week 4 Flashcards
1
Q
signs and symptoms of strep throat:
A
-begins quickly
-pain with swallowing
-fever
-red and swollen tonsils, sometimes with white patches or streaks of pus
-tiny red spots on roof of mouth
-swollen lymph nodes (anterior neck)
2
Q
symptoms to rule out strep throat:
A
-cough
-runny nose
-hoarseness
-conjuntivitis (viral)
3
Q
what is the centor score?
A
the probability that the pharyngitis is strep
criteria:
-age (3-14 most common)
-exudate or swelling
-tender/swollen anterior cervical lymph nodes
-temp
-cough
4
Q
what bacteria causes group A strep?
A
streptococcal pyogenes
gram + bacteria
5
Q
what are the characteristics of a scarlet fever rash?
A
-“sandpaper rash”
-small, numerous papular elevations
-blanches with pressure
-starts on trunk and extends outwards
6
Q
what is the treatment for BACTERIAL strep?
A
-penicillin (x10 day course)
7
Q
possible etiologies of a persistent strep?
A
GERD
abscess
malignancy
tonsillitis
allergies
8
Q
appearance of simple squamous:
A
-oval nuclei parallel to the basal lamina
-flattened, single layer of cells
lining blood vessel or lymph vessel: endothelium
lining a body cavity: mesothelium
9
Q
appearance of simple cuboidal:
A
-square cells
-single layer
-round nuclei
-little cytoplasm distributed evenly around nucleus
10
Q
appearance of simple columnar:
A
rectangular cells
single layer
usually oval nuclei (not always)
usually nuclei are towards the basal lamina (not always)
may have migrating immune cells
11
Q
appearance of stratified squamous:
A
multiple layers
top layer flattened
bottom layer can be cuboidal or columnar in shape
surface modifications
-non-keratinized (usually; means nuclei in the top layer)
-keratinized
-parakeratinized
12
Q
keratin vs. parakeratin
A
keratin does not have nuclei in the top layer; parakeratin looks like a keratin layer but nuclei ARE present
13
Q
where are stratified columnar and cuboidal cells found?
A
mainly in the ducts of larger glands
14
Q
what type of epithelium is respiratory epithelium?
A
pseudo-stratified columnar
cilia
goblet cells present
15
Q
what are stereocilia?
A
long microvili that clump together (paintbrush)
made of actin, therefore are NOT true cilia
16
Q
what are the features of transitional epithelium?
A
balloon or umbrella cells (larger cells) on the surface
type of pseudo-stratified epithelium because all cells touch the basal lamina but not all cells reach surface (picture says otherwise…)
commonly seen in uroepithelium
-these cells can stretch
-important with the expanding bladder w/ urine
17
Q
what are discoidal vesicles?
A
-part of the transitional epithelium
-not actually vesicles-membrane infoldings that are cut to look like vesicles
-artifact (artificial structure that is present from when the slide was cut/prepared?)
-allow for the expansion of the epithelium when the bladder fills with urine
18
Q
contrast the appearance of microvili on a TEM and a LM?
A
TEM: appear fingerlike, can distinguish them, can see linear features inside (microfilaments)
LM: cannot visualize them as separate structures, appear as a dense line
19
Q
what are microvili composed of?
A
microfilament core (actin)
20
Q
what are cilia composed of?
A
core of protein tubulin in a 9+2 arrangement (motor proteins move the cilia)
basal bodies (base of the microtubule arrangement) are composed of 9 triplets of microtubules
21
Q
what are the permanent type of cell-cell junctions?
A
-zona occuldens (tight junctions)
-zona adherens (belt desmosome)
-macula adherens (spot desmosomes)
-zonula communicantes (gap junction)
22
Q
transcellular vs paracellular
A
transcellular: movement through the cytoplasm
(transporters, channels)
paracellular: in between two cells, prevents movement through cells
(tight junctions, zona occuldens; made of protein strands, the more protein strands, the tighter the junction)
23
Q
what proteins are involved in zonula occuldens (tight junctions)?
A
Claudin and Occuldin
Claudin is the protein which confers the barrier properties.
24
Q
what proteins are involved in the structure of the zonula adherans?
