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239 Cards in this Set
- Front
- Back
|
what proportion of benign adenomas in the colon become malignant?
|
approx 10%
|
|
|
which morphological features of benign adenomas of the colon confer a risk of the adenoma becoming malignant?
|
large (>3cm)
villous sessile |
|
|
what prolongs the activation of ras?
|
impaired hydrolysis of GTP
|
|
|
t/f... malignant tumours are usually sessile (no stalk)
|
true
|
|
|
t/f... malignant tumours are usually pedunculated
|
false
|
|
|
what percentage of breast cancers are familial?
|
10%
|
|
|
mutations of which two genes account for most cases of familial breast cancer?
|
BRCA-1 and BRCA-2
|
|
|
mutation of which gene occurs in most colonic carcinomas?
|
DCC
|
|
|
what percentage of occupationally caused cancers are found in the lungs and pleura?
|
75%
|
|
|
what percentage of lung and pleural cancer is attributable (at least in part) to occupational exposure?
|
13-27%
|
|
|
what percentage of the workforce is exposed to occupational carcinogens?
|
1-5%
|
|
|
what is the cause of hypercalcaemia as a paraneoplastic syndrome?
|
overproduction of PTH-RP
|
|
|
which tumours are associated with hypercalcaemia?
|
myeloma
breast cancer NSCLC colon lymphoma renal |
|
|
what are the symptoms of acute hypercalcaemia?
|
renal effects (polyuria, polydipsia, RF)
neuro effects (drowsiness, confusion, coma, pain) gastro effects (N, V, constipation) other effects (arrhythmias, fatigue) |
|
|
what is the treatment of hypercalcaemia?
|
IV fluids
bisphosphonates |
|
|
which tumour most commonly causes ectopic ACTH?
|
small cell lung cancer
|
|
|
which tumour is most often associated with SIADH?
|
SCLC
|
|
|
what are the findings expected in SIADH?
|
hyponatraemia
decreased serum osmolality increased urine osmolality (compared with serum) and sodium normal renal, adrenal, thyroid function euvolaemia |
|
|
what are the symptoms of SIADH?
|
fatigue
headaches anorexia confusion seizures coma death |
|
|
why does anaemia occur with cancer?
|
suppression of maturation of red cell series
|
|
|
what type of anaemia occurs with cancer?
|
normochromic/normocytic anaemia of chronic disease
|
|
|
what is the cause of Eaton Lambert syndrome?
|
antibody against presynaptic nerve terminals, especially on VDCC
|
|
|
how does Eaton Lambert syndrome present?
|
proximal weakness, dysphagia
|
|
|
t/f... generally, fewer proto-oncogenes are damaged in a benign tumour than in a malignant tumour
|
true
|
|
|
what are the features of epithelial cells of pre-malignant lesions?
|
enlarged nuclei
loss of other differentiated features disorderly positional arrangement increased proliferative activity |
|
|
what is dysplastic tissue?
|
tissue that has lost the uniformit of the individual cells but will be returned to normal if dysplastic stimulus is removed
|
|
|
what proportion of benign adenomas in the colon become malignant?
|
10%
|
|
|
which morphological features of benign adenomas of the colon are an indicator they might become malignant?
|
large (>3cm)
villous sessile |
|
|
t/f... malignant tumours are usually pedunculated
|
false, they are usually sessile
|
|
|
what is the function of BRCA-1?
|
secreted from breast epithelium and is believed to inhibit cell growth
regulates a DNA repair protein, Rad51 |
|
|
what is the function of BRCA-2?
|
unknown
|
|
|
t/f... mutations in BRCA-1 and BRCA-2 account for most familial cases of breast cancer
|
true
|
|
|
what percentage of breast cancers are familial?
|
10%
|
|
|
what does the DCC gene code for?
|
cell surface-like protein that may be involved in cell-cell or cell-matrix communication
|
|
|
in which cancers is there a mutation of DCC?
|
most colonic carcinomas
some breast, prostate, pancreatic, endometrial |
|
|
what does APC code for?
