Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a pre clinical > microbiology > Flashcards

microbiology Flashcards

1
Q

pathogen

A

organism that causes or is capable of causing disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

commensal

A

organism which colonises the host but causes no disease in normal circumstance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

opportunistic

A

microbe that only causes disease if host defences are compromised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pathogenicity

A

the degree to which a given organism is pathogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

asymptomatic carriage

A

when a pathogen is carried harmlessly to a tissue site where it causes no disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

bacterial nomenclature

A

consists of genus and species

e.g. staphylococcus (genus) aureus (species)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

areas that are colonised

A

most mucosal surfaces

digestive tracr, nasal cavity, skin, urethra, vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

sterile areas

A

lungs
gallbladder
kidneys
upper urinary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bacterial morphology

A

divided into coccus (round) and bacillus (rod)

further divided into gram positive or negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

structures in bacteria

A 
inner and outer membrane
capsule
chromosome of circular DNA
pili
flagella
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

differences between gram positive and negative

A

different cell envelope
negative have 2 membranes and lipopolysaccharides

positive have much more peptidoglycan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

bacterial environment

A 
temp= -800 degrees to +80 degrees
pH= 4-9
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

growth of bacteria

A

lag phase
exponential phase
stationary phase- number of viable bacteria decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

endotoxin

A

component of outer membrane of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

exotoxin

A

secreted proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

gene mutation

A

base substitution
deletion
insertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

gene transfer

A

transformation e.g. via plasmid
transduction e.g. via phage
conjugation e.g. via sex pilus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

plasmids

A

proteins can be synthesised using plasmid DNA

tend to be spread during bacterial conjugation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

gram stain steps

A
  • apply primary crystal violet (purple)stain to fixed, heated bacteria
  • add iodide which binds to stain and fixes it to cell wall
  • decolourise with ethanol or acetone
  • counter stain with safranin (pink)
  • negative lipids interact with decolouriser and lose their other lipopolysaccharides and crystal violet- iodide (CV-I) so appear pink with counterstain
  • positive are dehydrated by decolouriser and the cell wall and CV-I are trapped in the multilayered peptidoglycan so are purple
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

gram stain of neisseria gonorrhoea

A

similar appearance to kidney beans with concave sides facing each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

staphylococci gram stain

A

appear in clusters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

catalase test

A

flavoproteins reduce O2 using superoxide dismutase- producing H2O2

2H2O2 -> 2H20 +O2

staph are catalase + but strep aren’t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

coagulase test

A

distinguishes s.aureus (positive) from other staphylococci (negative)

it activates prothrombin to convert fibrinogen to fibrin

a positive test- clot forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

latex test for staph. aureus

A

positive= agglutination occurring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

haemolysis

A

ability of a bacteria to breakdown red blood cells in blood agar

requires expression of haemolysin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

optochin sensitivity

A

strep. pneumoniae are optochin sensitive

other strep are resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

oxacillin disc

A

the oxacillin disc tests for penicillin sensitivity

resistant strains should have a MIC performed to penicillin to ascertain level of resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

selective indicator medial for fram negactive bacilli

A

MacConkey agar

cysteine lactose electrolyte deficient (CLED) media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MacConkey agar

A

o Bile salts inhibit Gram-positive bacteria and inhibits swarming of a Gram negative
bacterium Proteus spp.
o Crystal violet also inhibits some Gram-positive bacteria
o Neutral red acts as a pH indicator so that bacteria that ferment lactose (Lac+) and
release H+ appear pink or red
o Lactose is available for Lac+ micro-organisms
o Peptone is used by Lac- micro-organisms, resulting in production of NH3 and a rise in pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

cysteine lactose electrolyte deficient (CLED) media

A

o Electrolyte deficient media prevents swarming of Proteus mirbilis
o Bromothymol blue is indictor, lactose ferementation causes blue to yellow change,
decarboxylation of L-cyteine results in blue colour
o Used as media for urinary pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

lactose fermenter on CLED agar

A

A simple but important method of classifying members of the Enterobacteriaceae is based
upon lactose fermentation. Classically lactose fermenting organisms are E. coli, Klebsiella, Enterobacter and Citrobacter species.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

non-lactose fermenter on CLED agar

A

The non-lactose fermenting organisms usually belong to the genera other than those
mentioned in slide ‘Lactose fermenter on CLED agar’. However, some lactose fermenting organisms, because they are late lactose fermenters, may appear as a non-lactose
fermenter. Late lactose fermenters are recognised by a positive ONPG test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

motility

A

distinguishes bacteria
flagella staining patterns
swarming motility patterns on agar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

oxidase test

A

-Tests if micro-organism contains a cytochrome oxidase or indophenol oxidase
-Utilises a redox indicator such as N,N,N’,N’-tetramethyl-p-phenylenediamine (TMPD)
-In oxidised state indicator dark blue or maroon
-Implies organism able to use oxygen as the terminal
electron acceptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

