Week 2 Flashcards
(147 cards)
1
Q
Describe how B and T cell receptors recognize antibodies
what do each recognize?
A
B and T cells differ in the type of antigen they recognize
B cells = macromolecules
T cells = peptide fragments of protein antigens and only when these peptides are presented by MHC
2
Q
Explain how specificities of antibodies are determined
A
specificity is determined by antigen recognition region (variable region) at the tip of the antibody
3
Q
how can antibodies have so many ways to recognize antigens?
A
VDJ Recombination
- random rearrangements of VDJ gene segments –> results in novel AA sequences in antigen binding regions
4
Q
_____ portion of the heavy chains defines the class of Ab
A
Fc (trunk)
5
Q
antigen molecules have different ______
interacts with:
allows for:
A
epitopes
- interacts with B cell antigen receptors
- allows for expansion of immune responses
6
Q
what are the 5 isotypes of antibodies?
A
IgM
IgG
IgD
IgE
IgA
7
Q
IgM functions
structure
_____ antibody to be secreted
peaks:
good for:
A
pentameric (soluble) or monomeric (membrane bound)
first
peaks in 7-10 days
good for activating complement, agglutinating pathogens
8
Q
IgG (_____meric) functions
______ concentration in blood
peaks:
good for:
A
mono
highest concentration in blood
peaks in 2.5-3 weeks
complement activation, cause antibody dependent cellular cytotoxicity (ADCC)
9
Q
IgE (_____meric) functions
binds to receptors on ____ cells and activates:
Great for:
A
mono
mast cells, activates cells to cause histamine release when antigen binds
response to parasites, allergic reactions
10
Q
IgA (____meric) functions:
can cross ____, ____ immunity
main antibody secreted onto:
great for:
A
di
epithelium, passive
mucosal surfaces (tears, saliva, mucous, colostrum)
agglutinating pathogens
11
Q
what are the 4 major functions of antibodies?
A
1) act as central component of B cell receptors (BCR)
2) neutralization (or blocking) of pathogens and toxins
3) mediate responses to antigen by Fc receptor expressing effector cells
4) activation of the complement cascade
12
Q
Describe how TCR-MHC-CD4/CD8 work together
T cell receptors bind small ______ presented on either MHC I (_____ + _______ cells) or MHC II (____ + ______)
T cell receptors can only recognize antigens presented on _____
Mechanisms of killing by CD8 T cells
A
peptides
- MHC I (CD8 + cytotoxic T cells)
- MHC II (CD4 + helper T cells)
MHCs
- perforin/granzyme B
- Fas/FasL mediated killing
13
Q
Understand TCR-MHC affinity and restrictions
large number of recipient T cells react ______ to foreign MHCs on donor tissues (alloimmune response)
If a transplant contains donor T cells, many of them will react how?
A
large number of recipient T cells react strongly to foreign MHCs on donor tissues (alloimmune response)
If a transplant contains donor T cells, many of them will react strongly to foreign MHCs on recipient tissues (graft versus host disease)
- MHC-TCR affinity is random - Some T cells will do nothing
- Many T cells with high affinity to MHC will react strongly
14
Q
how do antibodies mediate responses to antigen by Fc receptor expressing effector cells?
A
Opsonization: Fc-dependent phagocytosis
1) antibody binds and neutralizes its antigen target
2) antibody then binds to Fc receptors on phagocytes via its constant Fc region
3) binding causes phagocytes to become activated, make oxidative burst, etc
15
Q
how does antibody dependent cytotoxicity (ADCC) work?
mediated by:
____, _____, and ______ can also mediate ADCC
A
1) antibodies bind antigens on the surface of target cells
2) natural killer cell CD16 Fc receptors recognize cell-bound antibodies
3) cross lining of CD16 triggers degranulation into a lytic synapse
4) tumor cells die by apoptosis
perforin and granzyme
macrophages, neutrophils, eosinophils
16
Q
how do antibodies activate complement/classical pathway?
A
initiated by binding of the C1 complex to antibody antigen complexes
only IgM and IgG can activate complement
17
Q
how do antibodies activate complement/classical pathway?
A
initiated by binding of the C1 complex to antibody antigen complexes
only IgM and IgG can activate complement
18
Q
T cells have both a _____ and _____ region
A
constant
variable
- each T cell receptor chain has 3 CDRs, thus highly diverse, allowing T cells to recognize millions of different peptides
19
Q
Naive T cell maturation flow chart:
A
naive T lymphocyte –> CD4
or CD8
CD4 –> T helper or T regulatory (CD4, CD8, CD25)
CD8 –> cytotoxic T cell or T regulatory (CD4, CD8, CD25)
20
Q
T helper cell function
A
activate cytotoxic T cells and B cells
21
Q
T regulatory cell function
A
help distinguish between self and non self, prevent autoimmune diseases
22
Q
what happens during T cell activation?
A
cytokines secreted due to interaction between PAMPs and PRRs
these cytokines drive the differentiation of the T cell response into appropriate effector T cell for that infecting pathogen
1) antigen presented on MHC –> starts activation of T cells
2) when T cells are activated by presented antigen, T cells secrete IL2 –> leads to proliferation of T cell that can recognize specific antigen –> can secrete different types of cytokines
depending on what cytokines are secreted, T cells can make appropriate effector cells that can get rid of pathogens
23
Q
how do super-antigens work?
what is the resulting cascade of events?
