesions are healed!

Reactivation may be silent, but the person is still infectious & the virus can still be transmitted. Up to 70% of new genital HSV infections are transmitted via asymptomatic reactivation and shedding

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14
Q

How do you diagnose HSV definitively?

A
  • viral culture of lesions
  • direct immunofluorescence of lesions
  • PCR of lesions
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15
Q

What is the treatment for HSV?

A

Acyclovir

C-section for pregnant women with active lesions at time of delivery

Severe infections: IV acyclovir

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16
Q

How is VZV transmitted?

A

Primarily respiratory, via droplet or aerosole secretions (coughing, sneezing)
Or contact with lesions

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17
Q

Describe the primary infection of varicella/chicken pox

A

Disease starts with fever, headache, malaise, +/- cough, and results in telltale rash

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18
Q

Describe the rash of varicella

A

Generalized, itchy, vesicular rash. First on face/trunk, spreads to limbs. Appears in successive waves.
Lesions in multiple stages (blisters/pustules/scabs), vs. smallpox where the lesions are all at one stage

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19
Q

What is the pathogenesis of varicella?

A

Entry via the respiratory tract and spread to regional lymphoid system
Viral replication in lymph nodes followed by a primary viremia
Virus replicates in the liver, spleen, and sensory ganglia
Secondary viremia to skin, causing the rash

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20
Q

What are the complications of varicella?

A

Secondary infection of the lesions (Group A Strep), pneumonia, necrotizing fasciitis, encephalitis, hepatitis, congenital varicella

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21
Q

What is the prophylaxis for varicella?

A

Live attenuated varicella vaccine:
2 dose series, given SQ (12-15 mos and 4-6 yrs)

May cause disease in pregnant and immunocompromised individuals

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22
Q

What does reactivation of VZV result in?

A

SHINGLES :( aka herpes zoster

Lesions develop in a single dermatome that do not cross the midline

Very painful; heal in about 2 weeks

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23
Q

What are some of the complications of herpes zoster?

A

Post-herpetic neuralgia!

Nerve palsies, encephalitis, secondary skin infections

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24
Q

What is the vaccine for shingles? Whom is it given to?

A

Zostavax, for use in persons 50+ years of age to prevent shingles

Live attenuated vaccine (contraindicated in those with immune deficiencies & pregnant)

Reduces risk for developing shingles by 50%; reduces risk of PHN

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25
Q

What happens if a woman gets varicella during pregnancy?

A

Very bad. Can lead to varicella pneumonia and death.

Can also get congenital varicella syndrome. Occurs when a pregnant woman gets VZV in first 8-20 weeks of pregnancy. Fetus can exhibit multiple tissue and organ abnormalities, such as microcephaly, mental retardation, hypoplasia of extremities, microphthalmia, and hypopigmentation.

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26
Q

Describe the primary infection of cytomegalovirus

A

For most healthy people, no symptoms and no long-term consequences.

In immunocompromised patients, serious –> can infect most organs. CMV retinitis and colitis in HIV patients

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27
Q

How is CMV transmitted?

A

Infected body fluids - saliva, breast milk sexual contact, blood, tears, contact with urine, blood transfusions, organ transplantations, in utero

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28
Q

What is the pathogenesis of CMV?

A

Affects the epithelial cells of the salivary gland or the genital tract, resulting in persistent infection and intermittent viral shedding

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29
Q

What happens if a mother has a primary CMV infection during pregnancy?

A

3-5% chance the child with be born with congenital CMV infection

Leads to low birth weight, microcephaly, hearing loss, mental impairment, skin rash (“blueberry muffin spots”), jaundice, etc.

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30
Q

How is serology useful for testing for CMV?

A

Negative IgM, negative IgG = patient has never been infected with CMV

Positive IgM, negative IgG = acute CMV disease

Negative IgM, positive IgG = patient has previously been infected with CMV
at some time in their life

Positive IgM, positive IgG = recent CMV REACTIVATION

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31
Q

What does CMV look like on histology?

