Week 9 Flashcards
what is ketamine?
dissociative antagonist
NMDA receptor antagonist
harms of hallucinogens?
OD, bad trips and hams from hallucinating
administration of inhalants and volatile substances?
sniffing
huffing
bagging
harms with volatile substances?
volatile substances are lipid soluble and damage cell membranes in the CNS: white matter damage optic damage, hearing loss cortical atrophy cerebellar damage peripheral neuropathy
acute management of volatile substances?
recognition be aware be alert monitor sats/ ECG O2 when needed decontamination - get substance away wait it out
chronic management of volatile substances?
address underlying issue
physical assessment and needs
harm minimization
psychosocial needs (psychotherapy / life skills)
recommended screening tool 1 for gambling?
bief biosocial gambling screen:
withdrawal: during the past 12 months, have you been restless, irritable or anxious when trying to stop/ cut down on gambling
deceive: during the past 12 months, have you tried to keep your family and friends from knowing how much you gamble?
bailout/ need money? during the past 12 months have you had financial trouble that you had to get help with living expenses from family, friends, welfare?
recommended screening tool 1 for gambling?
NODS-CLIP:
loss of control: have you ever tried to stop, cut down ir control your gambling?
lying: have you ever lied to family member or friends about how much you gamble or how much money you’ve lost gambling?
pre-occupation: have their been periods lasting > 2 weeks or longer when you spent a lot of time thinking about your gambling experiences or planning out future gambling ventures/ bets?
recommended screening tool 1 for gambling?
Lie-Bet screening instrument:
have you ever felt the need to bet more and more money?
have you ever had to lie to people important to you about how much you gamble?
what are the components of innate immunity in viruses?
complement (forms MAC complex)
interferons (activate NKC)
3 functions of interferon 1?
induce viral replication in all cells
increase expression of ligands for receptors on NKC
activate NKC to kill infected cells
what are the components of Ab adaptive immunity in viruses?
neutralize EC virus (Ab may block virus to bind to arrestor, aggregation of virus so its easier to phagocytose, block endocytosis)
enhancing complement cell mediated killing of virus directly or cell containing virus
promoting cytotoxicity and opsonization
evasion of immune response by viruses?
antigenic variation
encode proteins that bind complement, cytokines and cytokine receptors
interfere with Ag processing and presentation
produce molecules that sequester AB
interfere with CTL and NKC functions
evasion of host immunity from viruses?
DNA viruses have low mutation rates but large genomes meaning that they have large number of viral genes encoding immune subversion proteins
what is the extracellular immune response to protozoa?
innate: phagocytosis, complement
Ab: phagocytose, complement, ADCC
T cell: Th2 cytokines for Ab response ADCC and activation of eosinophils and mast cells
what is the intracellular immune response to protozoa?
Ab: neutralization to block entry to host cells
T cell: TH1 cells activate macrophages, CTLs kill infected cells
immune evasion by protzoa?
antigenic variation
antigenic drift
molecular mimicry
sequestration in immune privileged sites
immune evasion by helminths?
shedding of surface Ag
protease production to neutralize anti-parasite immune components
absorbing host Ag and making parasite Ag
what are the 6 basic stages essential for viral replication?
attachment penetration uncoating replication assembly viral release
how does HIV enter the cell?
HIV GP120 receptor attached to CD4 receptor and undergoes conformational change to avoid detection by neutralizing Abs
binds co receptors:
CCR5 - macrophages
CXCR4 - T cells
innate immune response in HIV?
Macs, DC, NKC
adaptive immune response in HIV?
