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Invaders and Defenders > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

reservoir of Ebola:

Characteristics of Ebola:

  • massive replication in:
  • necrosis of:
  • ______ of lungs
  • fatality %
  • ________ is similar
A

reservoir:

  • fruit bat
  • may also spread by non human primates - blood, body fluids, and tissues

characteristics

  • virus undergoes massive replicaiton in endothelial cells, phagocytes, hepatocytes
  • necrosis of liver, kidneys, gonads, spleen, lymph nodes
  • hemorrhage of lungs
  • severe - 80-90% fatality
  • Marburg Hemmorrhagic fever is similar
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2
Q

reservoir of hanta virus

characterisitcs of hanta virus

  • what starts initially?
  • what starts later on?
  • death percentage?
A

reservoir

  • rodents natural reservoir, specially deer mouse’s urine, droppings, saliva

characteristics

  • fatigue, fever and muscle aches initially
  • later coughing, shortness of breath, fluid filled lungs
  • death in ~40%
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3
Q

HPV’s E7 gene can bind to ______

–> leads to?

A

binds to Rb- gatekeeper off duty

–> leads to uncontrolled cell reproduction

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4
Q

HPV’s E6 protein can bind to?

–> leads to?

A

can bind to p53

–> repeated replication of cells with incorrect DNA information

–> no apoptosis of mutated cells

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5
Q

HPV’s E6 can also activate?

–> leads to?

A

can also activate telpmerase

–> maintains a repeated cell cycle that continues to produce viral cells

–> mutant cells continue to reproduce out of control

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6
Q

HPV: Verruca

details:

HPV types:

A

common skin wart

2, 4, 40

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7
Q

HPV: plantar wart

details

HPV types

A

sole of foot

1, 2, 4

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8
Q

HPV: condyloma acuminatum

details

HPV types

A

genital (also oral)

6, 11, 42, 43, 44, 55 and others

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9
Q

HPV: Hecks disease

details

HPV types

A

focal epithelial hyperplasia, oral

13, 32

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10
Q

HPV: cancer

details

HPV types

A

cervix, pharynx, oral

16, 18, 31, 33, 35, 39, 45, 51

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11
Q

Papilloma:

is it common?

_____ like surface

where can it be found?

color

keratinized?

is it high risk HPV?

A

common, pedunculated

cauliflower like surface

soft palate, tongue, uvula - anywhere

usually pink

non-keratinized

not high risk HPV

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12
Q

HPV: Verruca vulgaris - common wart

color?

keratin?

what does it look like?

high risk HPV?

A

white

more keratin than papilloma

elevated with crisp borders, flat verrucous or warty top

not high risk HPV

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13
Q

HPV: Papillomas and verrucas

____ disappear spontaneously

how to get rid of on skin?

how to get rid of intraoral?

A

2/3

on skin

  • surgical excision, liquid nitrogen, or keratinolytic agents

intraoral

  • surgical excision, cryotherapy or electrosurgery
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14
Q

HPV: Condyloma acuminatum (genital warts)

is it infectoius/how is it spread?

what does it look like?

larger or smaller than papillomas? can there be multiple?

high risk HPV?

how should it be removed?

A

infectious - can spread to other people and other sites

small and sessile to large, papillary proliferations, cauliflower shape

larger than papillomas, often multiple

not high risk HPV

surgically, laser removal may spread the virus to other sites or personnel through aerosol (non surgical management also available)

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15
Q

HPV: Hecks disease: focal epithelial hyperplasia, oral

  • do adults have symptoms?
  • is it high risk HPV?
  • what is the shape?
  • color?
  • does it have malignant transformation potential?
  • usually _____ viral infection
  • what can it mimic?
  • could be mistaken for what in children?
  • can be more florid and persistent in ____ patients
  • may be removed _____ if they interfere with function
A
  • adults usually have minimal symptoms
  • not high risk HPV
  • flat, smooth, soft, papules
  • same color as surrounding mucosa usually
  • no ulceration
  • no malignant transformation potential
  • usually self limiting viral infection
  • can mimic condyloma acuminatum
  • could potentially be mistaken for sxual abuse in children
  • can be more florid and persitant in HIV+ patients
  • may be removed surgically
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16
Q

Antiviral Agent Mechanisms of Action

Block:

A

viral attachment to cell membrane

entry of cell via endocytosis or fusion

uncoating of virus

viral DNA or RNA replication (and transcription for retroviruses)

viral protein synthesis by cell

viral exit from cell

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17
Q

Key Concepts For Antiviral Agents:

Only active against:

______ is best option, so ______ highly recommended

DNA viruses

  • easier to prevent with ______ vs RNA viruses due to:
  • more/less treatments than for RNA viruses

RNA viruses

  • more/less treatments compared to DNA viruses
  • breakthrough in ______ treatment in last decade
  • ________ treatment now highly effective
A

replication viruses, not latent viruses

prevention, vaccines

DNA viruses

  • vaccines
  • more

RNA viruses

  • less
  • Hep C
  • antiretroviral
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18
Q

Key Concepts for Antiretroviral Agents:

What are the mechanisms of action?

contemporary therapy uses combinations of ___ or ___ agents to maximize suppression and minimize ADRs

Treatments are life long/short

What are some ADRs?

What are the DDIs?

A

MOA:

  • reverse transcriptase inhibitor
  • protease inhibitor
  • integrase strand transfer inhibitor

2 or 3

treatments are life long

ADRs

  • metabolic effects with NRTIs, NNRTIs, PIs
  • clucose metabolism abnormalities
  • osteoporosis
  • QTc prolongation with PIs

DDIs

  • almost none for NRTIs, but many for other agents
  • check with pharmacist when prescribing a macrolide (bacterial infection) or triazole (fungal infection)
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19
Q

Key Concepts for Herpes Virus Agents

MOA:

Agents

ADRS:

DDI:

____ is safe to use during pregnancy and lactation

A

MOA

  • most agents are nucleoside inhibitors, competitively binding during DNA transcription and thus terminating it

Agents

  • Acyclovir
  • Valacyclovir
  • Famcyclovir
  • Docosanol (OTC)

ADRs

  • nausea
  • headache

DDIs

  • few with acyclovir/valacyclovir
  • famciclovir - almost none

acyclovir

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20
Q

Antiviral Agents for Herpes Infections

HSV-1 and HSV-2:

A

acyclovir/valacyclovir

famciclovir

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21
Q

Antiviral Agents for Herpes Infections

VZV:

A

acyclovir (chicken pox/shingles)

valacyclovir (shingles)

famciclovir (shingles)

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22
Q

Antiviral Agents for Herpes Infections

EBV

A

no agent approves - supportive care only

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23
Q

Antiviral Agents for Herpes Infections

CMV

A

valgancyclovir

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24
Q

Key Concepts for Influenza Agents

MOA:

Agents

ADRs:

DDIs

comments:

  • _____ safe in pregnancy
  • start treatment within ___ days of symptoms in otherwise healthy patients
  • in patients with high risk of severe illness there is a benefit seen even at start ___ days after symptom onset
  • later start ____ in immunocompromised, longer/shorter therapy needed
A

MOA

  • blocks viral RNA transcription and replication (baloxavir) or inhibit virus exit from cell (amivers)

Agents

  • oseltamivir dosed twice daily for 5 days
  • zanamivir 2 inhalations twice daily for 5 days
  • baloxavir as single oral dose

ADRs

  • nausea
  • vommiting
  • headache

DDIs

  • nothing notable

comments

  • oseltamivir
  • 2
  • 5
  • OK, longer
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25
Q

Key Concepts for Hepatitis C Agents

MOA:

  • referred to as:
  • these agents not taken up by:

Agents

  • Agents usually used in _______ and regimen selection depends on: ______, _______, and _______

ADRs

DDIs

Comments: agents used for ___-___ weeks

A

MOA

  • multiple MOAs for the 3 classes of agents
  • referred to as direct acting antiviral; these agents are not taken up by non-infected cells

Agents

  • NS3-4 protease inhibitors; suffix is -previr
  • NS5a inhibitors; suffix is -asvir
  • NS5b nucleoside/non-nucleoside inhibitors; suffix is –buvir
  • Agents usually used in combination and regimen selection depends on the viral genotype, the stage of disease, and response to prior therapy

ADRs

  • fatigue
  • headahce
  • insomnia

DDIs

  • potential for many
  • most are 3A4 substrates

comments: agents used for 8-12 weeks

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26
Q

COVID: asymptomatic

indicators:

treatment:

A

indicators: no symptoms
treatment: none

27
Q

COVID: mild disease

indicators

treatment

A

indicators

  • fever
  • cough
  • sore throat
  • diarrhea
  • notmal O2 sat and CXR

Treatment: none

28
Q

COVID: moderate disease

indicators

treatment

A

indicators:

  • mild disease + LRTI on CXR or O2 sat >94% room air

Treatment: monoclonal antibody if risk factors

29
Q

COVID: severe disease

indicators

treatment

A

indicators:

  • moderate disease
  • O2 sat <94%
  • CXR >50% infiltrates

treatment

  • remdesivir
  • steroid
  • tocilizumab
30
Q

COVID: critical disease

indicators

treatment

A

indicators

  • septic shock
  • intubated and or multisystem organ failure

treatment

  • steroid
  • tocilizumab
  • anticoagulation
31
Q

What components does the early pathway defects involve?

A

C1-C4

32
Q

what components does the late pathway defects involve?

A

C5-C9

33
Q

Early classical pathway defects (C1-C4) present in one of 2 ways:

A

invasive infections (sepsis, pneumonia, meningitis) with encapsulated organisms (s. pneumoniae, h. influenzae, N. meningitidis)

lupus or glomerulonephritis (autoimmune kidney disease that occurs in Lupus)

34
Q

Late complement pathway defects (C5-C9) present almost exlusively with _____ infections with _______ species

  • examples

Late pathway defects increase risk of meningococcal disease approx. _____ fold

Typically the first Neisserial infection occurs in the _____ decade of life

  • Capsular polysaccharides of the meningococcus are highly charged, hydrophilic structures that act as a:
  • _______ is an important alternate form of clearence for these organisms
  • Some Neisseria strains produce ______ which leads to ________
A

invasive infections (sepsis, meningitis, etc…)

Neisseria species (N. meningitidis, N. gonorrhoeae)

8000 fold

2nd

  • barrier to phagocytosis
  • complement mediated bacteriolysis
  • a human factor H-binding protein –> degredation of C3 and hinders bacterial lysis
35
Q

C1-INH and Kinin-Kallikrein System

Bradykinin: what is it and what does it cause?

what are the 2 levels that C1-INH inhibits?

C1-INH is important in _____ system where it is the major inhibitor of _______

the absence of C1-INH causes:

A

Bradykinin: small peptide that causes blood vessel dilation and increased vascular permeability, causes fluid to leak into the tissues (edema) and decrease blood pressure

after FXIIa and after Kallikrein

clotting, Kallikrein

heriditory angiodema

36
Q

hereditary angiodema

_____ deficiency

characterized by:

attacks can be triggered by:

A

C1-INH

attacks of rapid swelling in various tissues

can be triggered by trauma, surgery, emotional stress

  • dental procedures can cause life threatening swelling of the airways
37
Q

HAE in dental procedures

____ are the most affected

is there an obvious cause? what can it be triggered by?

Management:

A

Airways

no obvious cause, but can be triggered by anxiety, invasice procedures, and trauma

management

  • anxiety control during the operating phases
  • does not respond well to epinephrine, antihistamines, or glucocorticoids
  • treatment - androgenic hormones, C1 esterase inhibitor (Berinert)
38
Q

Neutropenia (low neutrophil counts)

1) neutropenia can either be _______ or _______
2) _______ neutropenia is most common
* causes:
3) symptoms:
4) bacterial entry from:
5) increased susceptibility due to:

A

1) congenital, aquired
2) aquired
* chemotherapy, drug induced, autoimmune
3) infections/sepsis (Ecoli, Pseudomonas), fever, mouth sores, peri-rectal pain and abscesses, skin infections, swelling/inflmmation of the gums
4) gut, mouth
5) decreased numbers of functioning PMN’s (neutrophils)

39
Q

Leukocyte Adhesion Deficiency (LAD)

different types caused by ______ that affect either the ______ step or the ______ step of leukocyte extravasation

all affect the ability of:

As a result:

  • impaired _____ function due to:
  • patients get reccurent ______ and ______ infections (by what bacteria?)
  • other symptoms:
A

genetic defects, tethering/rolling, firm adhesion

phagocytes to traffic into tissues normally

as a result:

  • neutrophil, impaired adhesions-dependent functions of leukocytes
  • skin and soft tissue infections (Staph, Ecoli, Fungal), absecces and boils but no pus
  • periodontitis, poor wound healing
40
Q

Chronic Granulomatous Disease

caused by:

cells do everything normal except:

  • _______ deficiency - cannot make ______

As a result?

A

defects in components of NADPH oxidase complex

they cant degrade what they have ingested

  • neutrophil deficiency - cannot make ROS

Patients have skin and soft tissue infections or lymphadenitis with catalase + organisms (Staph, Aspergillus, Burkholderia cepacia, etc)

41
Q

Patients with Primary Immune Defects

The principal consequence of immune deficiency is ____________ (frequency, severity or unusual organisms)

  • Patterns of specific organisms/infectious syndromes, other patient symptoms can suggest the source of the immune problem
  • Lab tests then help you narrow in on which immune compartment is affected and where!

Children with immunodeficiencies commonly show _________

Patients with immunodeficiencies are also susceptible to specific types of ______

Paradoxically, certain type of immune deficiencies are also associated with increased incidence of _________ problems

A

is an increased susceptibility to infection

failure to thrive

cancer

autoimmune

42
Q

Immune System Function Spectrum

Immune system deficiency:

Primary:

Secondary:

A

Primary:

  • born with a genetic defect that impairs innte or adaptive immunity (hereditary angiodema caused by C1-esterase deficiency)

Secondary

  • develops an immune deficiency as a result of a health event (HIV infection)
43
Q

Immune System Function Spectrum

System working as intended:

innate immunitt:

adaptive immunity

A

innate immunity

  • general response to pathogens that prevents immediate spread of disease
  • short acting response

Adaptive immunity

  • pathogen- specific
  • needs time to develop
  • long acting response
44
Q

Immune System Function Spectrum

Immune system over-responsiveness

autoimmunity:

hypersensitivity:

A

autoimmunity

  • the body’s self tolerance system fails and the immune system attacks its own healthy cells

Hypersensitivity

  • the body overreacts to a stimulus, usually an exogenous antigen
45
Q

what are the commo cells between the innate immune system and adaptive immune system?

A

ygT cell

NK T cell

46
Q

Immune system pro-inflammatory cytokines:

lost of _____

  • sustained _______ processes
  • a lot of _______ are pro inflammatory
A

cytokines - interleukins

  • inflammatory
  • interleukins
47
Q

_______ is part of the healing process

cells get rid of things and initiate:

why wouldnt you want to give an antiinflammatory after injury?

A

inflammation

tissue repair

dont want to inhibit the healing process

48
Q

NSAIDS

inhibit:

do not affect:

A
  • prostaglandin
  • prostacyclin
  • thromboxane production
  • leukotriene
  • tumor necrosis
  • interleukin production
49
Q

Corticosteroids

inhibit:

used for:

A
  • prostaglandin
  • prostacyclin
  • thromboxane
  • leukotriene
  • interleukin
  • indications other than just inflammation
50
Q

Key Concepts for NSAIDs

MOA

Agents

ADRs

DDIs

Comments

A

MOA: Either non-selective (COX-1 and COX-2) or selective (COX-2) inhibitors of cyclooxygenase and so prevent production of prostaglandins

Agents: Ibuprofen – Naproxen – Celecoxib

ADRs – GI effects are most worrisome—lower risk with celecoxib; edema; risk of CV events in patients with existing CV disease

DDIs – Many. Most concerned about risk of bleeding and AKI development in specific situations

Comments – Antipyretic, analgesic properties

51
Q

Key Concepts for Corticosteroids

MOA

Agents

ADRs

DDIs

Comments

A

MOA – Blocks protein synthesis of interleukins and the arachidonic acid pathway

Agents – see one-pager, know this information – Prednisone – Dexamethasone – Triamcinolone

ADRs – A plethora of short-term and long-term adverse effects

DDIs – Oral agents have several—when given with 3A4 inducer will decrease serum concentration of corticosteroids

Comments – Patients on chronic therapy with prednisone ≥ 7.5 mg daily may need extra stress dose on day of invasive dental surgery

52
Q

what do Anti-inflammatory agents do?

A

– Suppress inflammatory processes all over the body

53
Q

what do disease modifying drugs do?

A

– Slow or arrest the tissue-damaging process (e.g., impair cell division)

54
Q

what do direct immunosuppressants do?

A

– Have several effects on a smaller part of the immune process

55
Q

what do biological response modifiers do?