3 main types of gram positive bacteria

A

streptococcus
staphylococcus
corynebacterium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

coagulase

A

enzyme produced by bacteria that clots blood plasma

fibrin clot formation around bacteria protects it from phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

staphylococcus

A

coagulase +ve or -ve
s.aureus is most important (coag +ve)
coag -ve are important in opportunistic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

staphylococcus habitat

A

nose

skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

MRSA

A 
resistant to:
beta-lactams
genatmicin
erythromycin
tetacycline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

staph. aureus virulence factors

A

pore forming toxins
proteases
toxic shock syndrome toxin
protein A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

staph. aureus associated conditions

A

pyogenic- wound infections, pneumonia, endocarditis

toxic mediated- toxic shock syndrome, food poisoning

coag -ve - infected implants, septicaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

coagulase- negative staphylococci

A

s. epidermidis

s. saprophticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

s. epidermidis

A

infections in debilitated, prostheses - opportunistic

main virulence factor is ability to form persistent biofilms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

s. saprophticus

A

acute cystitis
haemagglutinin for adhesion
urease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

streptococci classification

A

haemolysis
lancefield typing
biochemical properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

alpha haemolysis

A

partial
greening
H2O2 reacts with Hb
e.g. s.intermedius

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

beta haemolysis

A

complete lysis
haemolysins O and S
e.g. s.pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

gamma haemolysis

A

no lysis

some s. mutans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

sero-grouping

A

method of grouping catalase negative, coagulase negative bacteria based on bacterial carbohydrate cell surface antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

infections caused by S. pyogenes

A 
wound infections
tonsillitis
otitis media
impetigo
scarlet fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

S. pyogenes virulence factors

A

capsule- hyaluronic acid
M surface protein- encourages complement degradation
enzymes
toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

s. pneumoniae

A

normally commensal in oropharynx in 30% of people

causes - pneumonia, otitis media, sinusitis, meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

s. pneumoniae predisposing factors

A

impaired mucus trapping
hypogammaglobulinaemia
asplenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

s. pneumoniae virulence factors

A

capsule
inflammatory wall constituents
cytotoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

viridans streptococci

A

collective name for oral streptococci
alpha or gamma haemolytic
some cause dental abscesses
important in infective endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

C. diphtheriae

A

droplet spread

can grow in the presence of potassium tellurite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

C. diphtheriae toxin

A

inhibits protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

C. diphtheriae prevention

A

vaccination with toxoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

most relevant gram negative bacteria

A

proteobacteria
chlamydiae
spirochaeta
bacteroidetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

proteobacteria

A

family of enterobacteriacaeae
rods
motile
facultatively anaerobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

e. coli infections

A 
wounds infections
UTIs
gastroenteritis 
travellers diarrhoea
bacteraemia
meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

why are some e.coli strains pathogenic

A

have additional DNA that causes them to be pathogenic

several pathovars, many serotypes or strains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

shigella

A

closely related to e. coli
four species- dysenteriae, flexneri, boydii, sonnei

severe bloody diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

pathogenesis of shigella

A

acid- tolerant

person-person or contaminated water and food transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

invasion of shigella

A

moves form cell to cell in colonic mucosa

cause damage to mucosa which results in diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

shigella virulence determinant

A

shiga toxin- causes cell death by blocking protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

salmonella

A

two species= enterica and bongori (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

salmonella infections

A

gastroenteritis
enteric fever
bacteraemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

salmonella pathogenesis

A
  • ingestion of contaminated food/water
  • invades gut epithelium of small intestine
  • intestinal secretory response
  • does not produce toxins
  • enters submucosa
  • intracellular survival/replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

vibrio cholerae

A

facultative anaerobe
curved rods with single polar flagellum
cholera= most severe diarrhoeal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

vibrio cholerae pathogenesis

A 
faceal-oral route
incubation
voluminous watery stools
no blood, pus or fever
60% mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

vibrio cholerae virulence determinants

A

TCP pili required for colonisation

cholera toxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

pseudomonas aeruginosa

A

single polar flagellum
opportunistic
antibiotic resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

pseudomonas aeruginosa acute infections

A

localised- burns, UTI, keratitis
systemic
ICU patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

pseudomonas aeruginosa chronic infections

A

cystic fibrosis patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

pseudomonas aeruginosa virulence determinants

A

twitching motility

multiple toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

legionella pneumophila

A

immunocompromised
severe 15-20% mortality
fastidious- charcoal agar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

legionella pneumophila pathogenesis

A

modulates trafficking of phagosome
avoids phagosome-lysosome fusion
differentiate to replicative phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

bordetella pertussis

A

whooping cough
short rods- coccobacilli
fastidious
non-invasive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

bordetella pertussis toxins

A

pertussis toxin

adenylate cyclase- haemolysin toxin (increases cAMP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

neisseria

A

non-flagellated diplococci
fastidious
2 species= meningitidis and gonorrhoeae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

n. meningitidis

A 
asymptomatic in nasopharynx of 5-10%
rises to 20-90% during outbreaks
aerosal transmission (person to person)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

n. meningitidis pathogenesis

A

crosses nasopharyngeal epithelium and enters blood stream

enters subarachnoid space after crossing blood brain barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

n. meningitidis virulence determinants

A

capsule is major determinant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

n. gonorrhoeae

A

asymptomatic in 30% of females
person-person sexually transmitted
proctitis, gingivitis, pharyngitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

n. gonorrhoeae virulence determinants

A

twitching motility

non-capsulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

campylobacter

A

spiral rods
unipolar or bipolar flagella
most common cause of food poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

bacteroides

A

non-motile rods
strict anaerobes
commensal flora of the large intestine is most abundant (30-40%)
most common cause of anaerobic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

chlamydia

A

small and non motile
obligate intracellular parasites
many live asymptomatically as endosymbionts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

growth cycle of chlamydia

A

2 developmental stages-

elementary bodies= infectious, enter cell through endocytosis, prevent phagolysosome fusion

reticulate bodies= replicative, non-infectious, possess tubular projections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

life cycle of chlamydia

A
  • entry as elementary bodies
  • prevent phagolysosome fusion
  • conversion into reticulate body
  • multiplication
  • convert back to elementary body
  • cell lysis and release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

chlamydia. trachomatis

A

most common std
can spread to uterus and ovaries
usually asymptomatic
can also cause conjunctivitis- hand to eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Chlamydophila. pneumoniae

A

respiratory tract

infects other mammals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Chlamydophila. psittaci