|
cytosplasmic protein linked to and presumably regulates E-cadherin (involved in intercellular junctions)
|
|
|
what does mutation of one APC allele result in?
|
numerous benign adenomas, a proportion of which eventually become malignant
|
|
|
in which cancer is mutation of E-cadherin seen?
|
invasive gastric carcinomas
|
|
|
where is p53 located?
|
chromosome 17
|
|
|
what percentage of cancers involve p53?
|
50%
|
|
|
which part of the cell cycle does p53 arrest damaged cells in?
|
G1
|
|
|
what are the two inherited conditions associated with the development of colorectal cancer?
|
familial adenomatous polyposis
hereditary non-polyposis colorectal cancer |
|
|
what is the population frequency of FAP?
|
1 in 10 000
|
|
|
what percentage of those with colorectal cancer have FAP?
|
1%
|
|
|
by what age does colocrectal cancer develop in those with untreated FAP?
|
40
|
|
|
which tumours occur in FAP?
|
colorectal cancer
stomach duodenum liver bone skin thyroid other sites |
|
|
what is FAP due to?
|
germline mutation in APC gene located on long arm of chromosome 5
|
|
|
which cancers (other than colorectal) occur with increased incidence in those with HNPCC?
|
endometrium
urinary tract |
|
|
what is HNPCC due to?
|
mutation in one of four DNA mismatch repair genes
|
|
|
what is the inheritance of FAP?
|
autosomal dominant
|
|
|
t/f... HNPCC is associated with a predominance of right sided lesions
|
true
|
|
|
what is the inheritance of HNPCC?
|
autosomal dominant
|
|
|
for which cancers is alcohol a risk factor?
|
mouth and pharynx
larynx oesophagus liver colon and rectum breast |
|
|
what is the commonest cause of cancer death in men? women?
|
lung
breast (followed by lung) |
|
|
what percentage of occupationally caused cancers are found in the lungs and pleura?
|
75%
|
|
|
what percentage of lung and pleural cancer is attributable in some part to occupational exposure?
|
13-27%
|
|
|
what percentage of the workforce is exposed to occupational lung carcinogens?
|
1-5%
|
|
|
what is squamous cell carcinoma associated with?
|
cigarette smoking
|
|
|
what is the most common type of lung cancer?
|
adenocarcinoma
|
|
|
which lung cancer has a lower rate of metastasis?
|
squamous cell carcinoma
|
|
|
t/f... small cell carcinoma is strongly associated with cigarette smoking
|
true
|
|
|
which type of lung cancer spreads early with few initial symptoms?
|
small cell carcinoma
|
|
|
where does large cell carcinoma usually develop?
|
airways
|
|
|
what are the mechanisms of metastasis?
|
seeding within a body cavity
spread through lymphatics haematogenous spread Pagetoid (intraepidermal) implantation (iatrogenic) mucosa to mucosa perineural |
|
|
how does malignant metastasis through the blood occur?
|
tumour adheres to basement membrane
proteolytic enzymes break down bm tumour cells undergo amoeboid movement to pass through ECM and bm cells intravasate through wall of blood vessel with decreased adhesion characteristics cells attach to lymphocytes to form tumour cell embolus and pass to distant site cells re-attach to blood vessel and extravasate type of tissue in which metastatic cell lodges determines growth |
|
|
where in the body is metastasis rare?
|
skeletal muscle
spleen |
|
|
what is the distribution of calcium in the blood?
|
50% ionised
40% bound to protein (maily albumin) 10% complexed (citrate and phosphate) |
|
|
what are the majority of cases of hypercalcaemia due to?
|
primary hyperparathyroidism
malignancy associated |
|
|
what is the mechanism of malignancy associated hypercalcaemia?
|
excessive bone resorption which overwhelms capacity of kidney to excrete the extra calcium
|
|
|
which hormone is made in excess by tumour cells causing excess bone resorption?
|
parathyroid hormone-related peptide (PTHrP)
|
|
|
what are the consequences of hypercalcamia?
|
impairment of concentrating ability of kidney resulting in increased urinary water loss
anorexia N/V (severe dehydration) nerve and muscle hyperpolarisation (causing constipation and cardiac arrhythmias) |
|
|
what is the immediate treatment of hypercalcaemia?
|
rehydration
|
|
|
what is the purpose of loop diuretics in hypercalcaemia?
|
may improve calcium excretion
|
|
|
what is the microscopic appearance of malignant cells?
|
enlarged nuclei (nuclear:cytoplasmic ratio >50%)
pleomorphic cells haphazard arrangement increased mitosis loss of architectural organisation |
|
|
which types of HPV are associated with cervical and other anogenital cancers?
|
types 16 and 18
|
|
|
what type of cancer is associated with EBV?
|
Burkitt's lymphoma
nasopharyngeal carcinoma |
|
|
which virus is associated with HCC?
|
Hep B
|
|
|
t/f... cervical cancers preferentially metastasise to the inguinal lymph nodes
|
false
|
|
|
t/f... cervical cancers frequently contain both squamous and adenomatous areas
|
true
|
|
|
t/f... cervical cancers arise in the transitional zone of the cervix
|
true
|
|
|
t/f... cervical cancers commonly cause remote bony mets
|
false
|
|
|
which virus induced tumours are associated with viral sequences integrated into the tumour cell genome?
|
HTLV1/human T cell leukaemia
HBV/HCC HPV16/cervical cancer |
|
|
what percentage of patients indicate they would prefer to receive as much information as possible?
|
80-90%
|
|
|
how many women with breast cancer want to have an active or collaborative role in making decision about their treatment?
|
2/3
|
|
|
what type of lymphomas occur in HIV?
|
B cell lymphomas
|
|
|
what is the mean time from exposure to onset of symptoms in HIV?
|
2-3 weeks
|
|
|
how long is seroconversion delay?
|
up to 3 months
|
|
|
which malignancies are associated with HIV?
|
non-Hodgkins B cell lymphoma
Kaposi's sarcoma HPV associated cancers (cervical, perianal) |
|
|
what is the most common mode of transmission of HIV worldwide?
|
mucosal transmission during sexual intercourse
|
|
|
in what percentage of HIV infected mothers does vertical transmission occur?
|
25%
|
|
|
how can vertical transmission rates of HIV be reduced?
|
treatment of mother pre-delivery and treatment of neonate
avoidance of breastfeeding (caesarian may possibly reduce risk) |
|
|
when does the immune response to HIV infection occur?
|
within several weeks in almost all cases
|
|
|
what is the antibody response to HIV infection?
|
antibody of IgM, IgA and IgG class produced
|
|
|
how does HIV enter lymphocytes?
|
by binding to CD 4 molecule and chemokine receptors
|
|
|
which cancers have high mortality?
|
lung
unknown primary pancreas stomach brain |
|
|
what mainly causes the geographical differences in cancers?
|
environmental influences
|
|
|
which cancers are associated with smoking?
|
lung
mouth larynx oesophagus pancreas bladder cervix |
|
|
what is the cancer most commonly caused by ionising radiation?
|
leukaemia
|
|
|
which cancers may be associated with ionising radiation?
|
leukaemia
thyroid cancer breast lung salivary glands |
|
|
what ages in men and women have the highest incidences of cancer?
|
males 45-54
females 30-64 |
|
|
which cancers frequently occur in children?
|
certain leukaemias
neurological tumours renal tumours |
|
|
what causes neoplastic transformation of a cell?
|
non-lethal cumulative genetic damage
|
|
|
how many mutations are involved in neoplastic transformation?
|
at least 6
|
|
|
why are tumour monoclonal?
|
tumour arises by clonal expansion of a single precursor cell that has undergone damage
|
|
|
which genes may mutate during neoplastic transformation?
|
proto-oncogenes
tumour suppressor genes genes that regulate apoptosis enzymes of DNA repair genes that regulate telomerase expression |
|
|
what type of mutations usually cause the inactivation of p53?
|
missense mutations
|
|
|
what is the effect of mutant ras?
|
slow to hydrolyse GTP i.e. longer duration of kinase activity
|
|
|
what chance of developing breast and ovarian cancer do people with BRCA-1 germline mutations have?
|
> 50% chance breast cancer
> 20% chance ovarian cancer |
|
|
what are the three primary mechanisms of activation of oncogenes?
|
point mutations
chromosomal translocations activation by gene amplification |
|
|
what is the lifetime risk of developing colorectal cancer before 75 for women and men?
|
female 1/28
male 1/18 |
|
|
what is the lifetime risk of developing colorectal cancer before 85 for men and women?
|
men 1/10
women 1/14 |
|
|
t/f... the incidence of colorectal cancer in men is constant but increasing in women
|
true
|
|
|
t/f... the mortality of colorectal cancer is increasing in both men and women
|
false, it is decreasing in bothmen and women
|
|
|
what are the dietary factors that reduce risk of colorectal cancer?
|
restrict energy intake
reduce dietary fat (<25% caloric intake) >4 portions F and V poorly soluble cereal fibre selenium supplementation |
|
|
what are the lifestyle factors that reduce risk of colorectal cancer?
|
physical activity
no smoking avoid excessive alcohol |
|
|
describe category 1 risk of colorectal cancer
|
at or slightly above average risk
no family hx or one 1st/2nd degree relative >55 RR less than or equal to 2 |
|
|
describe category 2 risk of colorectal cancer
|
1 x 1st deg rel<55 or 2 x 1st/2nd deg rel same side
RR 3-6 2% population |
|
|
describe category 3 risk of colorectal cancer
|
3 or more 1st/2nd deg rels same side
2 or more 1st/2nd deg rels smae side: multiple bowel cancers, < 50, one rel with endomet or ovarian cancer, definite family mutation APC or MMR risk 1/2 <1% population |
|
|
what effect does screening for colorectal cancer have on mortality?
|
reduction 40%
|
|
|
what is the risk of perforation in bowel cancer screening? death?
|
1/1500
1/10000-20000 |
|
|
where do colorectal cancers occur?
|
40% rectum
60% colon (left 30%, transverse 9%, right 21%) |
|
|
what percentage of colorectal cancers are genetic?
|
20%
|
|
|
how is colorectal cancer diagnosed?
|
colonoscopy
CT |
|
|
how does colorectal cancer spread?
|
haematogenous
lymphatic direct extension transcoelemic |
|
|
how is colorectal cancer staged?
|
CT
US CXR CEA EUS MRI/PET operative - liver/LN mets post-op - pathology, CT/US/MRI |
|
|
what are the layers of the bowel wall?
|
mucosa
submucosa muscularis propria subserosa serosa |
|
|
describe the T stages for colorectal cancer
|
T0 no tumour
T1 invasion limited to submucosa T2 invasion into muscularis propria but not beyond T3 invasion beyond MP and into subserosa T4 invasion beyond serosa or adj viscera |
|
|
describe the N stages for colorectal cancer?
|
N1 < 4 LN
N2 4 or more LN |
|
|
what is the 5 year survival for colorectal cancer (stages 1 to 4)?
|
stage I 90%
II 87% III 57% IV 10% |
|
|
which cancers tend to be drug resistant?
|
renal cancer
pancreas |
|
|
what are the side effects of alkylating agents?
|
anorexia, N, V
alopecia amenorrhoea/azoospermia mutagenic, 2nd malignancies myelosuppressive immunosuppressive |
|
|
what toxicity is associated with doxorubicin?
|
cardiotoxicity
|
|
|
what toxicity is associated with bleomycin?
|
pulmonary toxicity
|
|
|
which cytotoxics are associated with neurotoxicity?
|
vinca alkaloids - vincristine, vinblastine, vinorelbine
|
|
|
what are the side effects of taxanes?
|
neuropathy
arthralgia/myalgia |
|
|
what is imatinib used to treat?