A

Target a specific step in the immune process e.g., specific IL receptor or T-cell (e.g, CD28) or immune modulator or cell signaling pathway

Monoclonal antibodies (mabs): block, flag, or deliver

Small molecule kinase inhibitors (nibs): target enzymes that affect cell signaling, metabolism, growth, or survival

Biosimilars are biologic agents that do the same thing as a previously-introduced biological agent but are not quite the same exact molecule

56
Q

Immunosuppressive agents oral health effects:

A

aphthous stomatitis (ulcers in mouth)

herpes reactivation

oral candidiasis

DIGO (drug induced gingival overgrowth)

tongue edema

57
Q

Ibuprofen

MOA

ADRs

DDIs

Comments

A

MOA. Non-specific COX inhibitor—prevents prostaglandin production

ADRs:

  • epigastric pain, heartburn
  • nausea
  • avoid use in patients with known or history of gastroesophageal reflux disease (GERD) or peptic ulcer due to risk of GI bleed
  • can worsen pre-existing edema
  • tinnitus rare
  • increases risk of adverse cardiovascular event in patients with pre-existing heart disease (unstable angina, heart failure, prior MI)

DDIs: Many.

  • Can prolong bleeding time in patients on oral antiplatelet or anticoagulant agents
  • affect kidney function—use carefully in patients taking ACE inhibitors and thiazide diuretics as incautious use can lead to acute kidney injury

Comments: Has antipyretic, analgesic properties as well as anti-inflammatory properties

58
Q

Naproxen

MOA

ADRs

DDIs

Comments

A

MOA: Non-specific COX inhibitor—prevents prostaglandin production

ADRs: see ibuprofin

DDIs: see ibuprofin

Comments: Available as a base and sodium salt. 200 mg naproxen base = 220 mg naproxen sodium. Has antipyretic, analgesic properties as well as anti-inflammatory properties

59
Q

Celecoxib

MOA

ADRs

DDIs

Comments

A

MOA: COX-2 inhibitor—doesn’t affect prostaglandin production in GI tract, kidneys, platelets (COX-1 prostaglandin production)

ADRs:

  • diarrhea
  • dyspepsia
  • upper respiratory tract infection
  • may increase risk of adverse cardiovascular event in patients with pre-existing heart disease (unstable angina, heart failure, prior MI), but evidence points to risk among the lowest of all NSAIDs

DDIs:

  • Moderate CYP 2C9 substrate
  • weak 3A4 substrate
  • Weak 2D6 inhibitor
  • Many, but hard to distinguish from non-selective NSAIDs

Comments: Probably a better candidate for patients with a history of GERD or peptic ulcer than non-selective NSAID

60
Q

Diclofenac

A

A 3% gel was effective in one study for aphthous ulcer treatment

61
Q

Prednisone

MOA

ADRs

DDIs

Comments:

A

MOA: Blocks protein synthesis of interleukins (late phase inflammation) and the arachidonic acid pathway so blocks production prostaglandins and leukotrienes; some mineralocorticoid activity

ADRs:

  • Short-term: glucose intolerance, hypertension, dysphoria (dose related), GI toxicity, fluid retention, weight gain
  • Long-term: cataracts, glaucoma, osteopenia/osteoporosis, impaired wound healing, skin thinning, striae (particularly with topical use), moon face, edema, buffalo hump and other abnormal fat deposits, anemia

DDIs: Many.

  • Major CYP 3A4 substrate, so any inducer will decrease serum concentrations of prednisone
  • Concomitant administration will enhance GI toxicity of NSAIDs.
  • May enhance immune suppression effect of other immunotherapies.

Comments: 5 mg daily equals physiologic cortisol production

62
Q

Dexamethasone

MOA

ADRs

DDIs

Comments

A

MOA: Blocks protein synthesis of interleukins (late phase inflammation) and the arachidonic acid pathway so blocks production prostaglandins and leukotrienes; no mineralocorticoid activity

ADRs: See prednisone.

DDIs: See prednisone.

Comments: Preferred when no mineralocorticoid activity is desired

63
Q

Triamcinolone

MOA

ADRs

DDIs

Comments

A

MOA: Blocks protein synthesis of interleukins (late phase inflammation) and the arachidonic acid pathway so blocks production prostaglandins and leukotrienes; minimal mineralocorticoid activity Product options. 0.1% oral paste; intra-articular suspension 10 mg/mL, 20 mg/mL, 40 mg

ADRs: Less than with prednisone because topical or intra-articular administration

DDIs: minimal

Comments: Triamcinolone acetonide is a moderate potency corticosteroid that is widely used as a topical agent for many inflammatory dermatologic conditions

64
Q
A

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