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PMP > Week 3--lecture slides > Flashcards

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

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2
Q

what is the risk of cancer recurrence or second cancer in childhood cancer survivors

A

5-10x increased risk

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3
Q

what is a stage 3 wilms tumour

A

rupture with tumour spillage

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4
Q

how are wilms tumours treated

A

standard chemo–> vincristine, doxorubicin, actinomycin

+ whole abdo radiation

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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

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6
Q

what is the most common cause of death in childhood cancer survivors

A

recurrence of cancer

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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

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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)

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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

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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

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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

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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

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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

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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

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15
Q

does chemo usually cause a second cancer

A

no not usually

secondary leukemia can be associated with alkylating agents and hereditary issues

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16
Q

what cancers in children are often hereditary

A

bilateral retinoblastoma

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17
Q

what patients are particularly at risk for secondary cancers

A
  1. 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
  2. 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
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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

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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

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20
Q

what endocrine problems can childhood cancer survivors have after treament

A
  1. thyroid irradiation can cause hypothyroidism or thyroid malignancy–> requires screening with annual T4, TSH, exam, U/S
  2. cranial irradiation–> all pituitary hormones can be affected but GROWTH hormones most sensitive and often patients will require replacement
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21
Q

what condition is fairly common in childhood cancer survivors that received radiation or had cancer in the spine

A

scoliosis

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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)

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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

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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)

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25
Q

what is fibromyalgia

A

diffuse MSK pain arising in the soft tissues

no inflammation

lab tests are normal

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26
Q

how do you diagnose fibromyalgia

A

11/18 painful FM tender points–distributed in all 4 quadrants

9 pairs of points–> 6 pairs in upper body, 3 pairs in lower

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27
Q

what are the comorbidities associated with fibromyalgia

A

migraine headahe

vertigo and tinnitus

TMJ symptoms

atypical chest pain (must work it up tho)

IBS

interstitial cystitis/vulvodynia

leg cramps

chronic fatigue

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28
Q

how do you treat fibromyalgia

A

education, reassurance

night time meds–> TCAs or flexeril

analgesics

exercise

CBT

other drugs –> treat depression (SSRI), nerve modulating drugs (gabapentin)

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29
Q

what is myofascial pain syndrome

A

regional pain syndrome

localized area of soft tissue pain

painful “trigger” point

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30
Q

what is polymyalgia rheumatica

A

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

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31
Q

what serious condition is associated with polymyalgia rheumatica

A

temporal arteritis

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32
Q

what is temporal arteritis

A

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

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33
Q

how do you diagnose temporal arteritis

A

temporal artery biopsy

ESR is elevated at least two fold

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34
Q

how do you manage temporal arteritis

A

RHEUM EMERGENCY

treat with high dose steroids at 1 mg/kg/day

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35
Q

what history should you get RE osteoarthritis

A

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

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36
Q

ddx osteoarthritis

A

infection

trauma

non inflammatory (OA)

inflammatory–> seropositive: RA, other CVD/seronegative: psoriatic arthritis, reactive arthritis

crystal–>gout or pseudogout

idiopathic

sarcoid?

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37
Q

what should you look for on exam for OA

A

varus deformity (due to medial compartment narrowing)

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38
Q

what investigations should you do for OA?

A

synovial fluid analysis–?gram stain, C and S, cell count and diff, crystals, protein, glucose

Xray

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39
Q

what should you see on x ray for OA

A

radiographic evidence of calcification in hyaline and/or fibrocartilage

accumulation of calcium pyrophosphate dihydrate crystals in connective tissues

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40
Q

treatment of OA

A

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

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41
Q

acute treatment of gout

A

indomethacin (NSAID), colchicine or corticosteroids (PO, IV or IA)

do NOT start allopurinol during acute attack

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42
Q

chronic management of gout

A

start allopurinol after three or more attacks once the acute attack is over

keep on NSAID/colchicine/ prednisone for interval

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43
Q

risk factors for gout

A

overweight

heavy alcohol use (beer)

dehydration

renal failure

metabolic syndrome

drugs (HCTZ, low dose ASA)

