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Invaders and Defenders > Week 2 > Flashcards

Week 2 Flashcards

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

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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

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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

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4
Q

_____ portion of the heavy chains defines the class of Ab

A

Fc (trunk)

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5
Q

antigen molecules have different ______

interacts with:

allows for:

A

epitopes

  • interacts with B cell antigen receptors
  • allows for expansion of immune responses
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6
Q

what are the 5 isotypes of antibodies?

A

IgM
IgG
IgD
IgE
IgA

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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

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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)

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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

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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

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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

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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
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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
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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

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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

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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

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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

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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

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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)

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20
Q

T helper cell function

A

activate cytotoxic T cells and B cells

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21
Q

T regulatory cell function

A

help distinguish between self and non self, prevent autoimmune diseases

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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

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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

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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

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25
Q

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:

A

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
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26
Q

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:

A

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
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27
Q

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

A

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

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28
Q

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

A

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

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29
Q

Salmonella gastroenteritis/Salmonella enterica

_______ most common cause of:

____ production, inflammatory ____ - beneficial to salmonella because of:

________ hosts can develop:

A

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

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30
Q

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 ______

A

large

viable, nonculturable

survival, colonization of small intestine

enterotoxin

aquatic

adapted to the human host, causes outbreaks, epidemics, and pandemics

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31
Q

Campylobacter

post infection sequelae: (3)

A

reactive arthritis

irritable bowel syndrome

guillian barre syndrome (body’s immune system attacks own nerves, cause unknown - associated with COVID 19 and zika)

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32
Q

Does H pylori cause cancer?

____-____ of gastric cancer associated with H pylori

H pylori second only to _____ as a defined cause of cancer

transmission?

A

70-75%

smoking

transmitted within families

  • gastric-oral
  • oral-oral
  • oral-fecal
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33
Q

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 _____
A
  • 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
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34
Q

Who is at risk for H pylori disease? (bacterial factors)

  • what are the two factors and what do they do?
A

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
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35
Q

what are the respiratory infection causing gram negative bacteria?

A

1) Haemophilus influenzae
2) Bordetella pertussis
3) Legionella pneumophila
4) Chlamydia pneumoniae
5) Mycoplasma pneumoniae

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36
Q

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:

A

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

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37
Q

Respiratory Infection-causing Gram-negative Bacteria: Bordetella pertussis

causitive agent of:

production of ______ toxin

A

whooping cough

pertussis

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38
Q

Respiratory Infection-causing Gram-negative Bacteria: Legionella pneumophila

reservoir:

________ disease, ____ fever

no _____ to ______ transmission

A

Reservoir: Rivers/streams/amebae; Air-conditioning water-cooling tanks

Legionnaires disease (Atypical pneumonia); Pontiac fever

No human-to-human transmission

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39
Q

Respiratory Infection-causing Gram-negative Bacteria: Chlamydia pneumoniae

causes:

most common in:

A

Atypical pneumonia

Most common in school-aged children (mild pneumonia or bronchitis)

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40
Q

Respiratory Infection-causing Gram-negative Bacteria: Mycoplasma pneumoniae

causes:

mild/sever illness –> ______ pneumonia

A

Atypical pneumonia

Mild illness - “Walking pneumonia”

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41
Q

what results/causes pneumonia in general?

A

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
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42
Q

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:
A

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
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43
Q

Cell structure of Fungi

similar to _____

cell membrane with _____

____ cell wall with ____, _____, and ______

beta glucans

  • produces _____ that stimulates ______
A

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

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44
Q

what are the common commensal fungi on humans?

A

Candia albicans a common
commensal of mucosal
surfaces

Malassezia furfur a common
commensal of the skin

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45
Q

Aspergillus fumigatus:

______ pathogen that causes:

opportunistic or pathogenic?