A
some bacterial and viral proteins bind to MHC class II outside the peptide binding site and to T cell receptors
this leads to non specific T cell activation
Massive IFN gamma release –> large sacle macrophage activation –> massive TNF alpha release (cytokine storm) –> vasodilation, vascular leak, shock, organ failure
24
Q
Travelers’ Diarrhea
clinical features:
- large:
- can lead to:
- other symptoms:
pathogenesis:
- _____ mediated colonizatio of ______
- secretion of _____
- _____ mediated _____ and _____ loss
- low or no _____
- anbsence of ____ in stool
viruses:
bacteria: Most ecoli:
- pathogenic?
- normal or not normal flora?
- commensal/pathogenic?
protozoa:
how to prevent:
A
clinical features:
- large volume watery stools without inflammatory cells or blood
- can lead to dehydration
- nausea, vommiting, bloating, colicky abdominal pain
pathogenesis:
- fimbriae mediated colonization of intestine
- secretion of enterotoxin (LT and ST without tissue damage)
- toxin mediated fluid and electrolyte loss
- low or no fever
- absense of neutrophils in stool
viruses
- rotavirus
- norovirus
- adenovirus
bacteria
- Ecoli: non pathogenic, part of normal flora, commensal
- vibrio cholerae
protozoa
- giardia
- cryptosporidium
prevention: boil, cook
25
**Inflammatory or Bloody Diarrhea:**
Clincial features:
* frequent \_\_\_\_\_\_, amy have:
* symptoms:
* from:
* ______ also from poultry
* HUS:
* For HUS, ___ nto used
complications:
pathogenesis:
* damage to ____ with \_\_\_\_\_
* direct ____ and _____ damage
* _______ invasive
viruses:
Bacteria: (shigella)
* variant of:
* what route?
* low/high infectious dose?
protozoa:
Clincial features:
* frequent small volume stools, may have streaks of blood, mucosy from pus
* symptoms: pain on defication, ileocolitis, colitis, fever
complications:
* hemolytic uremic syndrome
pathogenesis:
* damage to enterocytes with local inflammatory responses
* direct invasion and cytotoxin damage
* locally invasive
viruses:
* none in immunocompetent
Bacteria:
* shigella (**a varient of ecoli, fecal oral, very low infectious dose)**
* shiga toxigenic
* ecoli
* EIEC
* campylobacter jejuni
* non typhi salmonella
* yersinia
protozoa:
* entamoeba histolytica
26
Antibiotic Associated Diarrhea
complications:
pathogenesis:
* most commonly associated with:
* mild or sever? requires treatment?
* what do antibiotics do?
* _____ produces toxins that damage colonic mucosa and are proinflammatory
viruses:
bacteria:
protozoa:
complications:
* C. difficile - pseudomembranous colitis, toxic magacolon, sepsis
pathogenesis:
* **most commonly associated with**: fluoroquinolones, cephalosporinsm penicillin, clindamycin
* mild, generally doesn't require treatment
* antibiotics kill normal flora and may afffect gut absorptive functions, C.
* C. difficile
viruses: none
bacteria:
* C. difficile in the context of antibiotic damage to normal microbiota
protozoa: none
27
**Intoxication**
comes from:
clinical features:
* ______ poisoning
* symptoms:
* onset:
* contagious?
* duration?
* _____ contaminated with ______ may not:
* are antibiotics effective against these toxins? what is the treatment?
pathogenesis:
viruses
bacteria
protozoa
**comes from:** contaminated food
**clinical features:**
* food poisoning
* nausea, vomitting, followed by diarrhea
* rapid onset in hours after digestion
* not contagious
* short duration
* food contaminated with staph toxin may not smell or look spoiled
* antibiotics not effective, oral IV/rehydration
**pathogenesis**: preformed toxins made by bacteria
**viruses**: none - mimicked by norovirus
**bacteria**
* staph aureus enterotoxins
* bacillus cereus enterotoxins
**protozoa**: none
28
Enteric fever/Typhoid fever
pathogenesis:
* most people in US become infected how?
* how effective are vaccines?
* are there carriers?
* how is it spread?