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44
Q

what foods to avoid if have gout

A

beef

seafood

beer

high fat dairy

soda pop

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45
Q

how to treat mild rheumatoid arthritis

A

plaquenil (hydroxychloroquine) or sulfalazine

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46
Q

how to treat moderate to severe RA

A

disease modifying anti-rheumatic drugs (DMARDs)

1st line–> methotrexate

can also try gold therapy, leflunamide, cyclosporine

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47
Q

which biologics can be used for RA (and also ankylosing spondylitis, psoriatic arthritis)

A

TNF inhibitors

rituximab (anti B cell Ab)

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48
Q

what is lupus

A

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

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49
Q

what are the diagnostic criteria for lupus

A

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

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50
Q

how do you monitor lupus

A

BUN
Cr
Uric acid

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51
Q

how do you treat lupus

A

plaquenil (hydroxychloroquine)

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52
Q

how might an inflammatory muscle disease like polymyositis or dermatomyositis present

A

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

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53
Q

what drugs should you ask about in the setting of new onset polymyositis or dermatomyositis

A

statins

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54
Q

what are the signs of dermatomyositis

A

heliotrope

gottren’s papules

V sign

shawl sign

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55
Q

how do you treat polymyositis or dermatomyositis

A

high dose prednisone

IVIG

sometimes imuran or methotrexate

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56
Q

how is worksafe funded

A

employer funded

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57
Q

what are some of the special services provided by worksafe BC

A

expedited specialist consults

expedited diagnostic imaging

expedited surgical care

nurse advisors

return to work support

psychology network

vocational rehab

multiple contracted rehab programs

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58
Q

how does RTW likelihood change with length of leave

A

decreases with longer leaves–50% return if have 12-24 wrrks of absence

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59
Q

define impairment

A

loss or abnormality of psychological, physiological or anatomical function that is observable

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60
Q

define disability

A

caused by impairments, always relative to a task

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61
Q

list methods of assessing GFR

A

serum urea

serum creatinine

serum cystatin C

timed urine collections with creatinine and inulin clearance calculated

nuclear medicine methods

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62
Q

why can calculating serum creatinine be problematic

A

confounded if someone taking creatinine supplements–not recommended on relying on serum creatinine alone

63
Q

how do you calculate GFR

A

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
Q

what are the stages of CKD (based on GFR)

A
  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
Q

why do we care about those with a low eGFR

A

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
Q

you see a low GFR–now what do you do?

A

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
Q

what meds can lower GFR

A

NSAIDs

ACEi/ARBs

aminoglycosides

IV contrast dye

OTC

68
Q

when should you refer a low GFR to nephro?

A
  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
Q

why are the elderly at increased risk for ARF

A

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
Q

what is the incidence of ARF in geriatric hospitalized pops?

A

3.5%

3x higher risk than all other hospitalized patients

mortality of 50%

CKD in 70%

71
Q

causes of kidney dysfunction in the elderly

A 
1. pre renal
decreased BP
decerased volume
sepsis
cardiac disease 
2. drugs
NSAIDs
ACEi/ARB
diuretics
contrast
  1. post renal
    BPH
    narcotics
    immobility
72
Q

what is the result of ARF in the elderly

A

dysnatremias

hypokalemia etc

73
Q

how do you treat ARF in the elderly

A

anticipation
prevention
early recognition
diagnosis

  • renal replacement therapy (50% mortality)
  • 30% progresses to CKD even with treatment
74
Q

is CKD usually progressive

A

no not usually

is a sign that patient is at risk for CV disease and increased mortality

75
Q

what are some complications of CKD in the elderly

A

anemia

Ca/Po4 disorders

76
Q

what anatomic structures should you consider when looking at a kidney biopsy

A

glomeruli

tubules

interstitium

vessels

77
Q

how does the kidney change structurally as it ages

A

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
Q

what functions are decreased in the aging kidney

A

renal blood flow

GFR

tubular sodium reabsorption

tubular potassium reabsorption (in part due to lower renin and aldosterone levels)

urinary concentration and dilution

79
Q

what % of the population has CKD

A

10%

80
Q

what is the primary cause of CKD in the elderly

A

primarily hypertensive +/- ischemic nephrosclerosis

can also be cause by diabetic nephropathy, “cardiorenal” syndrome

renal vasculitis syndromes also not uncommon

81
Q

what other disease risk increases with CKD

A

CVD

82
Q

what labs should be monitored in CKD

A

serum Cr/eGFR

electrolytes

HgB

minerals

PTH

urinalysis

urine ACR

83
Q

what comorbidities predispose to AKI

A

SVD

HTN

heart failure

malignancy

?cognition (i.e med errors)

failty–falls

propensity to UTI

84
Q

how do prostaglandins affect the kidney

A

vasodilatory

85
Q

how do ACEi/ARBs work

A

reduce angiotensin II mediated constriction

reduce efferent more than afferent arteriolar tone

this causes LOWER intraglomerular pressure, therefore reducing GFR

86
Q

how do NSAIDs affect the kidney

A

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
Q

why does GFR decline with age

A

nephrosclerosis

88
Q

what is the rationale for dosing drugs initially at very low doses

A

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
Q

define pharmacokinetics

A

what the body does to the drug

90
Q

define pharmacodynamics

A

what the drug does the the body

91
Q

why do most drugs fail

A

pharmacokinetics (39%)

92
Q

what is the therapeutic index

A

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
Q

name some drugs with a narrow therapeutic index (undesirable)

A

phenytoin
vancomycin
gentamycin
digoxin

94
Q

why might you pick a newer drug in a drug family to use

A

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
Q

what is digoxin

A

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
Q

what is vancomycin

A

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
Q

vanco adverse effects

A

renal toxicity

ototoxicity

more

98
Q

how should you dose vanco

A

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
Q

how is phenytoin metabolized

A

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
Q

why is phenytoin difficult to dose

A

small dose changes cause big serum level changes

there are quite a few drug interactions

101
Q

what symptoms indicate phenytoin toxicity

A

mild–> worsening coordination (usually chronic)

overt–> slurred speech, ataxia, coma

102
Q

what do you need to use to correct phenytoin levels

A

albumin, as phenytoin is highly albumin bound

103
Q

what id gentamycin

A

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
Q

should we be using gentamicin

A

no

105
Q

name 4 CYP P450 inhibitors

A

SSRIs
cimetidine
erythromycin
grapefruit juice

106
Q

name one common CYP P450 inducer

A

cigarette smoke

107
Q

what % of deaths in canada would benefit from palliative care

A

97.1% (2.9% are sudden and wouldnt benefit)

  1. 4% terminal illness
  2. 8% organ failure
  3. 3% frailty
108
Q

what are the most burdensome end of life sx for patients

A

pain and SOB

109
Q

define palliative care

A

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
Q

do non cancer deaths receive adequate palliative care?

A

no

studies show poor quality of death, inadequate access to palliative care, late referral to palliative care

111
Q

name a palliative care prognostic tool and describe how it works

A

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
Q

name some non cancer diseases that may benefit from palliative intervention

A
  1. advanced heart disease
  2. end stage pulmonary disease
  3. dementia
  4. advanced renal disease
  5. CVA
  6. multi-morbidity
113
Q

define NYHA stage IV heart disease

A

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
Q

what is the trajectory of advanced heart disease

A

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
Q

sx of advanced heart failure

A 
fatigue
dyspnea
PAIN
dry mouth
constipation
nausea
depression/anxiety
symptoms of other comorbid illnesses
116
Q

management of advanced CHF

A

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
Q

objective criteria for defining end stage pulmonary disease

A

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
Q

symptoms of end stage pulmonary disease

A 
dyspnea
depression/anxiety
fatigue/low function
pain
anorexia
cough/secretions
sleep
119
Q

when should you add an opioid in palliative care for COPD

A

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
Q

what meds are used in COPD palliative care

A

opioids when dyspnea at rest (on COPD meds)

neuroleptics (methotrimeprazine) can be a good adjuvant

anxiolytics help anxiety not dyspnea

121
Q

are opioids a risk for respiratory depression when used in end stage COPD appropriately

A

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
Q

define end stage dementia

A

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
Q

symptoms of advancing dementia

A 
confusion
urinary incontinence 
pain
low modd
constipation 
loss of appetite
124
Q

how much higher is the risk of UTI, pna, and pressure ulcers in those with dementia who cannot ambulate

A
  1. 4 x risk UTI
  2. 8 x risk pna

increased risk of pressure ulcers

125
Q

what is the mean survival from diagnosis for dementia

A
  1. 2 years men
  2. 7 years women

disease severity at diagnosis is most strongly associated with survival

126
Q

what is the mortality risk index score for dementia

A

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
Q

what are the objective criteria for advanced renal disease

A

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
Q

why do you need to be careful with your choice of opioid in CKD palliative care

A

active metabolites of opioids can build up due to poor clearance and lead to toxicity

129
Q

signs of opioid toxicity

A

myoclonus, drowsiness, confusion

130
Q

which opioids do not have active metabolites and are thus good choices in CKD palliative care?

A

oxycodone

fentanyl

methadone

(few metabolites–> hydromorphone)

131
Q

when should palliative care become involved in the setting of CVA

A

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
Q

what symptoms require management post CVA from a palliative standpoint

A

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
Q

challenges to dying well

A

isolation

marginalization (especially if demented)

fears and concerns

finding meaning and personal growth

loss of control

finance

vulnerability to abuse and neglect

134
Q

what are the phases of end of life care

A

pre-active–average 2 weeks

active–average 3 days

135
Q

as death approaches, how to the following things change:

food and fluid intake

A

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
Q

as death approaches, how to the following things change:

perception

A

hearing or vision may become altered

depth perception may be altered

may mistake common objects for other things

may have visions/hallucinations

137
Q

as death approaches, how to the following things change:

circulation

A

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
Q

as death approaches, how to the following things change:

breathing

A

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
Q

as death approaches, how to the following things change:

muscle tone

A

may become flaccid–skin slack on face, no movement in arms or legs

may lose control of bladder or bowels

may vomit

140
Q

as death approaches, how to the following things change:

consciousness

A

6-30% conscious until death

8-34% unconscious in last 24 hours

141
Q

signs and symptoms of impending death

A

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
Q

signs of active death

A

hypotension

apnea

major sx of last 48 hours: 
noisy, moist breathing
urinary dysfunction
pain
agitation/restlessness
143
Q

how to assess pain in the palliative patient

A

non verbal vocalizations

facial grimaces

bracing

rubbing

restlessness

verbal complaints

*most demented patients will directly answer pain questions

144
Q

name 3 drugs NOT affected by first pass metabolism

A

propanolol

fentanyl

nitroglycerin

145
Q

name 3 drugs that are affected by first pass metabolism

A

metronidazole

fluconazole

lorazepam

146
Q

define bioavailability

A

the % of the administered dose that reaches systemic circulation (100% for IV)

147
Q

why do we care about volume of distribution

A

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
Q

how do you calculate a good loading dose

A

loading dose concentration/ volume of distribution for that particular patient

Vd for a particular patient = average Vd x patients weight

149
Q

name 5 drugs that are highly protein bound in circulation (above 90% bound)

A

warfarin

furosemide

diazepam

phenytoin

valproic acid

150
Q

what conditions are associated with low albumin (and thus more unbound drugs)

A

ESRD

chronic liver disease

malnutrition

151
Q

what is. the main site of drug excretion

A

kidneys

152
Q

what is a drug steady state

A

where rate drug in = rate drug out

153
Q

how long does it take to reach steady state

A

4-5 half lives of the drug

154
Q

what loading dose of vanco should you always use

A

25 mg/kg (round up or down by 250 mg)

PMP (9 decks)

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