|
CML
GIST |
|
|
which tyrosine kinase inhibitor is used in treatment of renal cell carcinoma?
|
sunitinib
|
|
|
what effect has herceptin had on breast cancer mortality?
|
50% reduction
|
|
|
which side effects are common to all cytotoxics?
|
anorexia, N, V
alopecia myelosuppression gonadal damage |
|
|
which cytotoxics do not cause hair loss?
|
carboplatin
5FU mitoxantrone |
|
|
which cytotoxics are relatively marrow sparing?
|
bleomycin
vincristine cisplatin 5FU |
|
|
what symptoms in order of prevalence do cancer patients suffer from?
|
pain
fatigue/asthenia constipation dyspnoea nausea depression/suffering vomiting delirium |
|
|
according to the WHO pain ladder what is the treatment for mild (0-3), moderate (4-6) and severe (7-10) pain?
|
mild: acetaminophen (paracetamol)
moderate: codeine severe: morphine |
|
|
t/f... in the treatment of severe pain it is routine to start with slow release formulations
|
false, rarely start with slow release
|
|
|
what is the usual dose of oral morphine solution or oxycodone in treatment of severe pain?
|
2.5-5mg
|
|
|
what is given for breakthrough analgesia?
|
1/12 - 1/6 of 24hr dose or 50-100% of 4hr dose
|
|
|
how is analgesia titrated in the case of ferquent breakthroughs?
|
increase analgesia 25-50%
|
|
|
when does incident pain often occur?
|
bone mets
neuropathic pain intra-abd disease aggravated by respiration skin ulcer disimpaction catheterisation dressings |
|
|
what is fentanyl?
|
synthetic mu agonist opioid
|
|
|
how is fentanyl absorbed?
|
transmucosal
|
|
|
what is the duration of action of fentanyl?
|
1 hour
|
|
|
how strong is fentanyl in terms of morphine?
|
100x stronger than morphine
|
|
|
what are the side effects of opioids?
|
constipation
N/V urinary retention itch/rash dry mouth resp depression drug interactions neurotoxicity |
|
|
what are the features of opioid-induced neurotoxicity?
|
neuropsychiatric syndrome:
cognitive dysfunction delirium hallucinations myoclonus/seizures hyperalgesia/allodynia |
|
|
what are the risk factors for OIN?
|
high opioid doses
prolonged opioid treatment preexisting cognitive impairment dehydration renal failure psychoactive drugs advanced age advanced life-limiting illness |
|
|
why are corticosteroids useful adjuvant therapy for cancer pain?
|
reduce tumor mass effects (reduce inflamm, reduce oedema, reduce spontaneous nerve depolarisation)
|
|
|
what is the basic radiation effect?
|
xrays/gamma rays enter tissue and produce chemical damage and heat
direct damage to organelles, membranes, DNA indirect damage via free radicals |
|
|
what are the intracellular processes affected by radiation?
|
DNA repair
DNA replication DNA transcription membrane-DNA signal transduction acute response genes |
|
|
what are the tissue effects of acute radiation injury?
|
inflammation
oedema desquamation ulceration |
|
|
where does lung cancer spread?
|
lymph nodes
liver adrenals bone brain |
|
|
what is cachexia?
|
loss of both adipose tissue and lean body mass
|
|
|
which host derived cytokines are associated with cachexia?
|
TNF-a, IL-1, IL-6, IFN-g
|
|
|
which tumour generated substances are associated with cachexia?
|
proteolysis-inducing factor (PIF)
lipid-mobilising factor |
|
|
what is used to treat cachexia in cancer?
|
anti-TNF-a antibody (infliximab)
anti-IL-6 antibody steroidal meds omega-3 fatty acids |
|
|
which paraneoplastic syndrome is associated with inappropriately concentrated urine?
|
SIADH
|
|
|
which cancers are associated with SIADH?
|
small cell lung cancer
head and neck cancer |
|
|
what are the symptoms of SIADH?
|
may be asymptomatic
confusion seizures coma rarely death |
|
|
what is the treatment of SIADH?