A

mainly birds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

spirochetes

A

long, slender, helical, flexible
free living and non-pathogenic
modified outer membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

B. burgdoferi

A 
lyme disease
tick borne
bull's eye rash
spreads through ECM
culture in medium containing rabbit serum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

T. pallidum

A

syphilis
primary stage- localised infection, days to weeks
secondary stage- systemic, 1 to 3 months
tertiary stage- gummas in bone and soft tissue, neurosyphilis, several years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Gram-negative pathogens in the respiratory tract

A 
o Bordetella pertussis
o Haemophilus influenzae
o Pseudomonas aeruginosa
o Legionella pneumophila
o Chlamydia pneumoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Gram-negative pathogens in the GI tract

A 
o Vibrio cholerae
o Shigella dysenteriae/S. flexneri
o S. enterica sv enteritidis/typhimurium
o Some Escherichia coli serotypes
o Campylobacter jejuni/C. coli
o Helicobacter pylori
o Bacteroides fragilis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Gram-negative pathogens and meningitis

A

o Neisseria meningitidis
o Some E. coli serotypes
o Haemophilus influenzae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Gram-negative pathogens in the urinary tract

A

o Some E. coli serotypes
o Proteus mirabilis
o Klebsiella pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Gram-negative pathogens- STIs

A

o Neisseria gonorrhoeae
o Chlamydia trachomatis
o Treponema pallidum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Gram-negative pathogens in wound infections

A

o Some E. coli serotypes
o Bacteroides fragilis
o Pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

3 groups of worms

A

nematodes
trematodes
cestodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

nematodes

A

round worms

intestinal, larva migrans, tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

trematodes

A

flatworms, flukes

blood, liver, lung, intestinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

cestodes

A

tapeworms

non-invasive, invasive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

features of helminths

A

cannot usually reproduce without a period of development outside the body
although they usually produce a large number of larvae or eggs, they cannot increase the burden without re-exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

pre-patent period

A

interval between infection and appearance of eggs in the stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

intestinal nematodes

A

transmitted from human to human via egg or larvae

the egg or larva is not usually infectious when first passed and has to undergo a period of development in the soil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Ascaris lumbricoides: the large roundworm

A

cream coloured
15-30cm long
lives a year or more
pre-patent period is 60-75 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

loeffler’s syndrome

A

associated with larval migration through lungs
10-14 days after infection
cough, fever, wheeze, eosinophilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Ascaris lumbricoides effects of adult

A

often asymptomatic

can be mechanical e.g. intestinal obstruction or malnutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Ascaris lumbricoides odd presentation

A

emerging from nose

perforated eardrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

The Hookworm

A

white worm
1cm in length
life expectancy 1-5 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

The Hookworm 2 species

A

ancylostoma duodenale

necator americanus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

The Hookworm clinical features

A

ground itch- papules at site of entry of the larvae
pulmonary symptoms- mild due to pulmonary migration
most common cause of iron deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

The Hookworm diagnosis

A

stool microscopy for eggs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

The Hookworm treatment

A

iron supplements
pyrantel
mebendazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Enterobius vermicularis: the pinworm or threadworm

A

most common helminth infection in the uk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Enterobius vermicularis life cycle

A

adult is resident in large bowel
female adult emerges from anus at night to lay eggs on the perineum
the eggs are infectious after 4 hours are ingested by next host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Enterobius vermicularis clinical features

A

pruritus ani
appendicitis
vaginal penetration- endometritis, infertility
affects whole families

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Enterobius vermicularis diagnosis

A

microscopy of sellotape strip from perianal region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Enterobius vermicularis treatment

A

mebendazole
piperazine
pyrantel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Trichuris trichiura: the whipworm

A

2-5cm long
live 1 year
pre-patent period is 70-90 days
partially buried in the mucosa of large bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Trichuris trichiura clinical features

A

resident of large bowel
asymptomatic
co exists with ascaris lumbricoides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Trichuris trichiura diagnosis

A

stool microscopy for eggs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Trichuris trichiura treatment

A

mebendazole

albendazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Strongyloides stercoralis

A

causes strongloidiasis
2mm long
lies buried in small intestinal mucosa
pre-patent period is 17-28 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Strongyloides stercoralis clinical features

A

pruritus at site of entry
malabsorption
eosinophilia
hyperinfection syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

visceral larva migrans

A

caused by toxocara canis and t.cati (dog and cat roundworm)
mainly a disease of children
diagnose with eosinophilia and serology
treat with mebendazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

ocular toxocariasis

A 
larvae trapped in retina
see a granulomatous reaction
blindness
diagnose with serology and biopsy
treat with mebendazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

cutaneous larva migrans

A

creeping itchy skin eruption
dog hookworms
lesions at site where larvae penetrate
treat with topical or systemic thiabendazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Dracunculus medinensis: The Guinea worm

A

100cm long
lives one year subcutaneously
incubation period is one year
worm emerges from skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Dracunculus medinensis clinical

A

localised pain
blister bursting
tetanus or sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Dracunculus medinensis diagnosis

A

drop water on ulcer promotes egg release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Dracunculus medinensis treatment

A

local- wind out worm

mebendazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Dracunculus medinensis prevention

A

sieving of water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Wuchereria bancroftii

A

causes elephantiasis

adults live in lymphatic system and survive 30 years

140
Q

Wuchereria bancroftii diagnosis

A

demonstration of microfilaria in blood taken at right time of day (2300-0100)

141
Q

Wuchereria bancroftii treatment

A

diethylcarbamazine

142
Q

Trichinella spiralis

A

cause of trichinosis

143
Q

Trichinella spiralis clinical picture

A 
asymptomatic
GI disturbance associated with worm development
fever, headache, cough
periorbital oedema
myocarditis
pneumonitis
144
Q