CTLs lyse HIV cells and release cytokines
inhibit virus replication and block its entry into the cell
humoural immune response in HIV?
occurs later in the infection
first we get non-neutralizing Abs to structural proteins eg, p24
then we get neutralizing Ab to specific proteins involved in the entry of the virus in the cell
what is the route of transmission for hep A and E
ingestion of contaminated foods and drink
what is the route of transmission for hep B C D
parenteral contact with infected body fluids
hep B may be transmitted from mother to baby or sexual contact
what chemo drugs can cause secondary malignancies?
anthracyclines and alkylating agents
prognostic factors for early cancer?
size of primary level of differentiation node involvement receptor status age molecular markers
steps in staging?
to assess extent of disease
hx examination tumour markers (a-fetoprotein, hCG, PSA, CA125, CEA) FBC, LFT, BM histology x-ray, CT, MRI, bone scan, PET scan
indications for pet scan?
when we’re treating patient for curative intent and aggressive tx may offer prolonged surival
also decreases need for unnecessary/ intensive procedures if cancer is deemed incurable
what are some curative cancers with chemo?
lymphoma, leukemia, germ cell tumours, osteosarcoma
tumours curable with adjuvant therapy?
breast cancer, ovarian cancer and sarcoma
some features of telehealth?
improve patient access to health care
reduce travel/ inconvenience to patient, families, carers and health professionals
provide health professionals with access to peer support/ education
how does interferon 1 response work in innate immunity against viruses?
IFN alpha and IFN beta =
- induce resistance to viral replication in all cells
- increase expression of ligands for NKC receptors
- induce NKC killing of virus infected cells
where do NKC develop?
BM and circulate in the blood
how does hepatitis adhere to the host cells?
hepatitis virus gains entry into hepatocytes via interaction with receptor on hepatocytes
Ab can neutralize EC virus to stop it from entering the cell (adaptive viral immunity)
role of AB in adaptive immunity for viruses?
neutralize EC virus (block virus binding to a receptor, block endocytosis, form viral aggregates easier to phagcytose)
enhance complement mediated killing (directly - virolysis or cells containing virus - cytolysis)
promoting cytotoxicity and phagocytosis by NKC and phagocytes
how does CTL differentiate with the help of CD4 T cells?
APC stimulates CD4T cells to increase expression of B7 and CD40L
APC stimulation through CD4 increases B7 and 4-1BBLL which both co-stimulate naive CD8 T cell
what does AIDS stand for?
acquired immune deficiency syndrome
rough time course of HIV infection?
first few days HIV is starting to replicate and their are no signs of disease
6 days later we can detect virus in blood - look for nucleic acid via qPCR
few days later we can see Ab appearing in blood
12 days later we see specific Ab (non-neutralizing) p24
then neutralizing ABs appear specific for proteins, involved in the entry of virus into cell
2 types of eukaryotes?
trophozoite = reproducing/ feeding form cyst = dormant and infective form
examples of intracellular and extracellular protozoa?
extraceullular: amoebiasis
intracellular: malaria
malaria life cycle summary?
mosquito bites and injects sporozoites into the infected cell which travels to the liver and infects hepatocytes = hepatocyte shizont
shizont rupture in the liver releases merozoites which infect the RBCs
once in the RBC it is called a trophozoite
now it can either mature into a gametocyte which will be taken up by another mosquito and continue the spread of disease OR
develop into latent trophozoite and into a blood stage schizont which will burst and release more merozoites to continue cell cycle of infection
role of eosinophils in helminth infection?
produce MBP which kills parasite
can undergo ADCC
contains toxic granules - with toxic enzymes and free radicals which degrade wall of cuticle of from = interferes with worms ability to replicate
how is malaria parasite detected?
thick blood smear = detects parasite
thin blood smear = differentiates parasite type
dipstick = rapid Ag detection
evasion of host immunity in viruses?
dna viruses have low mutation rates but large viral genomes = large number of genes encoding immune subversion genes
how come neutralizing Abs don’t stop HIV from entering the cell?
their is a bit of lag time because HIV is a new virus so don’t have time for the production of enough Ab to prevent HIV entry into cell
which forms of Hepatitis are the cause of hepatic cirrhosis and liver cancer
hep B and C