|
fluid restriction
demeclocycline treat cancer |
|
|
give the formula for corrected serum calcium
|
corrected serum calcium = serum calcium + [(40 - serum albumin) x 0.02]
|
|
|
what are the causes of hypercalcaemia?
|
malignancy
associated with dialysis primary hyperparathyroidism no cause apparent |
|
|
what percentage of patients with lung cancer develop hypercalcaemia? breast cancer?
|
30%
25% |
|
|
what are the major symptoms of hypercalcaemia?
|
polydipsia
polyuria constipation confusion |
|
|
what is the cause of hypercalcaemia in malignancy?
|
due to cytokine/hormone production:
increases bone resorption in associated with reduced renal elimination of calcium |
|
|
what is the effect of PTHrP on calcium metabolism?
|
increased bone resorption
reduced renal elimination Ca |
|
|
what is the treatment of hypercalcaemia?
|
rehydration with normal saline
pamidronate calcitonin if rapid reduction required |
|
|
what is the source of ectopic ACTH?
|
small cell lung cancer (pancreas and others)
|
|
|
how is ectopic ACTH distinguished from CUshings?
|
ectopic ACTH more rapid onset
|
|
|
what will dexamethasone suppression test reveal in ectopic ACTH?
|
excessive cortisol not suppressed by dexamethasone
|
|
|
why do cancer patients have a greater risk of thrombosis?
|
circulating procoagulants released by cancer
|
|
|
why do cancer patients present?
|
symptoms from primary
symptoms from mets paraneoplastic syndromes screening |
|
|
which psychosocial elements are the strongest contenders in predicting cancers?
|
depression
emotional repression stressful life events |
|
|
which psychological factors are associated with poor outcome?
|
depression
hopelessness high concern |
|
|
which psychological factors are associated with better outcome?
|
self care
compliance active behavioural coping |
|
|
who is most vulnerable to problems in the context of cancer?
|
younger age
single having children under 21 poor social support history of psychiatric problems stressful life events poor marital or family functioning experiencing more side effects in treatment |
|
|
what cofactors are required for transformation of HPV lesions?
|
smoking
OCP |
|
|
what is the result of HPV integrating into host DNA?
|
E6/E7 oncogenes retained and expressed
(E6 interferes with p53, E7 interferes with pRb) |
|
|
when is the risk of breast cancer recurrence highest?
|
first 3 years
|
|
|
what is the risk of breast cancer recurrence every year (after first three years)?
|
2% per year
|
|
|
what is the typical pattern of spread of breast cancer?
|
lymph nodes
bone/bone marrow soft tissue lung/liver/brain |
|
|
what is the average number of symptoms in people on chemotherapy?
|
20 symptoms (13 physical, 7 psychosocial)
|
|
|
what does chemotherapy do in early breast cancer?
|
prolongs survival and reduces deaths
|
|
|
what is the role of chemotherapy in advanced breast cancer?
|
modest prolongation of survival but doesn't cure
|
|
|
t/f... small improvements are valued highly by those receiving chemotherapy
|
true
|
|
|
who reports HIV diagnoses to health department?
|
HIV testing labs
|
|
|
who reports AIDS diagnoses?
|
medical practitioners
|
|
|
t/f... HIV positive individuals must inform all potential sexual partners
|
true
|
|
|
who can disclose HIV results to a partner if required?
|
Director General of Health
|
|
|
how many people are living with HIV?
|
33 million
|
|
|
what is the major driver of Indonesia's HIV epidemic?
|
IVDU
|
|
|
what are the modes of HIV acquisition?
|
sexual
parenteral non-sexual exposure to blood or body fluids mother to child |
|
|
which factors increase risk of sexual transmission of HIV?
|
increased HIV viral load
ulcerative and inflammatory genital diseases |
|
|
which sexual behaviour has the highest risk of HIV transmission?
|
receptive anal sex (0.1-0.3%)
followed by receptive vaginal and insertive vaginal |
|
|
t/f... anti-retroviral therapy as soon as possible after exposure reduces the risk of HIV infection
|
true
|
|
|
t/f... knowledge of HIV status reduces risky behaviour
|
true
|
|
|
which body fluids will contain a high HIV viral load?
|
blood or blood-stained body fluids
semen cervical secretions CSF |
|
|
which body fluids will contain low HIV viral loads?
|
urine
faeces saliva tears |
|
|
what confers natural resistance to HIV infection?
|
CCR5 deficient (1% caucasions)
|
|
|
what are the four phases of HIV infection?
|
primary infection (seroconversion illness)
early immune deficiency (CD4 > 500) intermediate immune deficiency (CD4 200-500) late immune deficiency (CD4 < 200) |
|
|
what are the clinical features of seroconversion illness?
|
fever
rash adenopathy malaise myalgia/arthralgia meningo-encephalitis |
|
|
what percentage of people infected by HIV have a symptomatic seroconversion illness?
|
>75%
|
|
|
what loss of CD4 T cells occurs during seroconversion?
|
loss of 200-300
|
|
|
what are the two major coreceptors for HIV?
|
CCR5
CXCR4 |
|
|
which strains of HIV cause rapid T cell loss?
|
CXCR4 using HIV strains
|
|
|
what are the late infections in HIV (AIDS-defining)?
|
PCP
cryptosporidiosis toxoplasma encephalitis cryptococcal meningitis MAC CMV PML (JC virus) |
|
|
when is antiretroviral therapy started in treatment of HIV?
|
CD4 <200 (<350 in most)
pregnancy (and newborn) |
|
|
what classes of drugs exist to treat HIV?
|
reverse transcriptase inhibitors
protease inhibitors fusion inhibitors integrase inhibitor |
|
|
what is aim of antiretroviral therapy?
|
undetectable plasma HIV RNA (viral load)
|
|
|
what is critical for avoiding drug resistance in HIV treatment?
|
compliance (aim for 100%)
|
|
|
what percentage of HIV patients with 95% compliance to treatment achieve undetectable viral load?
|
80%
|
|
|
what percentage of HIV patients with 90-95% compliance achieve undetectable viral load?
|
45-64%
|
|
|
what are the side effects of HAART?
|
mitochondrial toxicity
hepatotoxicity metabolic abnormalities bone disease |
|
|
what is the prognosis of HIV infection untreated?
|
AIDS and death within 10 years
|
|
|
which cells are the targets of HIV virions?
|
T cells
|
|
|
what are the CD4+ cells?
|
T helper lymphocytes
dendritic cells cells of macrophage lineage (monocytes and microglia) |
|
|
which cells are preferentially affected in early HIV infection?
|
memory T cells
macrophages/DCs |
|
|
what determines immune status in HIV?
|
CD4 count
|
|
|
what is the normal range for CD4 cells?
|
600-1100/microlitre
|
|
|
what determines rate of disease progression in HIV?
|
viral load
|
|
|
how do opportunistic infections occur in HIV?
|
reactivation
reinfection |
|
|
what are the classic fungal opportunistic infections?
|
PCP
cryptococcus oesophageal candidiasis |
|
|
what are the classic bacterial opportunistic infections?
|
MAC
TB |
|
|
what are the classic parasitic opportunistic infections?
|
toxoplasmosis
cryptosporidium microsporidia |
|
|
what are the classic viral opportunistic infections?
|
CMV
JC virus |
|
|
what is the most common cause of pneumonia in AIDS?
|
pneumocystis jiroveci (carinii)
|
|
|
at what CD4 count will PCP occur?
|
200 or less
|
|
|
what are the clinical features of PCP?
|
subacute onset
dry cough dyspnoea fevers |
|
|
what is seen on imaging in PCP?
|
non-specific bilateral perihilar interstitial inflitrate
(but CXR normal in 6-23%) |
|
|
at what CD4 count is toxoplasmosis reactivated?
|
CD4 < 100
|
|
|
what is the most common cause of space occupying lesions in CNS in AIDS patients?
|
toxoplasmosis
|