A

Cells with CMV have characteristic “owl’s eye” appearance, with dark spot –> intranuclear inclusion

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32
Q

How is CMV treated?

A

In normal people, no need (asymptomatic)

In immunocompromised people, Ganciclovir (anti-viral). CMV-IG, an immunoglobulin preparation with high titer of CMV antibodies, together with Ganciclovir are sometimes used to treat CMV pneumonia.

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33
Q

What is Ehlers-Danlos Syndrome?

A

Genetic mutation leading to erroneous COLLAGEN production. Leads to hyperextensible skin, joints, fragile blood vessels, & poor wound healing.

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34
Q

Absence of what is strongly associated with Ehlers-Danlos Syndrome?

A

Inferior labial (100% sensitivity, 99.4% specificity) and lingual (71.4% sens, 100% spec) frenulum

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35
Q

What is a method of identifying the age of a person on a slide under the microscope?

A

Solar elastosis - sun damages elastin fibers in the skin over time. Has bluish-gray appearance.

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36
Q

What is a congenital problem of elastin fiber production?

A

Pseudoxanthoma elastin (PXE)

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37
Q

What happens in PXE?

A

Calcium deposits on the elastin fibers, causing them to become brittle.
Dx associated with “plucked chicken” skin, systemic HTN, and arterial ruptures in the eyes.

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38
Q

What are the components of ground substance?

A

(1) hyaluronic acid
(2) dermatan sulphate
“Glued” together with (3) fibronectin

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39
Q

What are two important types of nerve fibers in the skin?

A

Type A - myelinated, fast conductance
Carry sensations of proprioception, touch, pain, & muscle sensations.

Type C - unmyelinated, slow conductance
Carry sensations of itch, dull, non-localizing, temperature

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40
Q

What are two specialized skin receptors?

A

Meissner’s corpuscles: “pine cone like”; located near DEJ; involved in fine touch, in greatest amounts on fingers

Pacinian’s corpuscles: “onion like”; in dermis, involved in vibration and pressure, in greatest amount in genitals

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41
Q

What are the different glandular structures in the dermis?

A

Apocrine glands: sweat gland in armpits/groin; empties into hair follicles. Secrete thicker fluid; create BO smell :). Also in eyelids, ears, and breasts.

Eccrine glands: sweat glands over most of body

Apoeccrine glands: hybrid, located mostly in axilla. Secrete nearly 10x as much sweat as eccrine glands. Lots of fluid (like eccrine) but thicker (like apocrine). Lovely.

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42
Q

What type of hair is on the ears?

A

Vellus hair (thin, fine, apigmented)

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43
Q

What are the stages of hair growth?

A

Hairs randomly engaged in 1 of 3 stages:

(1) Anagen (growth): 85%
(2) Telogen (rest): 10-15%
(3) Catagen (involution): 1-5%

Anagen = 3 years
Telogen = 3 months
Catagen = 3 weeks (or less)
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44
Q

What is another name for male pattern baldness? What causes it?

A

Androgenic hair loss

Conversion of testosterone to DHT

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45
Q

What do holocrine glands secrete?

A

The whole cell

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46
Q

What neurotransmitter causes the causes of sweat from eccrine glands?

A

Acetylcholine

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47
Q

What is miliaria?

A

Skin disease marked by small and itchy rashes.

“Heat rash”. Caused by blocked sweat ducts.

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48
Q

What is a genetic cause of abnormal eccrine glands?

A

Anhidrotic Ectodermal Dysplasia

Genetically abnormal eccrine glands - can’t sweat. Also have funky teeth, sparse hair, & (obvi) poor temperature regulation.

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49
Q

When does a majority of atopic dermatitis start?

A

Before age 5

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50
Q

What is atopic diathesis?

A

Atopic dermatitis, asthma, and allergic rhinitis

Genetic predisposition to develop 1+ of the above

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51
Q

What are the diagnostic criteria for atopic dermatitis?

A

Itchy skin AND 3+ of the following:

(1) Involvement of skin creases
(2) Asthma or hay fever
(3) Dry skin in the last year
(4) Visible flexural eczema
(5) Onset under 2 years of age

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52
Q

What is the mutation associated with atopic dermatitis?