A
-interacts with the microfilaments of the terminal web (belt around the cell)
-receptors on either cell are cadherins (desmocollins, desmogleins)
25
what are junctional complexes?
symmetrical structures consisting of 3 components:
-zonula occuldens (tight junction)
-zonula adherans (belt desmosome)
-macula adherans (spot desmosome)
26
what proteins compose a gap junction (zonula communicantes)?
x6 connexins form a connexon with a gap in the middle
the connexon of one cell lines up with the connexon of another cell so that the holes line up
a gap junction consists of numerous connexons
allows for cell communication (e.g. electrical signal shared between cardiac cells)
27
what are the 2 layers of the basal lamina?
lamina rara (laminin, entactin, perlecan)
lamina densa (type IV collagen)
28
what are the 2 possibilities for having a basement membrane?
AKA a basal lamina that is thick enough to visualize with LM
1) cells have a basal lamina and a reticular lamina (reticular fibers made of collagen III)
2) cells have a fused basal lamina (cells pointing away from each other, each have a lamina rara with their lamina densas fused together)
29
describe the function and structure of hemidesmosomes:
function: adhere epithelial cells to the basal lamina
interact intracellularly with intermediate fibers
interact extracellularly with the matrix of the basal lamina
receptors: integrins
disruption: causes the epithelium to pull away (e.g. blisters)
30
what is the function of focal contacts?
adhere the cell to the proteins of the extracellular matrix
integrins=receptors of the ECM
ultimately connect the cell to the actin cystoskeleton
31
list the types of basal cell: matrix receptors?
-integrins: heterodimers (alpha and beta subunits)
-intergral membrane proteoglycans (e.g. syndecan)
-glyoproteins (e.g. CD44)
32
how are glands formed? how are the two kinds different from each other?
ORIGIN: epithelial, formed by the invagination of the surface epithelium
EXOCRINE: retain a connection to the surface, forming a duct
ENDOCRINE: lose the connection and secrete into the blood supply, endocrine
33
what type of glandular cell is a goblet cell?
exocrine (duct)
secretes mucus
found in the respiratory tract, secretes mucus that is moved by cilia
34
contrast the cellular appearances of mucous cells and serous cells:
mucous cells
-flattened nuclei
-cells appear washed out (mucous lost during processing)
-secrete mucous
serous cells
-rounded nuclei
-stains well
-secrete proteins
35
what are the 3 types of exocrine secretion?
merocrine
-exocytosis
-e.g. pancreas
apocrine
-piece of cell pinches off
-e.g. milk secretions
holocrine
-whole cell becomes the secretion
-e.g. sebaceous glands
36
name the 3 types of tonsils with location, cell type, distinguishing characteristics
PALATINE
-oropharynx
-paired
-stratified squamous with several crypts (also s. squamous)
PHARYNGEAL
-in the nasopharynx
-single
-pseudo-stratified columnar with cilia and goblet cells (AKA respiratory epi)
-no crypts but small folds
-adenoid (can become inflamed and hypertrophied)
LINGUAL
-base of the tongue
-numerous
-single crypt
-stratified squamous
37
what do the following factors cause?
histamine
bradykinin
prostaglandins
nitric oxide
-arteriolar dilation
-hyperemia (redness)
-slowing/stasis of the blood
-fluid extravasation into tissues (swelling)
38
what responses are the following factors responsible for?
complement C5a (anaphylotoxin/chemotaxin?)
leukotriene B4
chemokines
bacterial products
neutrophil activation
rolling and adhesion
emigration to tissue
chemotaxis
39
what responses are the following factors responsible for?
serotonin
histamine
C3a, C5a
bradykinin
leukotrienes
endothelial activation
adhesion molecules and increased permeability
plasma proteins "leak" into tissues
40
what are the 3 components of acute inflammatory exudates?
1. neutrophils migrating in response to chemotaxin signals (complement component C5a and LTB4)
2. spaces in the tissue that indicate fluid accumulation (edema)
3. several other plasma proteins are found in the tissue space - evidenced by fibrin threads (from plasma fibrinogen)
41
what are the 5 cardinal signs of inflammation?
-rubor (redness, hyperemia, vasodilation)
-tumor (swelling)
-calor (heat, due to hyperemia (vasodilation)
-dolor (pain due to bradykinin and PGE2)
-functio laesa (loss of function due to combined effects)
42
what suffix indicates inflammation?