* survives in \_\_\_\_
* may reseed the _____ and transmit through:
* survives in:
viruses:
bacteria:
protozoa:
\_\_\_\_ are only reservoir
pathogenesis:
* most people in US become infected how? **while traveling abroad**
* how effective are vaccines? **partially effective, booster needed in high risk group**
* are there carriers? **chronic carriers, not common but are capable of infecting others**
* how is it spread? **systemically**
* survives in **macrophages**
* may reseed the **bowel** and transmit through: **feces**
* survives in: **lymph nodes, liver, spleen, bone marrow, gall bladder**
**viruses**: none
**bacteria**:
* salmonella typhi
* para typhi
* listeria
* brucella
* non typhi salmonella
* yersinia
**protozoa**: none
**humans** are only reservoir
29
**Salmonella gastroenteritis/Salmonella enterica**
\_\_\_\_\_\_\_ most common cause of:
\_\_\_\_ production, inflammatory ____ - beneficial to salmonella because of:
\_\_\_\_\_\_\_\_ hosts can develop:
**salmonella enterica serovar typhi**, salmonella infection in the US
cytokine production, inflmmatory colitis - beneficial to salmonalla because of eliminating many commensal bacteria
immuno compromised hosts can develop bacteremia, spetic arthritis, meningitis
30
**Vibrio Cholerae**
need a **large/small** number of bacteria to cause disease
\_\_\_\_\_ but not ______ state of survival in gastric acid
large inoculum aids in \_\_\_\_\_\_, subsequent:
\_\_\_\_\_ - watery diarrhea
\_\_\_\_\_ environmental reservoir
\_\_\_\_\_\_\_ and ______ can cause gastroenteritis in humans from shellfish
a few strains of Vibrio cholerae are highly ______ and cause \_\_\_\_\_\_
large
viable, nonculturable
survival, colonization of small intestine
enterotoxin
aquatic
adapted to the human host, causes outbreaks, epidemics, and pandemics
31
Campylobacter
post infection sequelae: (3)
reactive arthritis
irritable bowel syndrome
guillian barre syndrome (body's immune system attacks own nerves, cause unknown - associated with COVID 19 and zika)
32
Does H pylori cause cancer?
\_\_\_\_-\_\_\_\_ of gastric cancer associated with H pylori
H pylori second only to _____ as a defined cause of cancer
transmission?
70-75%
smoking
transmitted within families
* gastric-oral
* oral-oral
* oral-fecal
33
**How does H pylori survive in the stomach? (acidic environemnt)**
* most abundant protein in H pylori is:
* what does this do?
* what can be used as a diagnostic test for H pylori?
Urea breath test only works if:
\_\_\_\_\_ is a common diagnostic tool
\_\_\_\_\_ test is another tool, needs high H pylori for this to wor
**H pylori and Immune tolerance:**
* ____ modified to avoid triggering \_\_\_\_
* _____ mutated to avoid \_\_\_\_\_
* _____ coated with sugar to mimic \_\_\_\_\_
* urease
* urease breaks down host derived urea into carbonic acid and ammonia which can locally neutralize gastric acid
* urease activity can be used as a diagnositc test (urea breath test)
H pylori is active
culturing of a gastric biopsy specimen
fecal Ag test
* LPS, TLR-4
* flagella, TLR 5
* O-antigens coated with sugar to mimic blood group Ags
34
Who is at risk for H pylori disease? (bacterial factors)
* what are the two factors and what do they do?
CagA
* Protein secreted into the
target epithelial cell
* Triggers reorganization
of actin cytoskeleton
* Disrupts cell signaling
VacA alleles
* Causes apoptosis of gastric epithelial cells
* Induces inflammatory cytokines
35
what are the respiratory infection causing gram negative bacteria?
1) Haemophilus influenzae
2) Bordetella pertussis
3) Legionella pneumophila
4) Chlamydia pneumoniae
5) Mycoplasma pneumoniae
36
Respiratory Infection-causing Gram-negative Bacteria: **Haemophilus influenzae**
\_\_\_\_\_ flora in ______ of 20-80% of healthy adult populatio n
causes:
peak incidence:
most virulent strains have:
**normal** flora in **nasopharynx** of 20-80% of healthy adult populatio n
**causes**:
* meningitis
* pneumonia
* bronchitis
* otitis media
**peak incidence**: 6mon-2yr age group
**most virulent strains have:** polysaccharide capsule
37
Respiratory Infection-causing Gram-negative Bacteria: **Bordetella pertussis**
causitive agent of:
production of ______ toxin
whooping cough
pertussis
38
Respiratory Infection-causing Gram-negative Bacteria: **Legionella pneumophila**
reservoir:
\_\_\_\_\_\_\_\_ disease, ____ fever
no _____ to ______ transmission
Reservoir: Rivers/streams/amebae; Air-conditioning water-cooling tanks
Legionnaires disease (Atypical pneumonia); Pontiac fever
No human-to-human transmission
39
Respiratory Infection-causing Gram-negative Bacteria: **Chlamydia pneumoniae**
causes:
most common in:
Atypical pneumonia
Most common in school-aged children (mild pneumonia or bronchitis)
40
Respiratory Infection-causing Gram-negative Bacteria: **Mycoplasma pneumoniae**
causes:
mild/sever illness --\> ______ pneumonia
Atypical pneumonia
Mild illness - “Walking pneumonia”
41
what results/causes pneumonia in general?
Disrupting or overwhelming these **defense mechanisms** can allow microbes to colonize the lungs, resulting in PNEUMONIA
defense mechanisms:
* Mucous entrapment
* Ciliary clearance
* Immune surveillance
* Intact epithelial barrier
* Secreted factors such as:
* Secretory IgA
* Surfactant proteins (SP-a, SP-d)
* Defensins
42
typical community aquired pneumonia
* presents with ______ infection
* infectious agent **is or is not** culturable/identifiable
* responsive to _______ antibiotics
* main species responsible:
atypical community aquired pneumonia
* presentation:
* causitive pathogens are **easy/difficult** to culture/identify?