Taenia saginatum

A

beef tapeworm
5-10metres long
pre-patent period is 12 weeks

145
Q

Taenia saginatum clinical

A

asymptomatic

proglottids may emerge from anus

146
Q

Taenia saginatum diagnosis

A

stools with eggs and proglottids

147
Q

Taenia saginatum treatment

A

niclosamide

praziquantel

148
Q

flukes

A

blood
liver
lung
bowel

all have snail as an intermediate host

149
Q

schistosomiasis

A

adult fluke is 12cm long
life span is 3-5 years
schistosoma haematobium- africa, Arabia, Mauritius
schistosoma mansoni- africa
schistosoma japonicum- china, japan, phillippines

150
Q

katayama fever

A 
initial immune complex mediated illness
2-4 weeks after exposure 
eosinophilia
diarrhoea
cough
hepatomegaly and splenomegaly
151
Q

liver flukes

A

adults resident in human biliary tree
invade liver via biliary tree

opisthorcis filenius
the bovine liver fluke

152
Q

lung flukes

A

resident in lung

paragonimus westermant
chinese lung fluke

153
Q

intestinal flukes

A

desident in gut
fasciolopiasis
giant chinese gut fluke

154
Q

intestinal flukes

A

desident in gut
fasciolopiasis
giant chinese gut fluke

155
Q

m. tuberculosis

A

tubercolosis

156
Q

m. kansasii

A

chronic lung infection

157
Q

m. maranium

A

fish tank granuloma

158
Q

m. ulcerans

A

buruli ulcer

159
Q

m.leprae

A

leprosy

160
Q

buruli ulcer formation

A 
nodule
small ulcer
large ulcer
deforming
bone destruction
(m. ulceran bacterium)
161
Q

buruli ulcer treatment

A

antibiotics for 8 weeks
wound management
surgery

162
Q

microbiology of mycobacteria

A

aerobic, non-spore forming, non-motile bacillus

cell wall= high molecular weight lipids

slow growing e.g. tb generation time is 15-20 hours

163
Q

mycobacteria cell wall

A

weakly gram positive
survives inside macrophages
contains mycolic acids and lipoarabinomannan

164
Q

mycobacterial slow growth

A

slow reproduction so slow growth in humans (slow onset of disease) and on agar
it responds slowly to treatment as well

165
Q

mycobacteria acid fast bacilli

A

need this stain as the high lipid content in the walls make it gram resistant

ziehl-neelsen- carbol fuchsin, acid alcohol, methylene blue

166
Q

mycobacterial slow growth in culture

A

first need decontamination steps to kill off other rapid growing bacteria

solid culture= egg based lowenstein jensen, microspoy positive material 2-4 weeks, negative 4-8 weeks

liquid culture= 1-3 weeks, automated systems BACTEC mycobacterial growth indicator tube

167
Q

TB reactivation risk after exposure

A

risk = 10% lifetime risk, most in first 2 years then 0.1% a year

increased risk= young infants and elderly, malnutrition, intensity of exposure and immunosuppression

168
Q

tuberculoid leprosy

A

associated with tissue hypersensitivity and granulomata
paucibacillary lesions with low numbers of mycobacteria
tissue damage e.g. nerves
predominate th1 biased cd4+ t cell responses- IFN-g and TNF-a production

169
Q

leptromatous leprosy

A

lesions full of bacilli but little or poorly formed granulomata
extensive skin lesions
predominant th2 biased cd4+ t cell response- IL4,5,10 production

170
Q

primary TB

A

bacilli taken into lymphatics to hilar lymph nodes

171
Q

latent TB

A

cell mediated immune response from t-cells
primary infection is contained but immune response persists

no clinical disease but detectable immune response to TB on skin test

172
Q

pulmonary tuberculosis

A

granuloma forms around -bacilli settle in the apex

  • the apex has more air and less blood supply so fewer cells for immune response
  • immune response and necrosis results in abscess of bacilli forming and caseous material coughed up leaving cavity
  • can occur immediately or after latent TB
173
Q

TB spreads beyond lungs

A

enters lymph nodes

genitourinary tb
tb meningitis
miliary tb
pleural tb
bone and joint tb
174
Q

TB spreads beyond lungs

A

enters lymph nodes

genitourinary tb
tb meningitis
miliary tb
pleural tb
bone and joint tb
175
Q

common viral infections

A 
respiratory viruses
rash causing viruses
herpes group
hepatitis group
enteroviruses
diarrhoea causing viruses
HIV
176
Q

diseases and viruses

A

same virus can cause different diseases e.g. enteroviruses cause resp infections and meningitis

different viruses can cause the same disease e.g. different hepatitis viruses

177
Q

basic properties of viruses

A

only grow inside cells
possess only one type of nucleic acid
have an outer protein coat, some have a lipid envelope as well
essentially inert outside the host cell

178
Q

are viruses living

A

have nucleic acid
have outer protein coat
can replicate once inside a living host cell and pass on its genetic code- using host enzymes

179
Q

are viruses non- living

A

non cellular
no cell wall
cannot replicate by themselves
have no organelles

180
Q

attachment (viral replication)

A

viral and cell receptors
viruses need specific receptors to attach to cells to enter them
this dictates the type of cells viruses can infect

181
Q

cell entry (viral replication)

A

only central viral core carrying nucleic acid and some proteins enter the cell

182
Q

interaction (viral replication)

A

using cell materials such as enzymes, amino acids and nucleotides
they replicate
subvert host cell defence mechanisms

183
Q

replication (viral replication)

A

may localise in nucleus, cytoplasm or both

produce progeny viral nucleic acid and proteins

184
Q

assembly (viral replication)