-itis
exceptions: pleurisy (inflammation of the pleura) and cellulitis (infection that causes inflammation)
43
what bacteria cause purulent inflammation?
pyogenic bacteria
staphylococci
strep pyogenes
e. coli
Neisseria spp. (N. meningitidis, N. gonorrhea)
44
what stage of inflammation is characterized by pus formation?
acute suppurative inflammation
45
clinical examples of purulent inflammation:
-lobar PNA
-bronchopneumonia
-acute appendicitis
-acute suppurative tonsillitis
46
contrast suppurative acute inflammation vs fibrinous acute inflammation:
SUPPURATIVE - high # of neutrophils, more cells than fibrin and fluid
FIBRINOUS - more fibrin compared to cells and tissue fluid
47
where is fibrinous inflammation most common?
in serous tissues such as the pericardium and the pleura
48
how does acute pericarditis occur?
inflammation causes a fibrin coat to form on top of the visceral layer of the serous pericardium
49
when is acute serous inflammation usually seen (what injuries and tissue types)?
burn injuries and in serous membrane lined cavities (e.g. pleural effusion)
50
what is a granuloma?
inflammation found in many diseases
characterized by the presence of giant cells
form when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate them
giant cells = macrophages fused together to form a multi nucleated cell
51
what are the 2 types of giant cells?
Langhan's giant cells
-immunological cause
-e.g. infectious organisms such as bacteria and fungi
Foreign Body giant cells
-non immunological cause
e.g. glass, splinters, silica, asbestos etc.
52
compare and contrast the appearance of Langhan's and Foreign Body giant cells:
although both are comprised of several macrophages fused together, the nuclei arrangement differ.
Langhan's - nuclei form a horseshoe shape and somewhat resemble one next to the other
FB cells - the nuclei are distributed randomly, no horseshoe shape
53
how can streptococcus be characterized?
gram (+) bacteria
cocci arranged in chains (or pairs)
non-motile
catalase negative (distinguishes from staph)
non-spore forming
most are facultative anaerobes (some obligate)
54
what 3 methods are used to classify each species within the streptococcal genus?
1. hemolytic patterns
2. Lancefield groupings
3. biochemical/physiological properties on other tests
55
what streptococcal species are capable of alpha hemolysis?
S mutans
S mitis
S pneumoniae
56
what streptococcal species are capable of beta hemolysis?
S agalactiae
S pyogenes
57
what streptococcal species are associated with gamma hemolysis?
nonenterococcus (S bovis)
enterococcus (E faecium, E faecalis)
58
what is the hemolytic patterns test used for?
distinguishes strep bacteria based on how well they can lyse RBCs in a blood agar
alpha: partial
beta: full
gamma: none
59
how is the serologic properties test used to distinguish strep?
-divide into groups based on the antibodies that recognize surface antigens (Lancefield groups)
-based on antigenic differences in cell wall carbs (group A - V), cell wall pili associated protein, and polysaccharide capsule group B (GBS)
60
how is the bacitracin sensitivity test used?
-divides B hemolysis groups into groups A and B
-bacitracin is an Abx that interferes with peptidoglycan synthesis
group A - inhibited (S agalactiae)
group B - not inhibited (S pyogenes)
B-BRAS
61
how is the optochin test used?
-distinguishes S pneumoniae from other alpha hemolytics
-optochin inhibits its growth
"overpass: OVRPS"
viridians - resistant
pneumoniae - sensitive
62
explain how the bile sensitivity test is used?
-another test that distinguishes S pneumoniae from other alpha hemolytics
-S pneumoniae is bile soluble
-viridians are bile insoluble
63
explain how the camp test is used:
-to distinguish S agalactiae from other B hemolytics
-releases CAMP factor
-not fully B hemolytic on its own but the CAMP factor helps enlarge its zone of hemolysis
-forms a characteristic arrow shape
64
S agalactiae colonization site:
vagina
65
S gallolyticus colonization site:
gut
66
S pneumoniae colonization site:
upper respiratory tract
67
S pyogenes colonization site:
throat, skin
68
Viridians group streptococci colonization site:
oral cavity
69
what are the 6 steps of a viral infection?