* species responsible:
typical community aquired pneumonia
* presentation: typical, severe, acute infection
* infectious agent is culturable/identifiable
* responsive to cell wall active antibiotics
* Streptococcus pneumoniae; Haemophilus influenzae
atypical community aquired pneumonia
* Presentation is usually sub-acute
* Causative pathogens are difficult to culture/identify by standard methods
* Mycoplasma pneumoniae (Lacks CW, so not responsive to penicillin); Legionella pneumophila; Chlamydia pneuminiae
43
**Cell structure of Fungi**
similar to \_\_\_\_\_
cell membrane with \_\_\_\_\_
\_\_\_\_ cell wall with \_\_\_\_, \_\_\_\_\_, and \_\_\_\_\_\_
beta glucans
* produces _____ that stimulates \_\_\_\_\_\_
similar to eukaryotes
cell membrane with ergosterol
rigid cell wass with mannan, beta glucans, chitin
beta glucans produce endotoxin like substances that stimulate the immune system
44
what are the common commensal fungi on humans?
**Candia albicans** a common
commensal of **mucosal
surfaces**
**Malassezia furfur** a common
commensal of the **skin**
45
Aspergillus fumigatus:
\_\_\_\_\_\_ pathogen that causes:
opportunistic or pathogenic?
Environmental pathogen that causes allergic aspergillosis and/or severe invasive pulmonary disease in neutropenic patients - hemorrhagic necrosis in the lung
opportunistic
46
Candida:
\_\_\_\_\_\_ yeast on _______ membrane
opportunistic or pathogenic?
causes:
Commensal yeast on mucous
membrane
Opportunistic
* Oral thrush: IC host
* Perleche/Angular cheilitis: Corners of mouth
* Esophagitis: AIDS-defining illness in HIV-infected individuals
* Endocarditis: IV drug abusers
* Yeast vaginitis
47
**Cryptococcus neoformans**
\_\_\_\_\_\_\_ _______ yeast
when inhaled, can cause:
patients with ______ defects are at high risk to develope severe \_\_\_\_\_\_
Encapsulated environmental yeast
When inhaled, can cause disseminated disease with predilection to the brain
Patients with CD4 T cell defects are at high risk to develop severe meningo-encephalitis
48
**Histoplasma capsulatum, Blastomyces dermatitidis, & Coccidioides immitis**
occur in what locations?
Infectious conidia are inhaled but can _________ and cause systemic disease
Occur in specific geographic locations (endemic)
Infectious conidia are inhaled but can disseminate and cause systemic disease
49
Histoplasma capsulatum
\_\_\_\_\_\_\_ flu
does it resolve on its own or with help?
fungus
self resolve
50
Blastomyces dermatitidis
acute and chronic ________ disease
does it self resolve?
pulmonary
less likely to self resolve
51
Coccidioides immitis
known as:
common where?
also known as
can cause systemic infections in what types of patients?
who else is a vulnerable population?
can lead to:
valley fever
south west US
desert bumps
systemic infections in AIDS and immunocompromised patients
pregnant women in 3rd trimester
oral lesions
52
Parastitic infections: Entamoeba leads to:
dysentery
53
parasitic infections: Giardia, Cryptosporidium leads to:
Traveler’s diarrhea
54
parasitic infections: trichomonas causes
STD: vaginitis, urethritis
55
parasitic infections: plasmodium causes
malaria
56
parasitic infections: Trypanosomes causes
Infect blood; Chagas disease,
African sleeping sickness
57
parasitic infections: Leishmania causes
Infect bone marrow, liver, spleen
58
parasitic infetions: Toxoplasma causes
CNS infection, encephalitis
59
parasitic infections: Pneumocystis causes
Pneumonia (in AIDS patients)
60
what is the importance of STDs in dentistry?
* chlamydia cases:
* gonorrhea cases
* syphilis cases
what are fators the CDC sites for this?
sexually transmitted diseases have been soaring
* #1 Chlamydia - 1.7M cases
* #2 Gonorrhea - 555,608 cases
* #3 Syphilis - 30,644 cases
poverty, stigma, discrimination, drug use
Diseases in the orofacial complex may affect other systems and may originate in other systems --\> refer to MD
61
What chlamydia causes mucous membrane disease (genitals, eyes, infant pneumonia)?
C trachomatis
62
what chlamydia causes respiratory disease (pharyngitis, bronchitis, pneumonia)?
C pneumoniae
63
what chlamydia causes psittacosis (from birds, mild fever, headache, dry cough, sometimes pneumonia)?
C psittaci
64
How is g**onococcal stomatits** spread?
Asymptomatic or symptomatic?
symptoms
Infection may possibly be spread by kissing an infected person, not just by genital contact.
Usually asymptomatic
Symptoms can include pharyngitis, tonsillitis, fever, and swollen lymph nodes
65
What is the causitive agent of **syphilis**?
shape/characteristics?
**can/cannot** be cultured in vitro?
**can/cannot** be viewed by normal light microscopy?
Caused by Treponema pallidum
Corkscrew-shaped, motile microaerophilic bacterium
Cannot be cultured in vitro
Cannot be viewed by normal light microscopy
66
Primary Syphilis
when does it appear?
primary \_\_\_\_\_, _____ at the site of inoculation
\_\_\_\_\_\_ progresses from _____ to _____ to \_\_\_\_\_
* pain/painless?