A

Environmental pathogen that causes allergic aspergillosis and/or severe invasive pulmonary disease in neutropenic patients - hemorrhagic necrosis in the lung

opportunistic

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46
Q

Candida:

______ yeast on _______ membrane

opportunistic or pathogenic?

causes:

A

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
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47
Q

Cryptococcus neoformans

_______ _______ yeast

when inhaled, can cause:

patients with ______ defects are at high risk to develope severe ______

A

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

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48
Q

Histoplasma capsulatum, Blastomyces dermatitidis, & Coccidioides immitis

occur in what locations?

Infectious conidia are inhaled but can _________ and cause systemic disease

A

Occur in specific geographic locations (endemic)

Infectious conidia are inhaled but can disseminate and cause systemic disease

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49
Q

Histoplasma capsulatum

_______ flu

does it resolve on its own or with help?

A

fungus

self resolve

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50
Q

Blastomyces dermatitidis

acute and chronic ________ disease

does it self resolve?

A

pulmonary

less likely to self resolve

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51
Q

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:

A

valley fever

south west US

desert bumps

systemic infections in AIDS and immunocompromised patients

pregnant women in 3rd trimester

oral lesions

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52
Q

Parastitic infections: Entamoeba leads to:

A

dysentery

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53
Q

parasitic infections: Giardia, Cryptosporidium leads to:

A

Traveler’s diarrhea

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54
Q

parasitic infections: trichomonas causes

A

STD: vaginitis, urethritis

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55
Q

parasitic infections: plasmodium causes

A

malaria

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56
Q

parasitic infections: Trypanosomes causes

A

Infect blood; Chagas disease,
African sleeping sickness

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57
Q

parasitic infections: Leishmania causes

A

Infect bone marrow, liver, spleen

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58
Q

parasitic infetions: Toxoplasma causes

A

CNS infection, encephalitis

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59
Q

parasitic infections: Pneumocystis causes

A

Pneumonia (in AIDS patients)

60
Q

what is the importance of STDs in dentistry?

  • chlamydia cases:
  • gonorrhea cases
  • syphilis cases

what are fators the CDC sites for this?

A

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
Q

What chlamydia causes mucous membrane disease (genitals, eyes, infant pneumonia)?

A

C trachomatis

62
Q

what chlamydia causes respiratory disease (pharyngitis, bronchitis, pneumonia)?

A

C pneumoniae

63
Q

what chlamydia causes psittacosis (from birds, mild fever, headache, dry cough, sometimes pneumonia)?

A

C psittaci

64
Q

How is gonococcal stomatits spread?

Asymptomatic or symptomatic?

symptoms

A

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
Q

What is the causitive agent of syphilis?

shape/characteristics?

can/cannot be cultured in vitro?

can/cannot be viewed by normal light microscopy?

A

Caused by Treponema pallidum

Corkscrew-shaped, motile microaerophilic bacterium

Cannot be cultured in vitro

Cannot be viewed by normal light microscopy

66
Q

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?

A

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, bilateral

Blood tests for syphilis may not be positive during early primary syphilis

67
Q

Secondary Syphilis

when does it appear?

may persist for how long?

what are the manifestations?

what do blood tests show during this phase?

A

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
Q

Tertiary (late) Syphilis

approx ___% of untreated patients progress to the stertiary stage within ___ to ____yrs

Why is it rare?

manifestations:

A

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
Q

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

A

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
Q

What are the possible orofacial features of congenital syphilis?

A

rhagades

frontal bossing

short maxilla

cleft or perforated palat

saddle nose

mucous patches

hutchinson triad

71
Q

what is rhagades?

A

infected fissures

may be seen on the oral commissures and other locations

72
Q

what is frontal bossing?

specific to syphilis?

A

unusually prominent forehead

not specific to congenital syphilis – it is seen in many other conditions too.

73
Q

perforation of the palate

not ______ in the normal sense

caused because:

A

not a “cleft palate” in the normal sense

The perforation or hole in the palate is caused because the bacteria have caused destruction.

74
Q

saddle nose

A

bridge of nose is depressed because the bacteria have destroyed it

75
Q

Mucous patches

can be seen in ______ too

we usually associate these with ______ syphilis

A

These can be seen in congenital syphilis too

we usually associate these with Secondary Syphilis.