A

occurs in nucleus e.g. herpes virus or cytoplasm e.g. polio or at cell membrane e.g. influenza

185
Q

release (viral replication)

A

via lysis of a cell or by exocytosis

186
Q

viruses causing disease

A
  • damage by destruction of host cells
  • by modification of cell structure or function
  • involving over-reactivity of the host as a response to infection
  • damage through cell proliferation
187
Q

pathogenesis of rotavirus

A
  • following ingestion, rotaviruses infect epithelia cells of the small intestine
  • there is shortening and atrophy of the villi and flattening of epithelia cells
  • decreases surface area of small intestine and limits production of digestive enzymes
  • they suffer malabsorption
  • causes diarrhoea
188
Q

infection with hepatitis B

A

majority are asymptomatic
there is a massive antibody and CTL response- destroying virally infected hepatocytes
can cause extensive liver damage

189
Q

hepatitis B virus and chronic carrier state

A
  • steady state between virus replication in host cells and host defence response
  • limited by sustained viral replication
  • hepatocyte regeneration
  • no clinical symptoms
190
Q

development of cervical carcinoma

A
  • HPV types 16 and 18 infect suprabasal layer of genital system
  • partial replication and gradual movement of cells to mucosal surface through natural wear and tear
  • HPV genome is integrated into host cell chromosome
  • viral gene expression by HPV E2 protein is lost and HPV E6 and E7 are expressed
  • two cell growth and proliferation suppressor proteins are prevented from operating
  • excessive cell growth and proliferation occurs and cervical cell carcinoma results
191
Q

viral evasion at cellular level

A

latency: allows viruses to cause life threatening disease in the immunosuppressed

spreads cell to cell

192
Q

viral evasion and molecular level

A

antigenic variability
prevention of host cell apoptosis
down regulation of interferon and other host cell defence proteins
interference with host cell antigen processing pathways

193
Q

viral diagnosis

A

electron microscope
cell culture
antigen- viral protein detection
serology

194
Q

viral treatment

A

treat with antivirals

prevent with vaccines

195
Q

viral treatment

A

treat with antivirals

prevent with vaccines

196
Q

fungi biology

A 
eukaryotic
chitinous cel wall
exist as yeast or mould
heterotrophic
move by means of growth or spores
197
Q

yeast vs mould

A

yeast= single celled organisms that divide by budding. small. <1% of fungal species
moulds= multicellular hyphae. form spores.
dimorphic fungi= switch between the two depending on the conditions

198
Q

common fungal infections

A

nappy rash
athletes foot
fungal nail infection
fungal asthma

199
Q

immunocompromised hosts and fungal disease

A

candida line infections
invasive aspergillosis
pneumocystis
mucormycosis

200
Q

post surgical patients and fungal disease

A

intra abdominal infection

201
Q

healthy host and fungal disease

A

fungal asthma

travel associated fungal infection

202
Q

diagnosing fungi

A

microscopy and histology
culture
serology

203
Q

mucosal candidiasis

A 
thrush
treat with topical antifungals and oral fluconazole
associated with:
- diabetes
- immunocompromised 
- antibiotics
- pregnancy
204
Q

invasive aspergillosis and galactaomannan

A

chest focus more common
culture is insensitive
can cause brain disease
more common in immunocompromised

205
Q

pneumocystis pneumonia

A

immunocompromised patients
unable to culture
treat with co-trimoxazole

206
Q

treating fungal disease- selective toxicity

A

aims of drug is to achieve inhibitory levels of agent at the site without host cell toxicity

relies upon identifying molecules with selective toxicity:

  • ones that dont exist in humans
  • different to human analogue
  • human cells recover from toxicity by alternative metabolic pathways
207
Q

fungal cell targets- DNA/RNA and protein synthesis

A

similar to mammalian

drug e.g. fluctosine

208
Q

fungal cell targets- cell wall

A

mannoproteins
B1,3 and 1,6 glucan
chitin
dont exist in humans

drug e.g. echinocandins

209
Q

fungal cell targets- plasma membrane

A

ergosterol
human membrane contains cholesterol instead

drug e.g. amphotericin, azoles, terbinafine

210
Q

ergosteol synthetic pathway

A

agents act early in pathway will be cidal

those acting at later stages will be fungistatic

211
Q

allylamines

A

reversible inhibition of squalene epoxidase
fungicidal
absorbed well but extensive first metabolism so bioavailability is 45%
used to treat dermatophytes

212
Q

azoles

A

dose dependent inhibitors of 14alpha-sterol demethylase

fungistatic
newer azoles have increase spectrum of activity

213
Q

spectrum of activity of azoles

A

determined by degree of inhibition of 14alpha-sterol demethylase and secondary targets

214
Q

azole adverse effects

A

relatively safe
drug interaction due to CYP450 metabolism
alopecia with long term fluconazole
30% on voriconazole suffer reversible visual disturbances

215
Q

azole resistance

A

multiple mechanisms in candida:
target site modification
-increased expression of ERG11
-efflux

216
Q

polyenes

A
  • amphoteric molecules
  • disruption caused by insertion of molecule into the membrane displaces and affects activity of membrane bound proteins
  • forms pores so fungicidal
  • 10x lower affinity for cholesterol but still can cause toxicity
217
Q

echinocandins

A 
inhibit 1,3 beta glucan synthase
fingicidal to susceptible yeasts
fungstatic to moulds with activity at hyphal tip
IV only
few side effects
218
Q

echinocandins

A 
inhibit 1,3 beta glucan synthase
fingicidal to susceptible yeasts
fungstatic to moulds with activity at hyphal tip
IV only
few side effects
219
Q

protozoa

A

single cell with nucleus

>30,000 species

220
Q

5 groups of protozoa

A 
flagellates
amoebae
sporozoan
ciliates 
microsporidia
221
Q

flagellates

A

leishmaniasis
trichomonas vaginalis
giardiasis

222
Q

amoebae

A

amoebiasis

223
Q

sporozoan

A

cryptosporidiosis
toxoplasma gondii
malaria (plasmodium)