* highly/not highly infectious?
* heals?
regional \_\_\_\_\_\_:
can blood tests during tis stage show positive?
**1-3 weeks** after contact
Primary **lesion**, **chancre**, at the site of inoculation
**Chancre** progresses from **macule** to **papule** to **ulcer**
* Typically painless, indurated
* Highly infectious
* Heals spontaneously within 1 to 6 weeks
Regional **lymphadenopathy**: **rubbery, painless, bilatera**l
Blood tests for syphilis **may not be positive** during early primary syphilis
67
**Secondary Syphilis**
when does it appear?
may persist for how long?
what are the manifestations?
what do blood tests show during this phase?
3 to 6 weeks after the primary chancre appears
May persist for weeks to months
Primary and secondary stages may overlap
Manifestations:
* Skin Rash (75%-100%) can affect hands and feet
* Lymphadenopathy (50%-86%)
* Malaise
* Mucous patches (6%-30%)
* Condylomata lata (10%-20%)
* Hair loss (Alopecia) (5%)
Blood tests are usually highest in titer during this stage
68
Tertiary (late) Syphilis
approx \_\_\_% of untreated patients progress to the stertiary stage within ___ to \_\_\_\_yrs
Why is it rare?
manifestations:
30%, 1-20 yrs
rare because of widespread availability and use of antibiotics
Manifestations
* Gummas or Gummatous lesions (hard palate is the classical oral site)
* Cardiovascular syphilis (aortic aneurysms)
* Neurosyphilis
69
Congenital syphilis
what stage and trimester does it spread?
risk is higher during _____ and _____ syphilis, why?
severity?
may lead to:
only _____ cases are clinically apparent at birth
Syphilis can be spread to fetus during any stage of syphilis and during any trimester of pregnancy
Risk is higher during primary and secondary syphilis – more circulating bacteria
Wide spectrum of severity
May lead to:
* stillbirth
* neonatal death
* deafness
* neurologic impairment
* bone deformities
Only severe cases are clinically apparent at birth
70
What are the possible orofacial features of congenital syphilis?
rhagades
frontal bossing
short maxilla
cleft or perforated palat
saddle nose
mucous patches
hutchinson triad
71
what is rhagades?
infected fissures
may be seen on the oral commissures and other locations
72
what is frontal bossing?
specific to syphilis?
unusually prominent forehead
not specific to congenital syphilis – it is seen in many other conditions too.
73
perforation of the palate
not ______ in the normal sense
caused because:
not a “cleft palate” in the normal sense
The perforation or hole in the palate is caused because the bacteria have caused destruction.
74
saddle nose
bridge of nose is depressed because the bacteria have destroyed it
75
Mucous patches
can be seen in ______ too
we usually associate these with ______ syphilis
These can be seen in congenital syphilis too
we usually associate these with Secondary Syphilis.
76
Cat Scratch Disease
type of:
ccaused by:
treated with:
90% acquired by contact with a cat
what is seen at the time of injury?
what is seen 1-3 weeks later?
Type of reactive lymphadenitis
Caused by Bartonella henselae, Gram negative bacillus
Treated with antibiotics
90% acquired by contact with a cat
Papule or vesicle, bump or blister at the site of injury
Painful swollen lymph nodes, low-grade fever, malaise nausea, sometimes abdominal pain
77
Diphtheria
what type of infection?
infection with:
what test is used?
what leads to cardiac and neurologic disturbances via toxin production
* interference with:
* paralysis of \_\_\_\_\_\_
* ______ failure
* ______ in throat can suffocate the patient
Infection with **Klebs-Loeffler bacterium / Corynebacterium**
**Schick test** used to be used for Dx
**Aerobic, Gram+ rod** may lead to cardiac and neurologic disturbances via toxin production
* **Interference with cardiac conduction**
* **Paralysis of palate**
* **Kidney failur**e
* **diphtheric membrane**
78
Oral Tuberculosis
Usually, patients who develop oral TB have severe ___________ and develop TB from:
most frequent oral locations for TB: why?
\_\_\_\_ and ____ lesions also common
also can occur in _____ after \_\_\_\_\_\_
lesions start as _____ and evolve into \_\_\_\_\_\_
can clinically resemble:
internal organ disease and develop TB from coughing up infected sputum
Tip and lateral margins of tongue most frequent oral locations for TB because patients often injure these locations and TB bacteria can enter the open wound
**Hard** and **soft palate** lesions also common.
Also can occur in **tooth sockets after extraction**
Lesions start as **red papules that evolve into painful, soft, punched-out, shallow ulcers**
Can clinically resemble **malignancies**
79
Scrofula
what is it?