1. attachment
2. penetration
3. uncoating
4. replication
5. assembly
6. release
70
where do DNA viruses replicate?
in the host nucleus, using the host's machinery
exception: pox viruses
71
where do RNA viruses replicate?
in the host's cytoplasm, using its own machinery and the host's ribosomes
exception: influenza virus which replicates in the nucleus
72
what is the most common cause of viral pharyngitis?
adenovirus
73
what is the most common cause of bacterial pharyngitis?
group A strep - S pyogenes
74
what is the most common cause of fungal pharyngitis?
candida albicans
75
term for "pain with swallowing"
odynophagia
76
describe the process for CD4 activation:
1. TCR binds to the antigen peptide presented by the MHC II molecule
2. co-receptor CD4 binds directly to MHC II
3. co-stimulator B7 (DC) binds to CD28 (CD4)
5. TCR and co-receptors move to the center of the TCR base to form a ring "immune synapse"
6. tyrosine kinase (Lyc) of CD4 co-receptor phosphorylates CD3 and zeta
7. activates transcription factors NF-kB and NFAT
8. increases IL-2 and IL-2Ra expression
9. autocrine stimulation
10. cell proliferation
77
in what x2 ways can helper T cells help CD8 cells during weak immune responses:
-directly secrete IL-2 that acts directly on the CD8 cells
-indirectly by activating more DCs to increase the expression of co-stimulator B7, therefore resulting in more DCs interacting with CD8s
78
in what ways is CD8 activation different from CD4 activation?
1. cross presentation - CD8 T cells can also be activated by the presentation of extracellular antigens by dendritic cells on MHC I (instead of MHC II)
2. CD8 may require help from CD4s if the immune response is weak and there isn't sufficient IL-2 being produced
79
what are the 3 major subsets CD4 cells and what kinds of pathogens do they respond to?
Th1 - intracellular pathogens
Th2 - helminths, injury
Th17 - extracellular pathogens
80
what cytokines differentiate a CD4 cell into Th1?
IL-12 and TFN gamma
81
what ligand does a Th1 cell express on its surface once it makes physical contact with the macrophage?
CD40
82
what cytokine does Th1 release once it binds to the CD40 receptor on macrophage?
IFN gamma
83
what cytokines do Th2 cells respond to?
IL-4 and IL-13
84
what cytokines do Th2 cells secrete in response to IL-13 and IL-4?
IL-4, IL-5, IL-13
85
what cytokines induce the differentiation/proliferation of Th17 cells?
IL-1, IL-6, IL-23, TGF-beta
86
what cytokines do Th17 cells secrete? What are the functions?
IL-17 - stimulate the recruitment of neutrophils and monocytes
IL-22 - increase the barrier integrity of the epithelial cells
both 17 and 22 - produce antimicrobial peptides
87
what type of antigens do T independent reactions detect?
non-peptide antigens
(i.e. polysaccharides, nucleic acids, lipids)
88
what type of B cells are involved with T independent reactions?
marginal zone B cells (B-7 cells)
89
what type of antigens do T dependent B cells detect?
peptide antigens only
90
what is the result of T dependent reactions?
-isotope switching
-affinity maturation
-long lived plasma cells and memory B cells
-the presence of helper T cells that can react with B cells that are specific for the same antigen
91
what is the result of T independent reactions?
-mainly IgM antibodies
-low affinity antibodies
-short lived plasma cells
-transient responses
92
what is the process for B cells recognizing antigens? (recognition/activation phase)
1. B cell antigen receptors cross-linked by antibody
2. Ig-alpha and Ig-beta are phosphorylated
3. other proteins get involved - series of intermediates
4. activation of transcription factors Myc, NFAT, NF-kB, Ap-1
5. increase of gene expression for proteins that are involved with B cell survival, proliferation/differentiation
93
what transcription factors are released by B cells during the activation phase?
Myc, NFAT, NF-kB, and AP-1
94
what is the post activation fate for T independent reactions?
-extensive cross-linking of BCRs due to multivalent antigens (i.e. repeating sugar units of polysaccharides)
-stimulates proliferation/differentiation without T cell help
-activated B cells synthesize IgM (may secrete some)
-early phase of humoral immune response
this response is enhanced when:
-antigens are multivalent
-antigen activates complement and innate receptors strongly
95
what is the post activation fate of T dependent reactions?
-interactions of T and B cells
-B and T cells specific for an antigen come together physically in the secondary lymphoid organ
RESULTS:
-increased survival, proliferation
-interaction with helper T cells
-responsiveness to cytokines
-increased expression of CCR7 - migration from the follicle to the T cell zone (where they meet the T cells)
-generation of plasma cells - Ig secretion
96
what x2 things do T cells use to promote B cell proliferation and differentiation?