A

Filaggrin

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53
Q

What is the bacteria associated with atopic dermatitis?

A

Staph. aureus (acts as a superantigen)

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54
Q

What is lichenification?

A

Areas of thickened areas of skin w/ greater creases; sign of chronic dx

55
Q

Where is atopic dermatitis located?

A

Areas of flexural skin

Antecubital fossa, popliteal fossa, neck, wrists, ankles

56
Q

What is keratosis pilaris?

A

Bumpy skin around the hair follicles

57
Q

Is contact dermatitis immunologically mediated?

A

NO.

Non-immunologically mediated; caused by direct cytotoxic effect from contact with irritant.

58
Q

What is intertrigo?

A

Irritant contact dermatitis in the folds of the skin, where they rub against one another

59
Q

What is allergic contact dermatitis?

A

IMMUNE MEDIATED

Type IV hypersensitivity

60
Q

What is the typical time span of a drug rash?

A

Usually occurs 7-14 days after starting a new medication

Starts sooner in cases of receiving an “old” medication

Eruption will resolve spontaneously in 1-2 weeks. However, it can take up to 3 months to resolve completely.

61
Q

In what contexts does stasis dermatitis occur?

A

In cases of venous insufficiency

Varicose veins, chronic LE edema, venous stasis ulcers

Can be BILATERAL

62
Q

Lichen simplex chronicus

A

Thickened plaques (“lichenification”) that result from chronic itching

Topic steroids are 1st line therapy. Antihistamines can be used for itching.

63
Q

Venous stasis ulcers. Where do they occur? After what? What do they look like?

A

Occur primarily just above ankle on medial leg. Occur after leg swelling, varicose veins, or in patients with a history of blood clots. Appear erythematous, with a yellow base. Irregular borders. Can be purulent if infected.

64
Q

Nummular dermatitis. Also called what? Where does it appear? What does it look like? In whom does it appear?

A

Also called discoid eczema. Appears mostly on legs, but also on arms/trunk. Looks like round pink circles with irregular borders. More common in men 50+

65
Q

What is cradle cap sebbhoreic dermatitis?

A

Flaky, white/yellow oily scales on scalp. Can become confluent & a thick scale on the scalp. Begins 1 week after birth and may persist for several months.

66
Q

What is sebbhoreic dermatitis characterized by? Where does it usually occur?

A

Flaky, greasy scales.

Occurs symmetrically on the face. Occurs in areas rich in sebaceous glands.

67
Q

What is the pathogenesis of seborrheic dermatitis?

A

Caused by a combination of overproduction in sebaceous glands and the yeast organism Malassezia furfur

68
Q

What is sebbhoreic dermatitis linked to?

A

Neurological disorders, like Parkinson’s, head injury, and stroke
Annnd HIV :(

69
Q

Guttate psoriasis is associated with what?

A

Strep throat

70
Q

What other diseases is psoriasis associated with?

A

Arthritis!
(5-20% of pts)

Metabolic syndrome, CVD, and MI

71
Q 
What are the locations of the following skin diseases?
Stasis dermatitis
Sebbhoreic dermatitis
Psoriasis
Atopic dermatitis
A

Stasis dermatitis - lower legs
Sebbhoreic dermatitis - scalp
Psoriasis - extensor surfaces (knees, elbows)
Atopic dermatitis - flexor surfaces (popliteal fossa, antecubital fossa)

72
Q 
What are the etiologies of the following diseases? 
Stasis dermatitis
Sebbhoreic dermatitis
Atopic dermatitis 
Irritant derm 
Contact derm
A 
Stasis derm - lower extremity edema
Sebbhoreic dermatitis - Malassezia furfur
Atopic derm - Filaggrin 
Irritant derm - common irritants
Allergic contact derm - common allergens
73
Q

What are the genetic transformations in BCC?

A

The majority of BCCs have a loss of function of PTCH1

PTCH1 normally blocks SMO (smoothened). Both are transmembrane proteins. If SMO is unchecked –> signals tumor growth –> cancer!

