Week 3--lecture slides Flashcards
1
Q
why are late effects of cancer more severe in childhood survivors than adult survivors
A
radiation and chemo inhibit normal tissue growth–kids still growing
–> organ growth, brain growth, development, psychosocial development, MSK growth can all be affected
treatment more intensive for children
survivors of childhood cancers have more years to survive for the late effects to show themselves than adults
2
Q
what is the risk of cancer recurrence or second cancer in childhood cancer survivors
A
5-10x increased risk
3
Q
what is a stage 3 wilms tumour
A
rupture with tumour spillage
4
Q
how are wilms tumours treated
A
standard chemo–> vincristine, doxorubicin, actinomycin
+ whole abdo radiation
5
Q
what are the concerning side effects of anthrocyclines like doxorubicin
A
can affect the heart and so they require yearly follow up
can caused decreased ejection fraction etc and may require cardiac meds to manage cardiac disease–> cause cardiomyopathy
this is dose and age dependent–> worsens with length of follow up, exacerbated by radiation to heart, pregnancy, obesity, sudden growth
6
Q
what is the most common cause of death in childhood cancer survivors
A
recurrence of cancer
7
Q
what is the second most common cause of death in childhood cancer survivors
A
cardiac disease
anthrocyclines (i.e doxorubicin) cause cardiomyopathy, and radiation to the chest can also cause heart problems
8
Q
how does chemo affect the female reproductive organs in childhood cancer survivors
A
alkylating agents (i.e cyclophosphamide) can cause ovarian failure–> dose and age dependent, may develop primary ovarian failure or premature menopause (process of losing eggs that happens normally throughout life is sped up due to chemo/radiation)
9
Q
how does radiation affect the female reproductive organs in childhood cancer survivors
A
abdo/pelvic radiation has direct effect on ovaries and uterus
cranial radiation can disrupt the pituitary-ovarian axis
10
Q
how should you monitor childhood cancer survivors who have female reproductive organs
A
monitor LH, FSH, estrogen
best predictor is antral follicle count, anti-mullerian hormone–> kind of like a “bank balance” of oocytes left–> not covered by MSP but costs about $100
consider oocyte storage, provide counselling at time of pregnancy
11
Q
how is pregnancy affected in childhood cancer survivors
A
no increases in abnormalities or cancer in offspring after mother treated with chemo
after radiation to abdo/pelvis, can have an increase in prematurity and pregnancy loss due to effects on uterine growth etc
12
Q
how does chemo affect the male reproductive system in childhood cancer survivors
A
alkylating agents have dose dependent and immediate effects on germinal cells in the testes
leydig cells which produce testosterone arent as affected
13
Q
how does radiation affect the male reproductive system in childhood cancer survivors
A
to testes–> germinal cells can be impaired, leydig cells more resistant
to brain–> at risk for hypogonadotropic hypogonadism, risk is lifelong
can advise sperm banking in the post pubertal patient but difficult to manage in pre pubertal boys
14
Q
what is the most important cause of secondary cancer in childhood cancer survivors
A
radiation
thyroid, brain, breast, skin and salivary glands are the most susceptible organs
important to know dose and site of radiation as you follow these patients in adulthood
15
Q
does chemo usually cause a second cancer
A
no not usually
secondary leukemia can be associated with alkylating agents and hereditary issues
16
Q
what cancers in children are often hereditary
A
bilateral retinoblastoma
17
Q
what patients are particularly at risk for secondary cancers
A
- those treated for hodgkins disease–> if female and received chest radiation during adolescence, have 25-35% chance of breast cancer by age 25, need mammograms or MR scans
- -> 5% risk of thyroid cancer is had chest, neck radiation and thus need thyroid function and regular ultrasound - those who received cranial radiation for ALL–> 12% risk of benign meningiomas by age 25, 2-3% risk of malignant brain tumour, need regular MR scans
18
Q
what are the effects of cancer treatment on intellectual development in childhood cancer survivors
A
XRT effects are age and dose related–> decreased intellectual function (poor attention, working memory, executive function); risk of leukencephalopathy which is rare but involved demyelination, loss of oligodendroglia
chemo or high dose IV methotrexate can also have effects
can have damage from brain tumour or surgery
can have hydrocephalus
19
Q
what side effect can cancer treatment cis platinum have on childhood cancer survivors
A
can get hearing loss
can sometimes predict who will get this loss but often dont have a choice whether to use or not because it is so effective
get high frequency hearing loss, happens very quickly
this hearing loss can affect speech and learning in school
20
Q
what endocrine problems can childhood cancer survivors have after treament
A
- thyroid irradiation can cause hypothyroidism or thyroid malignancy–> requires screening with annual T4, TSH, exam, U/S
- cranial irradiation–> all pituitary hormones can be affected but GROWTH hormones most sensitive and often patients will require replacement
21
Q
what condition is fairly common in childhood cancer survivors that received radiation or had cancer in the spine
A
scoliosis
22
Q
what MSK effects can be the result of treatment of childhood cancer
A
scoliosis
osteoporosis (after steroid tx for leukemias, replace vit D)
amputation (for bone tumours)
avascular necrosis of joins (from high dose steroids, worse in teens and females, will require joint replacement)
23
Q
what psychosocial effects can be seen in childhood cancer survivors
A
depression/anxiety/PTSD
career and financial effects
difficulty making friends, forming relationships
childhood cancer survivors tend to have lower paying jobs
generally miss alot of school
huge impact on the family as a larger unit
24
Q
what resources are there for you as a physician caring for childhood cancer survivors
A
cardio-oncology clinic at VGH
BMT f/u at VGH
LEAF clinic (late effect adult follow up)
25
what is fibromyalgia
diffuse MSK pain arising in the soft tissues
no inflammation
lab tests are normal
26
how do you diagnose fibromyalgia
11/18 painful FM tender points--distributed in all 4 quadrants
9 pairs of points--> 6 pairs in upper body, 3 pairs in lower
27
what are the comorbidities associated with fibromyalgia
migraine headahe
vertigo and tinnitus
TMJ symptoms
atypical chest pain (must work it up tho)
IBS
interstitial cystitis/vulvodynia
leg cramps
chronic fatigue
28
how do you treat fibromyalgia
education, reassurance
night time meds--> TCAs or flexeril
analgesics
exercise
CBT
other drugs --> treat depression (SSRI), nerve modulating drugs (gabapentin)
29
what is myofascial pain syndrome
regional pain syndrome
localized area of soft tissue pain
painful "trigger" point
30
what is polymyalgia rheumatica
in patients above 55 years old, can get aching and stiffness of the shoulder and hip girdle regions
**ESR often very high**
responds within 72 hours to low dose prednisone
about 1/3 are associated with TEMPORAL ARTERITIS
31
what serious condition is associated with polymyalgia rheumatica
temporal arteritis
32
what is temporal arteritis
large cell vasculitis
occurs in patients above 55
consider in new onset of headache in someone over 55
may or may not have associated swelling or tenderness of the temporal artery
jaw claudication may be present
33
how do you diagnose temporal arteritis
temporal artery biopsy
ESR is elevated at least two fold
34
how do you manage temporal arteritis
RHEUM EMERGENCY
treat with high dose steroids at 1 mg/kg/day
35
what history should you get RE osteoarthritis
duration of sx
diurnal variation? (worse in AM? AM stiffness?)
other joints affected
fever, chills, sources of infection, trauma, rashes (psoriasis/psoriatic arthritis?), family hx gout, rheumatology ROS
36
ddx osteoarthritis
infection
trauma
non inflammatory (OA)
inflammatory--> seropositive: RA, other CVD/seronegative: psoriatic arthritis, reactive arthritis
crystal-->gout or pseudogout
idiopathic
sarcoid?
37
what should you look for on exam for OA
varus deformity (due to medial compartment narrowing)
38
what investigations should you do for OA?
synovial fluid analysis--?gram stain, C and S, cell count and diff, crystals, protein, glucose
Xray
39
what should you see on x ray for OA
radiographic evidence of calcification in hyaline and/or fibrocartilage
accumulation of calcium pyrophosphate dihydrate crystals in connective tissues
40
treatment of OA
education anf physio
tylenol (1st line)--> 3-4g per day if liver and kidneys normal
NSAID + PPI, or celebrex 2nd line
consider viscosupplementation, corticosteroid injection of knee
41
acute treatment of gout
indomethacin (NSAID), colchicine or corticosteroids (PO, IV or IA)
*do NOT start allopurinol during acute attack*
42
chronic management of gout
start allopurinol after three or more attacks once the acute attack is over
keep on NSAID/colchicine/ prednisone for interval
43
risk factors for gout
overweight
heavy alcohol use (beer)
dehydration
renal failure
metabolic syndrome
drugs (HCTZ, low dose ASA)
44
what foods to avoid if have gout
beef
seafood
beer
high fat dairy
soda pop
45
how to treat mild rheumatoid arthritis
plaquenil (hydroxychloroquine) or sulfalazine
46
how to treat moderate to severe RA
disease modifying anti-rheumatic drugs (DMARDs)
1st line--> methotrexate
can also try gold therapy, leflunamide, cyclosporine
47
which biologics can be used for RA (and also ankylosing spondylitis, psoriatic arthritis)
TNF inhibitors
rituximab (anti B cell Ab)
48
what is lupus
an autoimmune disorder related to increased antibodies by B lymphocytes
often mild with mucocutaneous and joint manifestations/fatigue/ +ANA
can progress to involve other organs like kidneys, bone marrow
49
what are the diagnostic criteria for lupus
must have 4/11
"MD SOAP BRAIN"
Malar rash
Discoid rash
Serositis (pleuritis/pericarditis)
Oral or nasopharyngeal ulcers
Arthritis
Photosensitivity
Blood --hemolytic anemia, leukopenia, lymphopenia or tcp
Renal disorder
Antinuclear antibodies (99% sensitive, 49% specific)
Immunologic disorder (+ anti smith, anti-ds DNA, anti phospholipid)
Neuro disorder --seizures or psychosis
50
how do you monitor lupus
BUN
Cr
Uric acid
51
how do you treat lupus
plaquenil (hydroxychloroquine)
52
how might an inflammatory muscle disease like polymyositis or dermatomyositis present
NOT pain or stiffness but of chronic muscle weakness, weakness of the proximal large muscles
characteristic inflammatory features on EMG and muscle biopsy
often linked with malignancy
ask about statin drugs
high level CK
53
what drugs should you ask about in the setting of new onset polymyositis or dermatomyositis
statins
54
what are the signs of dermatomyositis
heliotrope
gottren's papules
V sign
shawl sign
55
how do you treat polymyositis or dermatomyositis
high dose prednisone
IVIG
sometimes imuran or methotrexate
56
how is worksafe funded
employer funded
57
what are some of the special services provided by worksafe BC
expedited specialist consults
expedited diagnostic imaging
expedited surgical care
nurse advisors
return to work support
psychology network
vocational rehab
multiple contracted rehab programs
58
how does RTW likelihood change with length of leave
decreases with longer leaves--50% return if have 12-24 wrrks of absence
59
define impairment
loss or abnormality of psychological, physiological or anatomical function that is observable
60
define disability
caused by impairments, always relative to a task
61
list methods of assessing GFR
serum urea
serum creatinine
serum cystatin C
timed urine collections with creatinine and inulin clearance calculated
nuclear medicine methods
62
why can calculating serum creatinine be problematic
confounded if someone taking creatinine supplements--not recommended on relying on serum creatinine alone
63
how do you calculate GFR
based on serum Cr
cockrift-gault forumla requires patients weight
MDRD is modification of diet in renal disease
*formulas are less reliable in those with near normal GFR and those with markedly abnormal body composition i.e extreme obesity, cachexia, paralysis, amputation
64
what are the stages of CKD (based on GFR)
1. normal--above 90
2. mild reduction --60-89
3. moderate reduction--30-59
4. severe reduction--15-29
5. established kidney failure--less than 15 or on dialysis
65
why do we care about those with a low eGFR
those with reduced GFR have uniformly poor outcomes
patients with CKD are more likely to die than go onto dialysis
have increased risk of ARF
66
you see a low GFR--now what do you do?
determine stability of patients eGFR--repeat test within 2-4 weeks and in 3-6 months
consider reversible illness, intercurrent illness, diuretics (volume dehydration?), meds, obstruction (stones)
abdo U/S if GFR under 60
UA for proteinuria (determine ACR) or hematuria
assess for complications from kidney disease--anemia, calcium, phosphate disorders
67
what meds can lower GFR
NSAIDs
ACEi/ARBs
aminoglycosides
IV contrast dye
OTC
68
when should you refer a low GFR to nephro?
1. acute kidney injury
2. GFR under 30
3. progressive loss of renal function
4. persistent proteinuria (ACR above 60)
5. GP unable to achieve BP targets, provide renoprotective/ cardioprotective tx, or is insufficiently prepared to manage patient with CKD
69
why are the elderly at increased risk for ARF
changes in kidney anatomy and function with age--
reduced GFR
decreased renal plasma flow
impaired autoregulation
imbalance between vasodilatory and constrictive mechanisms
higher chance of systemic vascular disease
generally on lots of meds (may have inappropriate dosing, direct nephrotixicity, combo)
70
what is the incidence of ARF in geriatric hospitalized pops?
3.5%
3x higher risk than all other hospitalized patients
mortality of 50%
CKD in 70%
71
causes of kidney dysfunction in the elderly
```
1. pre renal
decreased BP
decerased volume
sepsis
cardiac disease
```
```
2. drugs
NSAIDs
ACEi/ARB
diuretics
contrast
```
3. post renal
BPH
narcotics
immobility
72
what is the result of ARF in the elderly
dysnatremias
| hypokalemia etc
73
how do you treat ARF in the elderly
anticipation
prevention
early recognition
diagnosis
* renal replacement therapy (50% mortality)
* 30% progresses to CKD even with treatment
74
is CKD usually progressive
no not usually
is a sign that patient is at risk for CV disease and increased mortality
75
what are some complications of CKD in the elderly
anemia
| Ca/Po4 disorders
76
what anatomic structures should you consider when looking at a kidney biopsy
glomeruli
tubules
interstitium
vessels
77
how does the kidney change structurally as it ages
grossly--> cortical thinning, smaller kidney size
glomerular changes--> sclerosis, obsolescence
interstitial fibrosis
tubular atrophy
thickening of glomerular, tubular basement membranes
ateriolar hyalinosis, fibroelastic hyperplasia
78
what functions are decreased in the aging kidney
renal blood flow
GFR
tubular sodium reabsorption
tubular potassium reabsorption (in part due to lower renin and aldosterone levels)
urinary concentration and dilution
79
what % of the population has CKD
10%
80
what is the primary cause of CKD in the elderly
primarily hypertensive +/- ischemic nephrosclerosis
can also be cause by diabetic nephropathy, "cardiorenal" syndrome
renal vasculitis syndromes also not uncommon
81
what other disease risk increases with CKD
CVD
82
what labs should be monitored in CKD
serum Cr/eGFR
electrolytes
HgB
minerals
PTH
urinalysis
urine ACR
83
what comorbidities predispose to AKI
SVD
HTN
heart failure
malignancy
?cognition (i.e med errors)
failty--falls
propensity to UTI
84
how do prostaglandins affect the kidney
vasodilatory
85
how do ACEi/ARBs work
reduce angiotensin II mediated constriction
reduce efferent more than afferent arteriolar tone
this causes LOWER intraglomerular pressure, therefore reducing GFR
86
how do NSAIDs affect the kidney
reduce renal blood flow and GFR via reduction of vasodilatory prostaglandins (and thus reduce GFR)
can also cause Na retention and HTN
can cause AKI (hemodynamically mediated)
have intrinsic renal toxicity--> acute or chronic interstitial nephritis, papillary necrosis or glomerulonephritis (typically present as nephrotic)
hyperkalemia
87
why does GFR decline with age
nephrosclerosis
88
what is the rationale for dosing drugs initially at very low doses
there is rarely a need for an immediate response to a drug, and 3/4 of SEs are dose related
recommended starting dose is often much higher than needed
there is a wide range of patients responses to drugs (pharmcodynamics)
*does not apply to life threatening situations
recommend starting with half of the lowest marketed dose for older, established product
start with 1/2 or 1/4 of lowest available dose for newly marketed products and discuss with patients
89
define pharmacokinetics
what the body does to the drug
90
define pharmacodynamics
what the drug does the the body
91
why do most drugs fail
pharmacokinetics (39%)
92
what is the therapeutic index
ratio of a drug concentration that causes the therapeutic effect to the amount that causes toxicity
smaller is better (i.e 0.025 vs 0.5)
93
name some drugs with a narrow therapeutic index (undesirable)
phenytoin
vancomycin
gentamycin
digoxin
94
why might you pick a newer drug in a drug family to use
if all else equal, choose the newer drug in the family as the general trend is for "me too" drugs to have simpler pharmacokinetics
95
what is digoxin
common HF drug
antiarrhythmic
70-80% bioavailable, distributes readily, no known hepatic metabolism pathways--> linear kinetics!
because of linear kinetics, what you do to the dose is what happens to drug levels
is eliminated unchanged by kidneys
96
what is vancomycin
broad spectrum abx used for MDR gram + infections
(maybe for beta lactam allergic patients)
i. e MRSA, CONs, E faecium
* other than the above, not a great drug--> lower efficacy than beta lactams, narrow therapeutic index adverse effects
97
vanco adverse effects
renal toxicity
ototoxicity
more
98
how should you dose vanco
BOLUS
one dose is unlikely to cause harm
use the nomogram
have pharmacy dose it
do levels on everyone, twice weekly minimum
troughs pre 3rd or 4th dose
can do random levels as well
99
how is phenytoin metabolized
complicated metabolism by CYP P450
first order kinetics at therapeutic doses (fixed percentage is eliminated)
zero order kinetics at higher doses (fixed amount eliminated after enzymes saturate)
renally eliminated
100
why is phenytoin difficult to dose
small dose changes cause big serum level changes
there are quite a few drug interactions
101
what symptoms indicate phenytoin toxicity
mild--> worsening coordination (usually chronic)
overt--> slurred speech, ataxia, coma
102
what do you need to use to correct phenytoin levels
albumin, as phenytoin is highly albumin bound
103
what id gentamycin
abx with large gram - spectrum
used for ESBL, SPACE bugs, and is synergistic for enterococcus
falling out of favour due to renal and ototoxicity
104
should we be using gentamicin
no
105
name 4 CYP P450 inhibitors
SSRIs
cimetidine
erythromycin
grapefruit juice
106
name one common CYP P450 inducer
cigarette smoke
107
what % of deaths in canada would benefit from palliative care
97.1% (2.9% are sudden and wouldnt benefit)
28. 4% terminal illness
33. 8% organ failure
29. 3% frailty
108
what are the most burdensome end of life sx for patients
pain and SOB
109
define palliative care
an approach to care that improves the quality of life of patients and their families facing the problems associated with a life threatening illness, through the prevention and relief of suffering by means of early identification and impeccable assessment and treatment of pain and other problems--physical, psychosocial and spiritual
focus on quality of life
- -reduction in pain and non-pain symptoms
- -improved patient and family satisfaction
- -reduced hospital length of stay and cost
- -reduction in post death spousal mortality
110
do non cancer deaths receive adequate palliative care?
no
studies show poor quality of death, inadequate access to palliative care, late referral to palliative care
111
name a palliative care prognostic tool and describe how it works
Gold Standards Framework
"would you be surprised if this patient died in the next 6-12 months?"
should be patient choice for non intervention
general clinical indicators:
- declining function
- progressive weight loss
- frequent hospitalizations
112
name some non cancer diseases that may benefit from palliative intervention
1. advanced heart disease
2. end stage pulmonary disease
3. dementia
4. advanced renal disease
5. CVA
6. multi-morbidity
113
define NYHA stage IV heart disease
signs of CHF at rest/minimal activity, with already optimized cardiac med treatment
BP less than 100 and/or HR above 100
renal impairment (eGFR under 30)
cardiac cachexia
two or more episodes needing IV tx in last 6 months
114
what is the trajectory of advanced heart disease
the course of heart failure and the time spent processing through these illness phases is highly variable--important to emphasize that clinical deterioration and death may occur at any time
115
sx of advanced heart failure
```
fatigue
dyspnea
PAIN
dry mouth
constipation
nausea
depression/anxiety
symptoms of other comorbid illnesses
```
116
management of advanced CHF
optimal titration of cardiac meds
manage pain and dyspnea with opioids --> reduce preload and afterload, suppress CO2 sensitive respiratory centre which decreases dyspnea and leads to more efficient breathing
home care to monitor weight, symptoms, compliance with diet and meds
plan for terminal care--> i/e deactivate implanted cardiac defibrillators
inotropes improves sx and quality of life, but may shorten life
117
objective criteria for defining end stage pulmonary disease
disabling dyspnea at rest/minimal exertion despite optimal therapy
severe airway obstruction (FEV1 less than 30%) or restrictive deficit (vital capacity less than 60%)
increasing hospitalizations for COPD/infection
meets criteria for long term oxygen therapy
cor pulmonale and right heart failure secondary to pulmonary disease
pulmonary cachexia
increasing hospital visits for dyspnea
118
symptoms of end stage pulmonary disease
```
dyspnea
depression/anxiety
fatigue/low function
pain
anorexia
cough/secretions
sleep
```
119
when should you add an opioid in palliative care for COPD
dyspnea at rest on maximal COPD meds
opioids actually have greater benefit than oxygen, even for patients with hypoxia
opioids work through reduction of respiratory rate and workload
120
what meds are used in COPD palliative care
opioids when dyspnea at rest (on COPD meds)
neuroleptics (methotrimeprazine) can be a good adjuvant
anxiolytics help anxiety not dyspnea
121
are opioids a risk for respiratory depression when used in end stage COPD appropriately
no--are a risk for those who do NOT have pain or dyspnea, and for those who are opiate naive and receive more than needed for pain
BUT not an issue when opioids are used appropriately to treat pain and dyspnea even in those with cardiopulmonary disease
best measure is the rise in peripheral pCO2 and decline in peripheral pO2
122
define end stage dementia
unable to dress, walk or eat without assistance
increasing difficulty communicating meaningfully
progressive dysphagia
presence of co morbid conditions--aspiration pna, UTI, septicemia
urinary and fecal incontinence
123
symptoms of advancing dementia
```
confusion
urinary incontinence
pain
low modd
constipation
loss of appetite
```
124
how much higher is the risk of UTI, pna, and pressure ulcers in those with dementia who cannot ambulate
3. 4 x risk UTI
6. 8 x risk pna
increased risk of pressure ulcers
125
what is the mean survival from diagnosis for dementia
4. 2 years men
5. 7 years women
disease severity at diagnosis is most strongly associated with survival
126
what is the mortality risk index score for dementia
factors suggestive of less than 6 months of survival remaining
1. complete dependence for ADLs
2. male gender
3. cancer or CHF or unstable medical condition
4. needing oxygen, dyspnea
5. less than 25% of food eaten at most meals
6. bowel incontinence
7. bed ridden
8. not awake most of the day
*pain may be under reported and thus under treated
127
what are the objective criteria for advanced renal disease
stage 5 CKD (eGFR less than 15)
not appropriate for transplant or dialysis due to multi-morbidity
deteriorating on renal replacement therapy
persistent sx and/or increasing dependency
new life limiting condition or kidney failure as a complication of another condition or therapy
128
why do you need to be careful with your choice of opioid in CKD palliative care
active metabolites of opioids can build up due to poor clearance and lead to toxicity
129
signs of opioid toxicity
myoclonus, drowsiness, confusion
130
which opioids do not have active metabolites and are thus good choices in CKD palliative care?
oxycodone
fentanyl
methadone
(few metabolites--> hydromorphone)
131
when should palliative care become involved in the setting of CVA
during the acute phase/first few days-->
- coma beyond 3d duration
- absent response to pain
- absent brain stem responses
- multiple comorbidities
- progressive deterioration in physical and/or cognitive dysfunction despite optimal therapy
- recurrent aspiration pna
132
what symptoms require management post CVA from a palliative standpoint
post CVA thalamic pain syndrome (20%)--> damage to thalamus or spinothalamic tract can cause a burning pain on the contralateral side of the body
tx with gabapentin or opioids
also depression, anxiety
133
challenges to dying well
isolation
marginalization (especially if demented)
fears and concerns
finding meaning and personal growth
loss of control
finance
vulnerability to abuse and neglect
134
what are the phases of end of life care
pre-active--average 2 weeks
active--average 3 days
135
as death approaches, how to the following things change:
| food and fluid intake
decreased
lose interest in food/fluids
have no appetite
may forget to swallow
may refuse food/fluids
*dehydration not painful and not necessarily uncomfortable
136
as death approaches, how to the following things change:
| perception
hearing or vision may become altered
depth perception may be altered
may mistake common objects for other things
may have visions/hallucinations
137
as death approaches, how to the following things change:
| circulation
decreased
arms and legs may be cool to touch
arms and legs may look mottled, purple/bluish
mottling may also be to back, buttocks
skin may be very pale
138
as death approaches, how to the following things change:
| breathing
respiratory rate may increase or decrease
breathing may become irregular (Cheyenne's stokes, hyperventilation, apneuristic, ataxic, cluster)
secretions may pool in back of throat ("death rattle")
139
as death approaches, how to the following things change:
| muscle tone
may become flaccid--skin slack on face, no movement in arms or legs
may lose control of bladder or bowels
may vomit
140
as death approaches, how to the following things change:
| consciousness
6-30% conscious until death
| 8-34% unconscious in last 24 hours
141
signs and symptoms of impending death
rapidly increasing weakness and fatigue
decreasing intake of food and fluids
difficulty swallowing with loss of gag reflec
decreasing level of consciousness
terminal delirium or agitation
respiratory changes--> mandibular respiratory movement/chin breathing, apnoeic spells
in very last hours, evidence of CV changes--> acrocyanosis, absent radial pulse
142
signs of active death
hypotension
apnea
```
major sx of last 48 hours:
noisy, moist breathing
urinary dysfunction
pain
agitation/restlessness
```
143
how to assess pain in the palliative patient
non verbal vocalizations
facial grimaces
bracing
rubbing
restlessness
verbal complaints
*most demented patients will directly answer pain questions
144
name 3 drugs NOT affected by first pass metabolism
propanolol
fentanyl
nitroglycerin
145
name 3 drugs that are affected by first pass metabolism
metronidazole
fluconazole
lorazepam
146
define bioavailability
the % of the administered dose that reaches systemic circulation (100% for IV)
147
why do we care about volume of distribution
of a drug has a large volume of distribution, the first few doses "disappear" immediately from the blood stream into the tissues
loading doses are thus required to fill up the tissues and the plasma
important also if the site of a drugs action is in the tissues
148
how do you calculate a good loading dose
loading dose concentration/ volume of distribution for that particular patient
Vd for a particular patient = average Vd x patients weight
149
name 5 drugs that are highly protein bound in circulation (above 90% bound)
warfarin
furosemide
diazepam
phenytoin
valproic acid
150
what conditions are associated with low albumin (and thus more unbound drugs)
ESRD
chronic liver disease
malnutrition
151
what is. the main site of drug excretion
kidneys
152
what is a drug steady state
where rate drug in = rate drug out
153
how long does it take to reach steady state
4-5 half lives of the drug
154
what loading dose of vanco should you always use
25 mg/kg (round up or down by 250 mg)