-CD40 ligand (CD40L)
-cytokines
B cells are activated by CD40L engagement and cytokines
97
where does the initial T-B cell interaction take place?
in the T cell zone (outside of the follicle)
98
contrast primary and secondary follicles:
primary follicles do not have a germinal center
secondary follicles DO have germinal centers
99
what processes occur in the dark zone of the follicle?
B cell proliferation, somatic hypermutation
100
what processes occur in the light zone of the follicle?
isotope switching, affinity maturation, generation of plasma/memory cells
101
IgM effector function:
complement activation of classical pathway
M for Mozart, a classical composer
102
effector function of IgG:
recognize extracellular stages of most bacteria and viruses
coats/opsonizes microbes for phaGocytosis
transfer of neonatal antibodies from mother to fetus
103
IgE effector function:
elimination of helminths (too large for phagocytosis)
recognized by eosinophils, basophils, and mast cells
104
IgA effector function:
mucosAl immunity
105
IgD effector function:
signals that B cells are mature, ready to depart the bone marrow into circulation in search of its antigen
106
what is the process for isotope switching?
the constant region of IgM/IgD is switched for another antibody type, but antigen specificity (VDJ) remains UNCHANGED
-Tfc cells determine which isotope will be made
-induced by CD40L mediated signals and cytokines
-AID enzyme takes the mu heavy chain and moves it downstream to another constant chain region
(gene region is consistent with antibody name, e.g. alpha region - IgA)
107
what is the purpose of somatic hypermutation?
high frequency point mutations in Ig variable genes
-mediated by AID
-results in B cell clones with varying affinities for its antigen
-occurs in the dark zone
108
what is affinity maturation?
follicular dendritic cells display antigens to B cells
-successful B cells (bind antigen tightly) - survive
-unsuccessful (poor binding) - die
"survival of the fittest"
109
what are the 2 fates for successful B cells (passed through affinity maturation)?
Plasma Cells - will secrete antibodies, long lived
Memory B cells - do not secrete antibodies, circulate in the blood, mucosa, and tissues and wait for a second attack, can last a lifetime
110
what are the 5 effector functions of antibodies?
1. neutralization of microbes and microbial toxins (all isotypes)
2. opsonization for phagocytosis (IgG)
3. antibody dependent cellular cytotoxicity (IgG, natural killers)
4. recruitment of eosinophils, basophils, and mast cells (IgE)
5. complement activation - classical pathway (IgM, IgG)
111
contrast bacteriostatic and bactericidal drugs:
bacteriostatic: stop bacterial growth and allow the host immune system to kill the organism, it itself does not decrease bacteria
bactericidal: kills the organism itself, superimposes the effect of the host's defense, decrease in bacteria graphically
**bactericidal drugs are important for severe infections, necessary in immunocompromised patients
112
what enzyme do B-lactam antibiotics target?
-transpeptidase (PBP)
-blocks peptidoglycan cross-linking (cell wall formation)
-causes cell lysis
113
what are penicillin binding proteins (PBPs)?
-cell wall synthesizing enzymes
-binding sites for B-lactam antibiotics
-PBPs have varying affinities for B-lactam antibiotics
114
what is the function of Murein (peptidoglycan) hydrolases?
they are autolysins that degrade the cell wall, creating weak points through which the cell membrane can extrude, eventually rupturing and killing the cell
115
contrast gram (+) and gram (-) defenses against B-lactams:
gram +
-outer envelope composed of peptidoglycan, capsular proteins, and carbohydrates
-only have the one plasma membrane
-does not present a significant barrier to the Abx
gram -
outer envelope is a second membrane that is covalently linked to the peptidoglycan layer by lipoprotein bridges
-this outer membrane is a physical barrier to penetration
116
contrast the synthesis and dispersal of B lactamase in gram positive and negative bacteria:
gram +
-produced in large amounts but are released in the surrounding medium
-able to diffuse away
-relatively high substrate affinity
-inducible
gram -
-released in small amounts
-retained in the periplasmic space between the cytoplasmic and outer membranes (unable to diffuse away)
**therefore, antibiotics that traverses the porin pores of the outer membrane will encounter a B lactamase in the enclosed environment before it reaches the PBP (effective!)
117
what are the 3 inhibitors of B lactamase and how do they function?
