Exam 4 Flashcards
(64 cards)
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
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%
3
Q
HPV’s E7 gene can bind to ______
–> leads to?
A
binds to Rb- gatekeeper off duty
–> leads to uncontrolled cell reproduction
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
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
6
Q
HPV: Verruca
details:
HPV types:
A
common skin wart
2, 4, 40
7
Q
HPV: plantar wart
details
HPV types
A
sole of foot
1, 2, 4
8
Q
HPV: condyloma acuminatum
details
HPV types
A
genital (also oral)
6, 11, 42, 43, 44, 55 and others
9
Q
HPV: Hecks disease
details
HPV types
A
focal epithelial hyperplasia, oral
13, 32
10
Q
HPV: cancer
details
HPV types
A
cervix, pharynx, oral
16, 18, 31, 33, 35, 39, 45, 51
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
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
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
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)
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
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
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
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)
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
20
Q
Antiviral Agents for Herpes Infections
HSV-1 and HSV-2:
A
acyclovir/valacyclovir
famciclovir
21
Q
Antiviral Agents for Herpes Infections
VZV:
A
acyclovir (chicken pox/shingles)
valacyclovir (shingles)
famciclovir (shingles)
22
Q
Antiviral Agents for Herpes Infections
EBV
A
no agent approves - supportive care only
23
Q
Antiviral Agents for Herpes Infections
CMV
A
valgancyclovir
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
25
**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
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
26
COVID: asymptomatic
indicators:
treatment:
indicators: no symptoms
treatment: none
27
COVID: mild disease
indicators
treatment
indicators
* fever
* cough
* sore throat
* diarrhea
* notmal O2 sat and CXR
Treatment: none
28
COVID: moderate disease
indicators
treatment
indicators:
* mild disease + LRTI on CXR or O2 sat \>94% room air
Treatment: monoclonal antibody if risk factors
29
COVID: severe disease
indicators
treatment
indicators:
* moderate disease
* O2 sat \<94%
* CXR \>50% infiltrates
treatment
* remdesivir
* steroid
* tocilizumab
30
COVID: critical disease
indicators
treatment
indicators
* septic shock
* intubated and or multisystem organ failure
treatment
* steroid
* tocilizumab
* anticoagulation
31
What components does the early pathway defects involve?
C1-C4
32
what components does the late pathway defects involve?
C5-C9
33
Early classical pathway defects (C1-C4) present in one of 2 ways:
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
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 \_\_\_\_\_\_\_\_
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
**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:
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
**hereditary angiodema**
\_\_\_\_\_ deficiency
characterized by:
attacks can be triggered by:
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
**HAE in dental procedures**
\_\_\_\_ are the most affected
is there an obvious cause? what can it be triggered by?
Management:
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
**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:
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
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:
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
**Chronic Granulomatous Disease**
caused by:
cells do everything normal except:
* _______ deficiency - cannot make \_\_\_\_\_\_
As a result?
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
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
is an increased susceptibility to infection
failure to thrive
cancer
autoimmune
42
**Immune System Function Spectrum**
Immune system deficiency:
Primary:
Secondary:
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
**Immune System Function Spectrum**
System working as intended:
innate immunitt:
adaptive immunity
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
**Immune System Function Spectrum**
Immune system over-responsiveness
autoimmunity:
hypersensitivity:
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
what are the commo cells between the innate immune system and adaptive immune system?
ygT cell
NK T cell
46
**Immune system pro-inflammatory cytokines:**
lost of \_\_\_\_\_
* sustained _______ processes
* a lot of _______ are pro inflammatory
cytokines - interleukins
* inflammatory
* interleukins
47
\_\_\_\_\_\_\_ is part of the healing process
cells get rid of things and initiate:
why wouldnt you want to give an antiinflammatory after injury?
inflammation
tissue repair
dont want to inhibit the healing process
48
NSAIDS
inhibit:
do not affect:
* prostaglandin
* prostacyclin
* thromboxane production
* leukotriene
* tumor necrosis
* interleukin production
49
Corticosteroids
inhibit:
used for:
* prostaglandin
* prostacyclin
* thromboxane
* leukotriene
* interleukin
* indications other than just inflammation
50
**Key Concepts for NSAIDs**
MOA
Agents
ADRs
DDIs
Comments
**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
Key Concepts for Corticosteroids
MOA
Agents
ADRs
DDIs
Comments
**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
what do Anti-inflammatory agents do?
– Suppress inflammatory processes all over the body
53
what do disease modifying drugs do?
– Slow or arrest the tissue-damaging process (e.g., impair cell division)
54
what do direct immunosuppressants do?
– Have several effects on a smaller part of the immune process
55
what do biological response modifiers do?
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
Immunosuppressive agents oral health effects:
aphthous stomatitis (ulcers in mouth)
herpes reactivation
oral candidiasis
DIGO (drug induced gingival overgrowth)
tongue edema
57
**Ibuprofen**
MOA
ADRs
DDIs
Comments
**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
**Naproxen**
MOA
ADRs
DDIs
Comments
**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
**Celecoxib**
MOA
ADRs
DDIs
Comments
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
Diclofenac
A 3% gel was effective in one study for aphthous ulcer treatment
61
**Prednisone**
MOA
ADRs
DDIs
Comments:
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
**Dexamethasone**
MOA
ADRs
DDIs
Comments
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
**Triamcinolone**
MOA
ADRs
DDIs
Comments
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
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