76
Q

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?

A

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
Q

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
A

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 failure
  • ​diphtheric membrane
78
Q

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:

A

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
Q

Scrofula

what is it?

A

TB in neck involving skin and lymph nodes

80
Q

Pott’s disease

what is it?

what can it affect?

A

skeletal TB

can affect the spine and other bones

81
Q

Forms of candidiasis

A

pseudomembranous

atrophic

hyperplastic

angular cheilitis

linear gingival erythema (in HIV)

82
Q

Linear gingival erythema:

gingival candidiasis seen in patients with:

manifestation:

A

HIV

distinc red linear band along gingival margin

83
Q

Pseudomembranous candidiasis (thrush)

who does it affect?

symptoms

A
  • 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
Q

Atrophic candidiasis

epithelium signs

where is this seen?

manifestations with dentures:

A

epithelium thin and atrophic

often, but not exclusively seen under denture, especially if worn 24/7 or fits poorly

85
Q

hyperplastic candidiasis

manifestation/symptoms

symptomatic?

recognized?

A

white diffuse or pebbly areas that do not scrape off

thickened epithelium

may be mixed with atrophic areas

often asymptomatic

under recognized

86
Q

angular cheilitis

signs/symptoms

candidiasis often mixed with ____ or _____ infection

_____ can perpetuate it

treat ____ as well as _____

A

cracking at corners of mouth

mixed with staph or strep infection

drooling can perpetuate it

treat mouth as well as commissures

87
Q

chronic mucocutaneous candidiasis

what is it?

usually underlying _____ defect

sometimes _____ disorder

A

chronic candida infection of skin, scalp, fingernails, mucous membranes

usually underlying immune defect

sometimes endocrine disorder

88
Q

what is the causitive organism of candidiasis

other top 4 candida species

A

C albicans

  • C tropicalis
  • C glabrata
  • C parapsilosis
  • C krusei
89
Q

what is the micromedex?

A

general drug database

90
Q

what is lexicomp within UpToDate?

A

general drug database

91
Q

what is basic and clinical pharmacology within access pharmacy?

A

textbook on pharmacology for all drugs

92
Q

what is the sanford guide

A

antibiotics, infectious diseases

93
Q

MOA for Beta Lactams

A

Bacterial cell wall/membrane - bacteriocidal

94
Q

MOA for penecillins

A

bacterial cell wall/membrane - bacteriocidal

95
Q

MOA for cephalosporins

A

bacterial cell wall/membranes - bacteriocidal

96
Q

MOA for macrolides

A

bacterial protein synthesis - bacteriostatic

97
Q

MOA for tetracyclines

A

protein synthesis inhibitor - bacteriostatic

98
Q

MOA for lincosamides

A

protein synthesis inhibition - bacteriostatic

99
Q

MOA for folate antagonists

A

RNA/DNA function disrupter - bactericidal

100
Q

MOA for fluoroquinolones

A

RNA/DNA function disrupter - bactericidal

101
Q

MOA for nitroimidazoles

A

RNA/DNA function disrupter - bactericidal

102
Q

amoxicillin class

A

penicillin

103
Q

cephalexin, cefuroxime class

A

cephalosporin

104
Q

azithromycin class

A

macrolide

105
Q

doxycycline class

A

tetracycline

106
Q

clindamycin class

A

lincosamide

107
Q

trimethoprim-sulfamethoxazole class

A

folate antagonist

108
Q

levofloxacin class

A

fluoroquinolones

109
Q

metronidazole class

A

nitroimidazole

110
Q

what are good antibiotics to use for odontogenic infections?

A

clindamycin

penicillin

extended spectrum penecillin

macrolides

tetracyclines

111
Q

what would be a bad antibiotic to use for odontogenic infetions?

A

folate antagonists

112
Q

what are the 4 ways bacteria develop resistance to antibiotics?

A

1) limit uptake (entry) of an antibiotic
2) modify the intracellular drug target
3) inactivate the drug
4) drug efflux pumps

113
Q

how can bacteria limit uptake of an antibiotic?

A

1) high lipid content restricts hydrophilic drug access
2) thickened cell wall limits access
3) reducing number of membrane porin channels

114
Q

how can bacteria modify the intracellular drug target?

A

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
Q

how do bacteria inactivate a drug?

A

beta lactamases

116
Q

what are 2 ways bacteria develop resistance?

A

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
Q

what are 4 strategies to address antibiotic resistance?

A

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
Q

decrease unnescessary use of antibiotics:

this is the purpose of:

A

antibiotic stewardship

119
Q

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
A

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
120
Q

use an antibiotic from a different class:

the most ____ implemented strategy when encountering a resistant organism

A

widely

121
Q

Develop new antimicrobials

fast process?

A

long and slow process that is far outpaced by development of resistant strains of bacteria

122
Q

Penicillin:

MOA

Spectrum

Dosing

adverse drug rxs

drug interactions

comments

A

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.

123
Q

Amoxicillin/Amoxicillin-Clavulanate

MOA

Spectrum

Typical dosing

Adverse drug reactions

Drug interactions

Comments

A

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

124
Q

Clindamycin

MOA

Spectrum

Dosing

Adverse drug reactions

drug interactions

comments

A

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
Q

Metronidazole

MOA

Spectrum

Dosing

Adverse drug rxns

Drug interactions

Comments

A

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
Q

Doxycycline

MOA

Spectrum

Dosing

Adverse drug rxns

Drug interactions

comments

A

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
Q

Azithromycin

MOA

Spectrum

Dosing

Adverse drug rxns

Drug interactions

Comments

A

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
Q

what are 3 drug allergy masqueraders and how do they work?

A

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
Q

what are 3 ciral allergy masqueraders?

A

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
Q

why do patients with allergy labels need a work up?

A

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
Q

cutaneous rxns to drugs: Urticaria/hives

description

distribution

onset

treatment

A

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
Q

cutaneous rxns to drugs: angioedema

description

distribution

onset

treatment

A

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
Q

cutaneous rxns: maculopapular rash

description

distribution

onset

treatment

A

description: roundish or amorphous lesions usually bright or “drug” red
distribution: usually neck down, often confluent
onset: 6-48 hours
treatment: antihistamine

134
Q

cutaneous rxns: contact dermatitis

description

distribution

onset

treatment

A

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
Q

Stevens-Johnson syndrome/toxic epidermal necrolysis

description;

concern:

treatment

A

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
Q

antifungals: nystatin class

A

polyenes

137
Q

antifungals: fluconazole, itraconazole, posiconazole, voriconazole class

A

azoles, triazoles

138
Q

antifungals: anidulafungin, caspofungin, micafungin class

A

echinocandins

139
Q

antifungals: flucytosine class

A

pyrimidine analogs

140
Q

antifungals: ibrexafungerp class

A

triterpenoids

141
Q

Polyenes: Nystatin

MOA

ADR

DDI

Comments

A

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
Q

Azoles: Triazoles

MOA

ADRs

DDIs

Comments

A

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
Q

Azoles: imidazoles

MOA

ADRs

DDIs

comments

A

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
Q

Echinocandins

MOA

ADRs

DDIs

comments

A

MOA: Fungal membrane disrupter

ADRs: mild GI

DDIs: May increase concentration of a few transplant drugs

comments: IV only

145
Q

Pyrimidine analogs

MOA

ADRs

DDIs

comments

A

MOA: DNA/RNA function disrupter

ADRs: renal, GI toxicity

DDIs: none

comments: Oral, Expensive, Avoid use in pregnancy

146
Q

Triterpenoids

MOA

ADRs

DDIs

comments

A

MOA: Fungal membrane disrupter

ADRs: nausea, diarrhea

DDIs: CYP2C8 inhibitor

comments: expensive, Avoid use in pregnancy

147
Q
A

Invaders and Defenders (5 decks)

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