-clavulanate
-sulbactam
-tazobactam
possess the B lactam structure which make them substrates for B lactamases
irreversibly inhibit B lactamase enzymes
serve as a diversion so that more antibiotic can reach PBPs
the inhibitors in themselves do not possess antimicrobial affects but when they are combined with penicillin = SYNERGISTS/BACTERICIDAL EFFECT
118
how do macrolides exert a bacteriostatic effect?
bind to the 50s subunit and prevent bacterial protein synthesis
119
mechanisms of resistance against macrolides:
1. drug efflux by an active pump mechanism
2. production of methylase enzymes that modify the ribosomal target and decrease drug binding
3. hydrolysis of macrolides by esterases
120
to what degree are each of the macrolides absorbed?
erythromycin - inactivated by acid, administered in enteric coated capsules or as an ester
clarithromycin - absorbed rapidly but undergoes first pass metabolism
azithromycin - absorbed rapidly
121
how are each of the macrolides excreted?
erythromycin - bile and urine, no need to adjust for renal failure patients
clarithromycin - renal and non-renal, decrease dose in renal failure
azithromycin - biliary excretion, very long half life (40-70 hrs) due to tissue binding
122
what is the drug of choice for group A strep pharyngitis?
x10 day course of penicillin V or amoxicillin
macrolide if allergic to penicillin
one time dose of penicillin G benzathine
(10 days maximizes bacterial eradication)
123
what collagen type is associated with the lamina densa?
collagen IV
124
what collagen type is associated with the reticular lamina?
type III
125
what collagen type is associated with anchoring fibrils?
collagen VII
126
where is a fused basal laminae basement membrane seen (which organ)?
in the kidney glomeruli; forms a filtration barrier
127
how do collagen VII anchoring fibrils appear on microscopes?
striated
perpendicular to the basal lamina
128
what is an example of a unicellular exocrine gland?
goblet cell
129
what are serious demilunes?
serous cells that secrete proteins
form a cap on mucous acini clusters
"half moon" shape
secrete proteins into the mucous excretion
130
what are cytocrine secretions?
passing the secretion directly to another cell
melanocytes
131
what is the name of the mucosal lymphoid tissue?
MALT
mucosa associated lymphoid tissue
involved in the immune response
132
what are the symptoms of post-streptococcal glomerulonephritis? (PSGN)
result of untreated strep (dark urine 2-4 weeks post-strep)
sx:
-periorbital edema
-cola colored urine/hematuria
133
what are the symptoms of N gonorrhea caused pharyngitis?
sore throat
pharyngeal exudates
anterior cervical lymphadenopathy
134
symptoms of allergic pharyngitis:
presents with system allergic sx
e.g. allergic conjunctivitis, cobble stoning of posterior pharynx
135
who are at most risk for developing fungal pharyngitis?
immunocompromised patients
136
treatment for N gonorrhea pharyngitis?
ceftriaxone
137
what does bacitracin do?
interferes with peptidoglycan synthesis in some bacterial species
138
what infections does S agalactiae cause?
MOPS!
Meningitis
Osteomyelitis
Pneumonia
Septicemia (sepsis)
Common population: newborns following vaginal birth
139
what infections do S gallolyticus cause?
bacteremia
subacute endocarditis
most common population: patients with colon CA
140
S pneumoniae infections:
MOPS!
Meningitis
Otitis Media **
Pneumonia
Sepsis
most common population: children and elderly, immunocompromised, asplenic individuals
141
S pyogenes infections:
pyogenic infections
toxin mediated infections
autoimmune sequelae
necrotizing fasciitis
most common: children
142
viridians group infections:
S mutans and S mitis:
dental caries
S mutans:
subacute bacterial endocarditis
S sanguinis:
subacute endocarditis, damaged heart valves
most common: S mutans and mitis in all populations, S sanguinis in patients with damaged heart valves
143
what are some examples of dsDNA viruses?
adenovirus
viral conjunctivitis
pox viruses/small pox
144
example of ssDNA viruses:
parovirus B19 (fifth disease)
145
example of ssRNA virus:
ebola
rabies
measles
146
example of dsRNA virus:
rotavirus
147
what type of RNA do retroviruses contain? what enzyme?
ssRNA (+) - sense
reverse transcriptase (RT)
148
example of a retrovirus:
HIV
149
what kind of cells do HIV viruses target?