74
Q

What is the chemotherapy for BCC?

A

Vismodegib (inhibitor of SMO)

75
Q

What is actinic keratosis?

A

Pre-cancer

Most common type of pre-cancer. Approx 65% of SCCs and 36% of BCCs started as AKs.

76
Q

What is SCC in situ?

A

SCC only in the epidermis

77
Q

What is a keratoacanthoma?

A

A subtype of SCC.

Rapid growth over 6-8 weeks. 1-3 cm papule/nodule. Has crater in the middle like a volcano!

78
Q

When is metastasis of SCC more common?

A

When it’s on the lip

79
Q

What are the risk factors for skin cancer?

A

Age, skin type, UV radiation
Genetic factors
HPV
Level of immunosuppression: CD4 count, meds, transplant (heart > kidney > liver)

80
Q

What type of skin cancer are transplant pts more likely to get? Non-transplant?

A 
Transplant = SCC:BCC 4:1
Non-transplant = BCC:SCC 4:1

Transplant = you’re SCrewed

81
Q

ABCDE for melanoma?

A 
Asymmetry
Border irregularity 
Color changes
Diameter >6mm
Evolution
82
Q

What is the Breslow Depth for skin cancer?

A

Tumor invasion in mm

83
Q

What are Clarks Levels for skin cancer?

A 
I. Epidermis
II. Papillary dermis
III. Mid dermis
IV. Reticular dermis
V. Subcutaneous fat
84
Q

What is the most frequent mutation in melanoma?

A

BRAF

BRAF acts on MEK –> –> –> acts on genes affecting growth & proliferation

85
Q

What is the chemotherapy used to treat melanoma?

A

Vermurafenib

86
Q

What is Kaposi’s sarcoma?

A

Endothelial malignancy triggered by HHV-8. Slowly progressive.

87
Q

What are the types of Kaposi’s sarcoma?

A

Classic - occurs primarily in elder men of Eastern European descent

Lymphadenopathic - aggressive form primarily in equatorial Africa. Affects young men and is rapidly fatal.

AIDS-associated - incidence is declining with better ARTs

88
Q

What do infantile hemangiomas stain with?

A

Glut-1, a placental antigen

89
Q

What is one complication of a port wine stain?

A

Sturge Weber Syndrome
10-15% of port wine stains in V1 distribution are associated with ocular and neurologic abnormalities, including glaucoma, seizures, and developmental delay

90
Q

What is nevus sebaceus?

A

A hamartoma that most commonly presents as a papillomatous yellow-orange linear plaque on the face or scalp

On the scalp, associated with alopecia

Somatic mutations in HRAS and KRAS

Epithelial neoplasms occur in 10-30%

91
Q

What is the term for nuclear shrinking?

A

Pyknosis

92
Q

What is the term for cell fusion?

A

Syncytia

93
Q

Influenza - basic structure?

A

Genome is 8 pieces of ssRNA

94
Q

Influenza - important proteins?

A

The hemagglutinin (H) and neuraminidase (N) glycoproteins. Both are surface proteins. Names of viruses are based on the numbers of each on the viral coat.

95
Q

Influenza - what does it look like in neonates/children/adults?

A

Neonates - lethary, decreased eating, mottling, apnea
Children - GI symptoms, fever, anorexia, respiratory symptoms
Adults - we know

96
Q

Describe the antigenic drift of influenza that is a result of reassortment of genome segments

A

Because influenza has a segmented genome, gene segments can be “swapped” between strains.
Pigs can be infected by pig, bird, & human strains of influenza - simultaneous infection might allow for reassortment of genes.

Pigs = “mixing vessel”

97
Q

What is the fomite contamination of influenza?

A

Steel & plastic - 24-48 hours
Cloth, paper, & tissue - 8-12 hours
Hands - 5 min

98
Q

What are the two types of influenza vaccine?

A

(1) Inactivated influenza vaccine - injectable, killed virus. All people 6 mos+. Trivalent or quadrivalent.
(2) Live attenuated influenza vaccine - intranasal. For people 2 yrs - 49 years. Quadrivalent.