224
Q

leishmaniasis

A

spread by bite of the sandfly

>20 species that affect humans

225
Q

leishmaniasis clinical pictures

A 
cutaneous= ulceration
mucocutaneous= ulceration

both can cause social rejection and scarring

visceral= fever, weight loss, hepatomegaly, anaemia

226
Q

thrichomonas vaginalis

A 
sexually transmitted
asymptomatic
dysuria
yellow frothy discharge
treat with metronidazole
227
Q

giardiasis

A 
giardia lamblia
faecal-oral spread
diarrhoea
cramps
treat with metronidazole
228
Q

amoebiasis

A 
enteraemoeba histolytica 
faeco-oral spread
dysentery 
liver and lung abscesses
treat with metronidazole
229
Q

cyrptosporidiosis

A 
waterborne
diarrhoea
womiting
oocytes seen in stool
sever in immunocompromised
230
Q

toxoplasmosis

A

ingestion of contaminated food and water

acute maternal infection can be fatal in pregnancy

231
Q

toxoplasmosis can cause

A

disseminated disease
toxoplasma encephalitis
chorioretinitis

232
Q

5 species of malaria

A 
Plasmodium falciparum 
Plasmodium ovale
Plasmodium vivax
Plasmodium malariae 
Plasmodium knowlesi
233
Q

test for malaria

A

blood film

234
Q

symptoms of malaria

A 
fever
chills
headache
myalgia
fatigue
diarrhoea
235
Q

signs of malaria

A

anaemia
jaundice
hepatosplenomegaly (big spleen and liver)

236
Q

life cycle of malaria

A
  • mosquito bites infected human and ingests plasmodium gametocytes
  • the gametocytes are within midgut and undergo development- becomes sporozoites in salivary gland
  • they’re injected into blood and infect human liver hepatocytes
  • develop into schizont and bursts out and infects red blood cells
  • this stage lasts 48 hours with haemolysis causing anaemia and jaundice
237
Q

p. falciparum

A

-The pathophysiology of complicated malaria is mostly down to the infected RBCs ability to
adhere to endothelial cells
-RBCs infected with p. falciparum have proteinaceous knobs on the surface that bind to
endothelial cells in the vessels and other RBCs
-This can cause small vessels to become obstructed by clumps of red blood cells causing hypoxia of the tissues, microinfarcts in brain and lung

238
Q

complicated cerebral malaria

A 
vascular occlusion
drowsiness
raised intracranial pressure
seizures
coma
239
Q

complicated malaria and acute respiratory distress

A 
vascular occlusion
anaemia
lactic acidosis
increased vascular permeability
hypoxia
pulmonary oedema
240
Q

complicated malaria and renal failure

A

vascular occlusion
dehydration- hypotension
haemolysis- haemoglobulinuria

proteinuria
fatigue
haematuria

241
Q

complicated malaria and bleeding

A

thrombocytopenia
activation of coagulation cascade
worsened anaemia

242
Q

complicated malaria and shock

A

anaemia
bleeding
gram -ve sepsis
increased vascular permeability

hypotension
tachycardia
pale

243
Q

malaria treatment

A

complicated= IV artesunate, IV quinine+doxycycline

244
Q

supportive measures for malaria

A 
cerebral= anti-epileptics
ARD= oxygen, diuretics, ventilation
renal failure= dialysis
sepsis= antibiotics
bleeding= blood products
245
Q

malaria relapses

A

p.ovale and vivax can form hypnozoites in the liver- lying dormant

primiquine eliminates this

246
Q

antibiotics

A

agents produced by microorganisms that kill or inhibit the growth of other microorganisms

247
Q

antimicrobials

A

most agents currently used are semi-synthetic derivatives so = antimicrobials

antifungal, antibacterial, antihelminitic, antiprotozoal and antiviral

248
Q

antibiotics as antibacterials

A

antibiotic tends to= antibacterial
bind to target site on bacteria
give time and support for the immune system to deal with an infection

249
Q

antibiotics affecting bacterial cell wall synthesis

A

beta lactams= penicillins, cephalosporins, carbapenems, monobactams

glycopeptides= vancomycin and teicoplanin

250
Q

beta lactam antibiotics

A

disrupt peptidoglycan production by binding covalently and irreversibly to PBPs
to do so it diffuses through the cell wall
cell wall is disrupted and lysis occurs
gram positive is more susceptible

251
Q

antibiotics affecting bacterial nucleic acid synthesis

A

DNA gryase- quinolines

RNA polymeras- rifampin

252
Q

antibiotics affecting bacterial protein synthesis

A

ribosome 30s subunit- tetracyclines, aminoglycosides

ribosome 50s subunit- macrolides, chloramphenicol

253
Q

antibiotics affecting bacterial folate synthesis

A

sulphonamides

trimethoprim

254
Q

bacteria and accidental damage

A 
destroy phagocytes or cells in which bacteria replicate
endotoxins
exotoxins
inflammation
diarrhoea
255
Q

bacteriostatic

A 
prevents growth
by preventing multiplication
kill >90% in 18-24 hours
inhibit protein synthesis, DNA replication or metabolism
MBC to MIC ratio >4
256
Q

bactericidal

A

kill bacteria
>99.9% killed in 18-24 hours
inhibit cell wall synthesis

257
Q

minimum inhibitory concentration

A

concentration required to stop bacteria from multiplying

258
Q

lowest MIC does not equal best antibiotic

A

drugs must attach to binding site and occupy an adequate number of binding sites

to work effectively they should remain on binding site for a sufficient period in order for metabolic processes to be inhibited