CD4
also monocytes, macrophages, and dendritic cells
150
products of dsRNA viruses:
multiple RNA molecules that code for MULTIPLE proteins
151
product of (+) ssRNA viruses:
genome is directly translated
single large protein that can be processed into smaller proteins
152
product of (-) ssRNA:
needs RNA replicase to synthesize a sense RNA strand
then produces one protein that can be processed into multiple smaller proteins
153
what are the 3 infection types?
persistent infections
-replicate for long periods of time
-integration into host genome, evasion of host defenses, viral mutations
-e.g. HBV
latent infections
-lacks trigger for replication, lays dormant
-"reactivated" - immunosuppression therapies
-e.g. herpes, cold sores
abortive infections
-error prone replication, effective host defenses
-cell cannot successfully replicate
154
what are F fusion proteins?
fuse multiple cells together, called syntica
therefore, don't have to leave to infect other cells
e.g. RSV, retroviruses, herpes
155
what are inclusion bodies?
viral particles aggregate inside the affected cell
i.e. Molluscum bodies
156
what two enzymes do neutrophils, in conjunction with lysosomes (phagosomes), use to kill antigens?
perforin
granzymes
157
characteristics of lobar PNA:
suppurative inflammation - pyogenic
alveoli filled with WBCs (mainly neutrophils), fibrin, and fluid
become solidified vs. its normal spongy nature
158
what are the 3 types of inflammation:
acute serous
acute fibrinous
acute suppurative
159
transudate vs exudate
transudate has a low specific gravity with low protein content
exudate has higher specific gravity with high protein content
160
how are neutrophils and necrotic tissue removed once the inflammation/infection resolves?
phagocytosis (macrophages) and leave via lymph drainage
161
describe abscess formation:
acute inflammatory response fails to destroy/remove the cause of the tissue damage
continues, usually with a component of chronic inflammation
most common cause: pyogenic bacteria
inflammation progresses producing a liquefaction of tissue into pus
fibrous tissue seals off the cavity
162
how can plasma cells be identified?
purplish cytoplasm and "clock face" nuclei
(differentiated B cells that produce antibodies)
163
how can lymphocytes be identified?
dark round nuclei with a very thin rim of basophilic cytoplasm
164
how can macrophages be identified?
oval/kidney beaned nuclei, pale cytoplasm
(phagocytic and antigen presenting cells)
165
how can eosinophils be identified?
bilobed nuclei, bright pink granules
(hellminths)
166
role of fibroblasts?
secrete ECM, including collagen
when an injurious stimulus has been removed, they disappear from the tissue over the course of weeks/months
167
what is a granuloma?
inflammation characterized by the presence of giant cells (macrophages fused together)
Langhans (immunological)
Foreign Body (non-immunological)
168
example of immunological granuloma:
tuberculosis
areas of infected/caseous tissue (tubercles) are surrounded by Langhans giant cells
169
what is flux?
the number of molecules that pass through a permeable membrane at a given time
170
flux depends on what variables?
-temperature
-molecule mass
-viscosity of medium
-thickness of membrane
-surface area of membrane
171
doubling the concentration of one molecule will _______ the flux as a result
double
172
magnitude and direction of diffusion depends on the _______ of concentrations
net difference
173
what is permeability coefficient?
rate at which polar/charged molecules diffuse across membranes
rate limiting factor: hydrophobic interior of membranes
174
what is Fick's Law of Diffusion?
J=PA(Co-Ci)
J=rate of diffusion
P=permeability
-KD/x
K-lipid solubility (good for diffusing across membranes)
D=diffusion coefficient, based on size and viscosity
x=thickness of membrane
A=surface area of the membrane
Co-Ci = concentration difference
175
membranes have the highest permeability for what ion? why?
K+
has the most open K+ channels on the membrane
176
extracellular ions:
Na+
Ca2+
Cl-
HCO3-
177
intracellular ions:
K+
anions
"K in"
178
simplified Nernst Equation:
membrane potential = (60/ionic valence) x log (concentration outside/concentration inside)
179
equation for net driving force of an ion:
net driving force = actual membrane potential - equilibrium potential
180
what is ionic current?
AKA current flow
occurs when there is a movement of an ion across a cell membrane
2 conditions:
1. there is a driving force for the ion
2. membrane has conductance to the ion (membrane channels are open)
I = ionic conductance x (driving force)
conductance = 1/resistance
181
what is the Chord Conductance Equation?
calculates membrane potential based on the conductances of ions
low conductance = low contribution to the membrane potential
182
what is the role of adhesion molecules during T cell activation?
TCR only binds peptide-antigen complex with a low affinity
adhesion molecules on T cells recognize their ligands on APCs
stabilize the binding of the T cell to the APC
183
what are the variant and invariant parts of the T cell receptor?