TB in neck involving skin and lymph nodes
80
Pott's disease
what is it?
what can it affect?
skeletal TB
can affect the spine and other bones
81
Forms of candidiasis
pseudomembranous
atrophic
hyperplastic
angular cheilitis
linear gingival erythema (in HIV)
82
Linear gingival erythema:
gingival candidiasis seen in patients with:
manifestation:
HIV
distinc red linear band along gingival margin
83
Pseudomembranous candidiasis (thrush)
who does it affect?
symptoms
* Newborns
* HIV
* recent antibiotics
* denture wearers
* very dry mouth
Curd like plaques can be scraped off, leaving sore red mucosal base
sore, burning +/- unpleasent metallic taste
84
Atrophic candidiasis
epithelium signs
where is this seen?
manifestations with dentures:
epithelium thin and atrophic
often, but not exclusively seen under denture, especially if worn 24/7 or fits poorly
85
hyperplastic candidiasis
manifestation/symptoms
symptomatic?
recognized?
white diffuse or pebbly areas that do not scrape off
thickened epithelium
may be mixed with atrophic areas
often asymptomatic
under recognized
86
angular cheilitis
signs/symptoms
candidiasis often mixed with ____ or _____ infection
\_\_\_\_\_ can perpetuate it
treat ____ as well as \_\_\_\_\_
cracking at corners of mouth
mixed with staph or strep infection
drooling can perpetuate it
treat mouth as well as commissures
87
chronic mucocutaneous candidiasis
what is it?
usually underlying _____ defect
sometimes _____ disorder
chronic candida infection of skin, scalp, fingernails, mucous membranes
usually underlying immune defect
sometimes endocrine disorder
88
what is the causitive organism of candidiasis
other top 4 candida species
C albicans
* C tropicalis
* C glabrata
* C parapsilosis
* C krusei
89
what is the micromedex?
general drug database
90
what is lexicomp within UpToDate?
general drug database
91
what is basic and clinical pharmacology within access pharmacy?
textbook on pharmacology for all drugs
92
what is the sanford guide
antibiotics, infectious diseases
93
MOA for Beta Lactams
Bacterial cell wall/membrane - bacteriocidal
94
MOA for penecillins
bacterial cell wall/membrane - bacteriocidal
95
MOA for cephalosporins
bacterial cell wall/membranes - bacteriocidal
96
MOA for macrolides
bacterial protein synthesis - bacteriostatic
97
MOA for tetracyclines
protein synthesis inhibitor - bacteriostatic
98
MOA for lincosamides
protein synthesis inhibition - bacteriostatic
99
MOA for folate antagonists
RNA/DNA function disrupter - bactericidal
100
MOA for fluoroquinolones
RNA/DNA function disrupter - bactericidal
101
MOA for nitroimidazoles
RNA/DNA function disrupter - bactericidal
102
amoxicillin class
penicillin
103
cephalexin, cefuroxime class
cephalosporin
104
azithromycin class
macrolide
105
doxycycline class
tetracycline
106
clindamycin class
lincosamide
107
trimethoprim-sulfamethoxazole class
folate antagonist
108
levofloxacin class
fluoroquinolones
109
metronidazole class
nitroimidazole
110
what are good antibiotics to use for odontogenic infections?
clindamycin
penicillin
extended spectrum penecillin
macrolides
tetracyclines
111
what would be a bad antibiotic to use for odontogenic infetions?
folate antagonists
112
what are the 4 ways bacteria develop resistance to antibiotics?
1) limit uptake (entry) of an antibiotic
2) modify the intracellular drug target
3) inactivate the drug
4) drug efflux pumps
113
how can bacteria limit uptake of an antibiotic?
1) high lipid content restricts hydrophilic drug access
2) thickened cell wall limits access
3) reducing number of membrane porin channels
114
how can bacteria modify the intracellular drug target?
1) alteration in structure or function of penecillin binding proteins
2) ribosomal mutation or subunit methylation
3) mutation in enzymes involved in folate biosynthesis (TMP/SMX)
115
how do bacteria inactivate a drug?
beta lactamases
116
what are 2 ways bacteria develop resistance?
1) intrinsic resistance - bacterium possess a trait that makes an antibiotic ineffective
2) acquired resistance - bacteria can mutate or can transfer resistance between one another (plasmids)
117
what are 4 strategies to address antibiotic resistance?
1) decrease unnescessary use of antibiotics
2) use antibiotic in combination with another drug that provides protection
3) use an antibiotic from a different class
4) develop new antimicrobials
118
decrease unnescessary use of antibiotics:
this is the purpose of:
antibiotic stewardship
119
**use of antibiotic in combo with another drug that provides protection:**
this is the purpose of:
\_\_\_\_\_\_\_\_ and ________ are beta-lactam compounds that act as “suicide inhibitors” in that they:
The beta-lactam antibiotic in the preparation is then able to:
\_\_\_\_\_\_\_\_\_\_\_ is the beta-lactam/beta-lactamase inhibitor most commonly used by dentists
* Without the clavulanate component, amoxicillin can be:
* With the clavulanate, amoxicillin is more effective against \_\_\_\_\_\_-sensitive Staph aureus, E coli, H influenzae, and (important to dentists) some species of Prevotella and Fusobacterium, compared to amoxicillin alone
beta-lactamase inhibitors used in combination with a beta-lactam
Clavulanate, tazobactam, bind to one or more beta-lactamases produced by the bacteria, leading to permanent enzyme inactivation
take out the bacterial cell wall without being activated.
Amoxicillin-clavulanate
* cleaved by several penicillinases
* methicillin
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**use an antibiotic from a different class:**
the most ____ implemented strategy when encountering a resistant organism
widely
121
**Develop new antimicrobials**
fast process?
long and slow process that is far outpaced by development of resistant strains of bacteria
122
**Penicillin:**
MOA
Spectrum
Dosing
adverse drug rxs
drug interactions
comments
**MOA**. Lysis of bacterial cell walls
**Spectrum**. Most aerobic gm (+) Strep and most anaerobic gm (+) bacteria. Not great for anerobic gm (-) organisms.
**Typical dosing**. 500 mg TID or QID, depending on symptom severity
**Adverse drug reactions**. ADRs rare: potentially nausea.
**Drug interactions.** Uncommon
**Comments.** Drug of choice for acute Strep pharyngitis. Will need rapid Strep test to confirm.
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**Amoxicillin/Amoxicillin-Clavulanate**
MOA
Spectrum
Typical dosing
Adverse drug reactions
Drug interactions
Comments
**MOA**. Lysis of bacterial cell walls
**Spectrum**. Most aerobic gm (+) Strep and most anaerobic gm (+) bacteria. Clavulanate will add anaerobic gm (-)
coverage and sinus organism H flu over amoxicillin alone.
**Typical dosing**. Amoxicillin 500 mg TID - 1000 mg BID. Amoxicillin-clavulanate 500 mg/125 mg TID or 875 mg/125
mg BID
**Adverse drug reactions.** Diarrhea most common (10% +), nausea (2-3%)
**Drug interactions.** Uncommon
**Comments.** Spectrum does not offer advantages over penicillin
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**Clindamycin**
MOA
Spectrum
Dosing
Adverse drug reactions
drug interactions
comments
**MOA**. Binds to bacterial 50S ribosomal subunit, inhibiting protein synthesis
**Spectrum.** Excellent anti-Strep agent and good coverage for both gm (+) and gm (-) anaerobes
**Typical dosing.** Dosing ranges from 150 mg to 450 mg TID to QID, with max 1.8 g/day. A dose of 300 mg TID is not
uncommon.
**Adverse drug reactions.** Clostridioides difficile-associated diarrhea is the one to watch for. Otherwise, nausea,
headache, taste disturbance
**Drug interactions.** Uncommon. St. John’s wort can decrease
**Comments.** Most commonly used agent in the penicillin-allergic patient
125
**Metronidazole**
MOA
Spectrum
Dosing
Adverse drug rxns
Drug interactions
Comments
**MOA.** Destabilizes anaerobic cell DNA
**Spectrum.** No aerobic organism coverage. Excellent coverage of anaerobic gm (-) organisms and some coverage of
anaerobic gm (+) organisms.
**Typical dosing.** 250 – 500 mg BID - TID
Adverse drug reactions. Metallic taste, “furry” tongue, nausea (\> 10%); neuropathy rare
**Drug interactions.** Disulfiram reactions (nausea, vomiting, flushing, tachycardia) with alcohol
**Comments**. Can use in tandem with agent that has good Strep and some gm (+) anaerobe coverage, e.g., penicillin
or, if penicillin allergy, cefaclor
126
**Doxycycline**
MOA
Spectrum
Dosing
Adverse drug rxns
Drug interactions
comments
**MOA**. Binds to bacterial 30S ribosomal subunit, inhibiting protein synthesis
**Spectrum**. Good coverage for both gm (+) and gm (-) anaerobes; aerobic Strep coverage less reliable
**Typical dosing.** 100 mg po BID
**Adverse drug reactions.** Nausea, erosive esophagitis if taken dry; photosensitivity; deposition in forming teeth lower than with tetracycline, but can discolor if used in children , 8 years; low risk of C difficile colitis, but reports exist
**Drug interactions**. Carbamazepine ( doxycycline effect), warfarin ( INR)
**Comments.** If used for odontogenic infection, may need additional agent for aerobic gm (+) coverage. One of the few oral agents active against methicillin-resistant Staph aureus (MRSA)
127
**Azithromycin**
MOA
Spectrum
Dosing
Adverse drug rxns
Drug interactions
Comments
**MOA**. Binds to bacterial 50S ribosomal subunit, inhibiting protein synthesis
**Spectrum**. Good coverage for sinus pathogens; some activity against anaerobic gm (+) organisms but not great
**Typical dosing**. 500 mg day 1, then 250 mg daily days 2-5
**Adverse drug reactions.** Nausea, diarrhea uncommon (5% or less); QTc interval prolongation potential—monitor HR
**Drug interactions.** A number of drug-drug interactions, particularly with other agents affecting QT interval. Will see
enhanced effect of direct acting anticoagulants (e.g., apixaban) and immunosuppresants (e.g., cyclosporine, tacrolimus)
**Comments**.
128
what are 3 drug allergy masqueraders and how do they work?
1) opiods:
* Selectively cause release of histamine from mast cells only in skin.
* Most patients will experience pruritis and possibly some flushing.
* Dose-related
2) vancomycin
* Causes selective release of histamine from mast cells in skin.
* Most patients experience facial and upper trunk flushing, mild pruritis; occasional abdominal cramping.
* Dose-related
3) amoxixillin
* Two out of every three rashes reported with amoxicillin are non-allergic rashes.
* Non-allergic rashes appear later in course (\> day 3) and are more benign than allergic rashes.
* The rash does not recur with subsequent amoxicillin exposure.
* A common reason for penicillin allergy label.
129
what are 3 ciral allergy masqueraders?
1) **Viral exanthem**
* mistaken for drug reaction.
* Echovirus, Coxsackie virus, adenovirus, other (measles, chicken pox, etc) can all cause rashes.
* Viral exanthem lesions usually discrete (vs drug rashes are confluent), pink or brown (vs red), often non-pruritic or only mildly itchy, and often localized.
* Fever and lymphadenopathy often present.
* Patient will describe having an upper respiratory tract infection within the past 1-2 weeks.
**2) Pityriases rosea**
* A rash that is probably viral in origin but virus unknown.
* Patient develops reddish or brownish “herald patch” usually on the trunk and over the next few days more lesions start appearing on
trunk and even extremities.
* May spare face.
* Itchy.
**3) Epstein-Barr Virus**
* Patients with this virus will develop a rash about 80% of the time if given amoxicillin or penicillin.
* The rash does not recur once the viral infection is over.
130
why do patients with allergy labels need a work up?
need to address the likelihood of recurrence upon drug re-exposure so that you can recommend whether the allergy label shoulf be continued or discontinued
131
cutaneous rxns to drugs: **Urticaria/hives**
**description**
**distribution**
**onset**
**treatment**
**description**: pink, raised, small look like mosquito bites, large lesions, have blanched interior
**distribution**: can be anywhere, does not spare face, often starts on upper trunk
**onset**: minutes to hours, usually disappear within 6-24 hours, can migrate
**treatment**: antihistamine
132
cutaneous rxns to drugs: **angioedema**
description
distribution
onset
treatment
description: raised, swollen, pink area of soft tissue swelling
distribution: facial, food allergy usually only mouth, throat
onset: minutes to hours, can take 24+ hours to fully subside
treatment: antihistamine
133
cutaneous rxns: **maculopapular rash**
description
distribution
onset
treatment
description: roundish or amorphous lesions usually bright or "drug" red
distribution: usually neck down, often confluent
onset: 6-48 hours
treatment: antihistamine
134
cutaneous rxns: **contact dermatitis**
**description**
**distribution**
**onset**
**treatment**
**description**: usually erythematous lesion at first, developing into a thick
scaly lesion with chronic exposure
**distribution**: wherever the allergen contacts the skin
**onset**: several hours to a few days; usually subsides within a few days
**treatment**: topical corticosteroid, antihistamine
135
Stevens-Johnson syndrome/toxic epidermal necrolysis
description;
concern:
treatment
**description**: Brown to purple maculae on skin turn into blisters within 48 hours; blisters spread to generalized skin desquamation (10-30% of body for SJS; \> 30% detachment TEN)
**concern**: fluid loss leading to hypovolemia and secondary infections.
**treatment**: IV NS; cyclosporine (± benefit); silver-encrusted gauze dressings; ocular lubricant
136
antifungals: nystatin class
polyenes
137
antifungals: fluconazole, itraconazole, posiconazole, voriconazole class
azoles, triazoles
138
antifungals: anidulafungin, caspofungin, micafungin class
echinocandins
139
antifungals: flucytosine class
pyrimidine analogs
140
antifungals: ibrexafungerp class
triterpenoids
141
**Polyenes**: Nystatin
MOA
ADR
DDI
Comments
**MOA**: fungal membrane disrupter, forms pores in fungal cell membranes so intracellular contents leak out
**ADR**: unpleasent taste, nausea, diarrhea
**DDI**: none
**Comments**: topical (oral) suspension, 4x day use of suspension inconvenient
142
Azoles: Triazoles
MOA
ADRs
DDIs
Comments
**MOA**: fungal membrane disrupter, blocks fungal CYP450 enzymes involved of ergosterol synthesis, disrupting the cell membrane
**ADRs**: **QT prolongation**, headache, nausea, vomiting, abdominal cramping
**DDIs**: inhibitors of CYP2C9, CYP2C19, CYP3A4
**Comments**: Oral, Avoid use in 1st trimester of pregnancy
143
**Azoles: imidazoles**
MOA
ADRs
DDIs
comments
**MOA**: Fungal membrane disrupter, pores in cell membranes
**ADRs**: (troche) nausea, LFT increases
**DDIs**: Inhibitor of CYP3A4 (weak), may increase serum concentrations of sulfonylureas
**comments**: Buccal tab, Oral troche (lozenge)
144
**Echinocandins**
MOA
ADRs
DDIs
comments
MOA: Fungal membrane disrupter
ADRs: mild GI
DDIs: May increase concentration of a few transplant drugs
comments: IV only
145
**Pyrimidine analogs**
MOA
ADRs
DDIs
comments
MOA: DNA/RNA function disrupter
ADRs: renal, GI toxicity
DDIs: none
comments: Oral, Expensive, Avoid use in pregnancy
146
**Triterpenoids**
MOA
ADRs
DDIs
comments
MOA: Fungal membrane disrupter
ADRs: nausea, diarrhea
DDIs: CYP2C8 inhibitor
comments: expensive, Avoid use in pregnancy
147