259
Q

concentration dependent killing

A

key parameter is how high the concentration is above MIC

260
Q

time dependent killing

A

key parameter is the time the serum concentrations remain above the MIC during dosing interval

261
Q

antibiotic considerations

A

release and absorption
distribution to site
half life and elimination

262
Q

other antibiotic considerations

A 
are they safe
side effects
renal function
liver function
pregnancy 
drug interactions
263
Q

changing antibiotic target site

A

bacteria changes molecular configuration of binding site or masks it

264
Q

destroying the antibiotic

A

e.g. beta lactam ring of penicillin is hydrolysed by bacterial enzyme beta lactamase

265
Q

preventing antibiotic access

A

modify bacterial membrane porin channel size, numbers and selectivity

266
Q

removing bacteria from bacteria

A

proteins in bacterial membranes act as an export or efflux pumps- so antibiotic levels are reduced

267
Q

intrinsic resistance

A

subpopulations of a species will be equally resistant

268
Q

acquired resistance

A

bacterium that was previously susceptible obtains ability to resist the activity of an antibiotic

269
Q

MRSA

A

staphylococcal cassette chromosome mec, contains resistance gene

270
Q

VRE

A

plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding

271
Q

ESBL

A

mutation at the active site extended range of antimicrobial resistance to form extended spectrum beta lactamase (ESBL) inhibition

plasmid spread resistance

272
Q

AmpC b-lactamase resistance

A

broad spectrum penicillin, cephalosporin resistance

encoded on the chromosome in bacteria

273
Q

beta lactams

A

group of drugs that contain beta lactam ring- detroy cell walls
penicillin V, amoxicillin, cephalexin

274
Q

cephalosporins

A

beta lactams
good for penicillin allergy
better for resistance bacteria

275
Q

gram positive antibiotics

A

thick cell wall so need simple cell wall weapon

276
Q

gram negative antibiotics

A

thin cell wall so need a different weapon

277
Q

methicillin resistant staphylococcus aureus

A

describes all staph that are resistant to beta lactams

278
Q

macrolides

A

clarithromycin and erythromycin
for gram positives and atypical pneumonia pathogens
use in penicillin allergy and severe pneumonia

279
Q

linosamides

A

clindamycin
gram positives e.g. s. aureus
use for cellulitis or necrotising fasciitis

280
Q

tetracyclines

A

doxycycline
broad spectrum but mainly gram positive
use for cellulitis if penicillin allergy and chest infections

281
Q

quinolones

A

ciprofloxacin
for gram negatives
urinary tract infections, gall bladder infections, abdominal infections

282
Q

beta lactams for gram negative

A

amoxicillin- clavulante, cefuroxime, meropenem, ceftriaxone

283
Q

beta lactams for gram negative

A

amoxicillin- clavulante, cefuroxime, meropenem, ceftriaxone

284
Q

HIV genome

A 
codes for 9 genes
Gag
Pol
Env
Tat
Nef
Vif
Vpr
Vpu
Rev
285
Q

prevention strategies for HIV

A 
HIV testing
early diagnosis
sti testing
HAART
screening of blood products
microbicides
male circumcision
post-exposure prophylaxis 
Pre-exposure prophylaxis 
behavioural prevention strategies for HIV
future
286
Q

features that make HIV successful

A

transmitted by sexual intercourse
latency so individuals don’t know they’re spreading the disease
stops immune system functioning
ineffective at replication so mutates every time

287
Q

HIV origins

A

HIV-1 = transmission of simian immunodeficiency virus (SIV cpz) from chimps to humans

HIV-2 = arose from SIV sm

288
Q

HIV types

A

Main, outlying and new groups

main separated into A-D, F-H, J-K

289
Q

HIV replication

A
  • attachment via gp120 to CD4 receptors
  • entry
  • uncoating
  • reverse transcription -error prone
  • genome integration by integrase enzyme
  • transcription of viral RNA
  • splicing of mRNA and translation into proteins
  • assembly
  • budding
290
Q

HIV receptors

A

their glycoprotein- gp120 binds to human CD4 receptors

291
Q

HIV genes: Pol

A

encodes reverse transcriptase, integrase, protease

292
Q

HIV genes: Env

A

encodes envelope proteins

293
Q

HIV genes: Nef

A

increases infectivity

294
Q

HIV genes: Tat

A

contributes to viral replication

295
Q

HIV genes: Gag

A

encodes structural proteins

296
Q

HIV genes: Rev

A

binds to viral RNA and allows export from nucleus and regulates RNA splicing

297
Q

cell tropism- infected cells in HIV

A 
CD4 cells
macrophages
dendritic cells
CD34 bone marrow progenitors
astrocytes
298
Q

initial HIV infection

A
  • virus enters via mucosa (vaginal, rectal etc.)
  • local infection within mucosal macrophage then spreads to other cells
  • as these are APCs they will migrate to local lymph nodes and T cells
  • infection spills into blood stream
299
Q

mechanism for CD4+ T cell depletion

A

direct cytotoxicity of infected cells
activation induced death
decreased production due to infected progenitors in bone marrow

300
Q

immune system consequences of HIV

A

decreased number and function of CD4 t lymphocytes
excessive activation of immune system
decreased proliferation in response to antigens
decreased macrophage function

301
Q

sanctuary sites for HIV

A

genital tract
CNS
GI tract
bone marrow

302
Q

reservoir cells for HIV

A

macrophages
T cells
microglia

303
Q

UNAIDS 90/90/90 goals

A

90% of people with HIV diagnosed
90% of diagnosed on ART
90% viral suppression for those on ART by 2020