TCR is variant (differs between clones, specific to each antigen, lacks ability to transmit signals to the nucleus)
CD3 and zeta chain are invariant (invariant among T cell clones, bind to TCR and perform signaling functions)
184
what are M1 macrophages?
"classical macrophage activation"
activated in response to IFN-gamma in the Th1 pathway
185
what are M2 macrophages?
"alternative macrophage activation"
in response to IL-4, IL-13 during Th2 injury pathway
result: enhanced fibrosis, tissue repair, scarring
186
what 2 things do T cells rely on to get to their target/effector site?
adhesion molecules
chemokines
187
in what 2 ways can the T independent response be enhanced?
if the antigen crosslinks the B cell antigen receptors
if the antigen triggers the innate/complement response well
188
what is the binding process for phagocytosis by antibody coated antigens?
The Fc portion of the phagocyte receptor recognizes the Fc portion of the antibody
189
antibody mediated phagocytosis is a major defense against_______.
encapsulated bacteria
i.e. strep pneumoniae
190
where does antibody mediated phagocytosis take place?
spleen
191
what antibodies do natural killer cells bind to during antibody mediated cytotoxicity?
IgG
192
what causes post streptococcal glomerulunephritis (PSGN)?
IgM or IgG, complement antigen complex deposition in the basement membrane of the glomerulus
193
what type of Abx is penicillin?
B-lactam
194
important structural feature of penicillin:
carbonyl carbon - nitrogen (amide) bond
195
what stage of cell wall synthesis do B lactam antibiotics inhibit?
inhibit peptidoglycan cross linking
occurs outside of the cell
196
what are the B lactam binding sites?
penicillin binding proteins (PBP)
they are cell wall synthesizing enzymes
197
what is penicillin's binding site?
transpeptidase (PBP)
198
what is the next step after the antibiotic binds the PBP?
Murein (peptidoglycan) hydrolases are autolysins that degrade the cell wall, creating weak points for the cell membrane to extrude through the cell wall. leads to lysis.
199
how are the genes for B lactamase conferred?
in a plasmic, either via transduction or conjugation
200
contrast Penicillin G and Penicillin V absorption (in acid):
Penicllin G: unstable in acid, absorption is highest when the stomach is empty (30% absorbed)
Penicillin V: acid stable, more consistent blood levels can be achieved
201
how is Benzathine Penicillin G administered?
parental preparation, IM injection
202
what is the absorption like for Benzathine Penicillin G?
blood levels low but sustained
203
when is Benzathine Penicillin G used?
only use for groups that are notably sensitive to the antibiotic (due to the low levels)
AKA group A B hemolytic strep (GAS, S pyogenes)
204
distribution of penicillin?
widely distributed in the body except for in the CSF, joints, and occular fluids (EXCEPT in times of inflammation)
205
how are penicillin G and aminopenicillins (amoxicillin) excreted?
primarily by the kidney, so you have to adjust for renal failure/decreased renal function
206
what is Probenecid?
an organic acid that competes for secretion in the kidneys (would prevent penicillin G and aminopencillins from being excreted) but rarely used because of its toxic side effects
207
what is the major determinant of penicillin hypersensitivity?
penicillenic acid
208
how does penicillenic acid cause hypersensitivity reactions?
reacts with sulfhydryl groups in tissues to form HAPTEN-protein conjugates
209
what is a minor determinant of penicillin hypersensitivity?
penicilloyl
a derivative is used for skin testing for penicillin allergy
210
adverse effects of penicillin?
Oral - GI distress or diarrhea
Parenteral- phlebitis (IV) and pain (IM)
211
when does neurotoxicity occur in Penicillin administration?
myoclonus or seizures, confusion, agitation, hallucinations, lethargy
seen in high plasma levels due to failure to adjust for renal patients
212
why is interstitial nephritis sometimes seen with penicillin G?
sx: fever, rash, hematuria with eosinophilia, proteinuria
reversed when drug is stopped
cause: allergic reaction in which penicillin binds to the basement membrane of the glomerulus, forming an antigen elicited production of antibodies
213
distribution of macrolides?
wide distribution into intracellular fluids EXCEPT for CNS
214
side effects of erythromycin:
n/v/d, cramps (oral or IV)
QT prolongation
cholestatic jaundice w/ erythromycin estolate
OVERALL: worst tolerated macrolide