99
Q

What is H5N1?

A

A highly virulent strain circulating in bird populations in Asia, with mortality up to 40%. Currently cannot infect humans effectively; however could mutate the hemagglutinin alpha 2,3 linkage into an alpha 2,6 linkage, leading to human susceptibility.

100
Q

RSV - basic structure?

A

ssRNA, non-segmented

2 subtypes, A & B
A causes more severe disease

101
Q

RSV - important proteins?

A

F protein: causes fusion of viral envelope to host cell. Fusion of membranes of infected cells to each other to cause “syncytia”

G protein: Initial binding of virus to the host cell

102
Q

RSV - pathophys?

A

Invades conjunctiva & nasopharynx; 3-5 day incubation period.

Results in collection of fluid in alveoli & bronchioles. Causes constriction of SM in bronchioles –> respiratory symptoms (hypoxia, hyperexpansion by mucus plugging, wheeze, etc.)

103
Q

RSV - whom does it affect?

A

90% of children have had it by 2 years of age

can be asymptomatic to severe

104
Q

Is there a vaccine for RSV?

A

Nope. They tried in the 1960s and made the infections considerably worse. Serum antibody without local respiratory antibody may worsen the disease.

105
Q

What is Respigam?

A

Human pooled Ab with high RSV titer –> decrease in dx severity & hospitalization

Once-monthly IM injection for high risk groups. Expensive :(

106
Q

Ebola - basic structure?

A

Filo virus
7 structural proteins and 2 non-structural proteins
(-) sense RNA

107
Q

Ebola - important proteins?

A

Glycoprotein spikes on envelope - key for pathogenicity

Matrix proteins VP40 and VP24 - virus structure, assembly, budding, etc.

Nucleocapsid & nucleoproteins

Polymerase complex: VP35 & L. Function is replication.

108
Q

Ebola - pathophys?

A

Enters body through mucosal surfaces or cuts; travels to lymph nodes.
End result: CYTOKINE STORM. T cell depletion, hemorrhage/fluid imbalance, hepatic dysfunction (preventing shutting off of cytokine storm), DIC.
Die from hypovolemia +/- end-organ failure.

109
Q

What enables ebola virus to evade the immune system?

A

Glycoprotein on the surface

Masks sites on virus that our Ab bind to
Can mutate to evade
Shields/blocks proteins on the surface of host cells from recognized as infected by immune cells

Secreted GP (sGP) acts as a “decoy” and tricks our immune system - Ab secreted against it are non-neutralizing for virus

110
Q

What are the drugs that are inhibitors of viral neuraminidase (for the influenza virus)?

A

Oseltamivir (Tamiflu), Zanamivir (Relenza), and Peramivir (Rapivab)

111
Q

What is the mechanism of action of oseltamivir, zanamivir, and peramivir?

A

Block the activity of the viral enzyme neuraminidase. The enzyme cleaves sialic acid from the cell’s plasma membrane, allowing for interaction between viral hemagglutinin and cell sialic acid. Without the enzyme activity, viral particles cannot translocate within & bud out of the cell.

112
Q

What are the pharmacokinetics of oseltamivir, zanamivir, and peramivir?

A

Oseltamivir: ORALLY as prodrug. Renal elim.
Zanamivir: INHALED bid x 5 days. Renal.
Peramivir: Single IV dose

113
Q

When are influenza drugs used during the course of influenza?

A

If started within 48 hours, can reduce duration of symptoms by 1-2 days.
Can be used prophylactically in contacts of sick person.

114
Q

What are some of the adverse reactions of oseltamivir, zanamivir, and peramivir?

A

Oseltamivir: minor, occasional nausea and vomiting (reduced by taking with food)

Zanamivir: bronchospasm reported uncommonly in patients with asthma or COPD

Peramivir: diarrhea and GI effects; neutropenia has occurred; rarely serious skin reactions

115
Q

What is the mechanism of amantadine (Symmetrel) and rimantadine (Flumadine)?

A

They block the virally-encoded H+ ion channel (M2 protein) that’s necessary for membrane fusion & viral content release when it’s in the endosome (uncoating)

116
Q

What are the pharmacokinetics of amantadine and rimantadine?

A

Effective orally - accumulate in the lungs
Amantadine - excreted in urine
Rimantadine - hepatic elimination

117
Q

What are the clinical uses of amantadine and rimantadine?

A

Prophylaxis and treatment of influenza A infections

118
Q

What are some of the adverse reactions of amantadine and rimantadine?

A

Amantadine - may cause dizziness, lightheadedness, difficulty concentrating
Rimantadine - better tolerated because of poorer CNS penetration

119
Q

What are the mechanisms of antiherpes drugs (acyclovir, valacyclovir, penciclovir, famciclovir)?

A

Broadly: they inhibit the viral DNA polymerase.

When they enter the nucleus, get initially phosphorylated by a VIRAL enzyme (usually thymidine kinase). Then, cell enzymes convert the monophosphate to a triphosphate form.

Drug-TP competes with cell dGTP for the viral DNA polymerase & gets incorporated into the replicated DNA strand –> terminates further replication and elongation, AND binds & inactivates viral DNA polymerase.

120
Q

What are the pharmacokinetics of the antiherpes drugs?

A

Acyclovir: poor oral absorption; available as topical & IV
Valacyclovir: prodrug of acyclovir –> oral availability good
Penciclovir: topical only
Famciclovir: prodrug of penciclovir –> oral availability good

Neonatal acyclovir clearance is only 1/3 of adults.

121
Q

What does Docosanol (Abreva) do?

A

Prevents fusion between cellular & viral envelope –> blocks viral entry into cell

Topical treatment 5x daily to lips begun within 12 hours reduces healing time about one day in HSV.

122
Q

What is the most common form of resistance to antiherpes drugs?

A

Reduction or loss of expression of viral thymidine kinase

123
Q

What is the drug for RSV?

A

Ribavirin
Oral: Copegus®, Rebetol®
Aerosolized: Virazole

124
Q

What is the mechanism of action of ribavirin?

A

Ribavirin-TP inhibits GTP-dependent 5’ capping of viral mRNA

125
Q

What are the pharmacokinetics of ribavirin?

A

Oral absorption is good; increases with fatty foods

Elimination is via hepatic metabolism and renal excretion of unchanged drug

126
Q

What are the adverse reactions of ribavirin?

A

Inhalation: generally well tolerated
Oral-systemic: high incidence of hemolytic anemia!!
TERATOGENIC. Should not be administered during pregnancy. Pregnant health care workers should not care for pts using aerosolized ribavirin.

127
Q

What is Palivizumab?

A

Humanized mAb to RSV F glycoprotein that is indicated for RSV immunoprophylaxis in infants and young children with congenital heart disaese

128
Q

What is the mechanism of action of gancyclovir and valgancyclovir?

A

Cell uptake, initial phosphorylation by viral enzyme (main mechanism of selectivity). Gancyclovir-TP gets incorporated by viral DNA polymerase –> stops elongation.

129
Q

What are the clinical uses of gancyclovir?

A

Treatment & chronic suppression of CMV retinitis in immunocompromised patients. Also good at controlling CMV in transplant patients.

130
Q

What is the major adverse reaction with gancyclovir?

A

Myelosuppression with neutropenia and thrombocytopenia

131
Q

What is the mechanism of action of foscarnet?

A

DOES NOT REQUIRE CELL ACTIVATION

Binds to pyrophosphate binding site of DNA/RNA polymerases –> blocks viral replication.

132
Q

What are the clinical uses of foscarnet?

A

Effective against CMV retinitis, particularly in immunocompromised patients

Also effective against ganciclovir-resistant CMV infections and acyclovir-resistant HSV and VZV
infections

133
Q

What are the adverse reactions of foscarnet?

A

Major side effect is nephrotoxicity and hypocalcemia, can be quite severe or even fatal

CNS abnormalities also have been reported

Disease & Defense (3 decks)

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