304
Q

HIV transmission routes

A

blood
sexual
vertical- mother to child

305
Q

post-exposure prophylaxis

A

PEP
treatment commences within 72 hours of exposure
continued for one month

306
Q

Pre-exposure prophylaxis

A

PrEP
good evidence for effectiveness
ongoing trial in the UK to address questions such as duration of dose

307
Q

behavioural prevention strategies for HIV

A

sex education
avoid concomitant sexual partners
reduce high risk sexual partners
consistent condom use

308
Q

future prevention strategies for HIV

A

vaccines

309
Q

benefits of knowing HIV status

A

access to appropriate treatment
reduction on mortality
reduction in vertical transmission
reduction of sexual transmission

310
Q

high risk behaviours of HIV

A

sex with people from high prevalence groups e.g. subsaharan africa and thailand etc.
multiple sexual partners
rape in high prevalence localities

311
Q

consider HIV if recurring conditions, e.g.

A 
shingles
oral candidiasis 
flu like symptoms
rash
unexplained weight loss/ diarrhoea
unexplained lymphadenopathy
312
Q

screening tests for HIV

A

p24 antigen test

test at 4 weeks, if negative repeat at 8 weeks if high suspicion

313
Q

managing the result of HIV

A

negative- repeat if within window

positive-arrange appointment within 48 hours, explain test is reactive and needs further investigation

314
Q

partner notification and HIV

A

discuss with all HIV infected people
length of look back depends on circumstances
encourage them to inform their partners or agree to notification
document discussion
discuss consequences of reckless transmission

315
Q

criminalisation of HIV

A

only those who know their status are criminally liable

316
Q

confidentiality definition

A

Right of an individual to have personal, identifiable medical information kept private. Such information should be available only to the physician of record and other health care and
insurance personnel as necessary

317
Q

confidentiality and HIV

A

allows disclosure to known sexual partner if at risk and unaware
must inform patient you are doing so unless it endangers the contact
don’t reveal identity of patient

318
Q

markers of HIV

A

CD4 count

HIV viral load

319
Q

seroconversion

A

period of time during which HIV antibodies develop and become detectable

320
Q

acute HIV syndrome

A

usually takes 2-4 weeks
similar to glandular fever or flu
can present with opportunistic infections
non-specific symptoms

321
Q

HIV clinical latency

A

undiagnosed- the immune system takes control and CD4 increases
overtime CD4 does begin to decline
can then present with more opportunistic infections

322
Q

development of HIV symptoms

A

shingles
candida
oral hairy leukoplakia
recurring infections

323
Q

acquired immune deficiency syndrome

A

AIDs

CD4<200 and/or AIDs defining illness present

324
Q

AIDS defining illnesses

A

pneumocystis pneumonia
other respiratory infections
TB

325
Q

pneumocystis pneumonia

A

most common AIDS defining illness

most common opportunistic infection

326
Q

symptoms of pneumocystis pneumonia

A

fevers
dry cough
chest pain
drop in O2 sats

327
Q

tests for pneumocystis pneumonia

A

chest xray- can be normal
ABG test for hypoxia
induced sputum

328
Q

treatment of pneumocystis pneumonia

A

antibiotics- co-trimoxazole

and steroids

329
Q

HIV clinical latency

A

undiagnosed- the immune system takes control and CD4 increases
overtime CD4 does begin to decline
can then present with more opportunistic infections

330
Q

development of HIV symptoms

A

shingles
candida
oral hairy leukoplakia
recurring infections

331
Q

acquired immune deficiency syndrome

A

AIDs

CD4<200 and/or AIDs defining illness present

332
Q

AIDS defining illnesses

A

pneumocystis pneumonia
other respiratory infections
TB

333
Q

pneumocystis pneumonia

A

most common AIDS defining illness

most common opportunistic infection

334
Q

symptoms of pneumocystis pneumonia

A

fevers
dry cough
chest pain
drop in O2 sats

335
Q

tests for pneumocystis pneumonia

A

chest xray- can be normal
ABG test for hypoxia
induced sputum

336
Q

treatment of pneumocystis pneumonia

A

antibiotics- co-trimoxazole

and steroids

337
Q

TB and HIV

A

can present at any CD4 count
atypical presentations with lower CD4 count
all patients with TB should be tested for HIV

338
Q

CNS presentations of HIV

A

toxoplasmosis- reactivation of latent infection

meningitis- higher incidence and mortality in HIV

339
Q

cancers and HIV

A

increase in any cancer associated with a virus
HepB/B- hepatocellular carcinoma
human papilloma virus- cervical cancer
herpes 8- kaposi’s sarcoma

340
Q

kaposi’s sarcoma

A

single to multiple lesions

on the skin, mouth, respiratory tract, GI tract

341
Q

late diagnosis of HIV

A

increased transmission
increased morbidity
increased mortality

342
Q

highly active antiretroviral therapy

A

HAART
3+ antiretroviral drugs
act on different points in HIV replication cycle
aim to reduce viral loads to undetectable levels- not a cure

343
Q

how do antiretroviral drugs function

A

fusion/entry inhibitors
reverse transcriptase inhibitors
integrase inhibitors
protease inhibitors

344
Q

HIV resistance

A

1 mutation in every 2 new viruses produced
develop drug resistance through:
non-adherence (missing one or two doses)
drug-drug interactions

345
Q

avoiding HIV resistance

A

good drug adherence

checking drug interactions

346
Q

groups at risk of HIV

A 
men who have sex with men
heterosexual women
injecting drug users
commercial sex workers
heterosexual men
truck drivers
migrant workers
347
Q

problems for antiretroviral treatment in developing countries

A 
awareness
procurement/delivery
clinical services
cost
adherence
efficacy
co-morbidities

Phase 2a pre clinical (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions