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Preparation For Medical Practice > Wk 3 > Flashcards

Wk 3 Flashcards

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USMLE® Step 1 flashcards
0
Q

Key counselling pts re sun safety

A

Avoid btwn 10-2
Hydrate
ReapplyFace/ears/ back of legs.
SPF30 or greater.

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1
Q

Before what age should sunscreen not be used?

A

6 mo

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2
Q

What are the age-appropriate deet concentrations?

What about clothes considerations and washing off?

A

2 10% up to tid

Adult: 30 %

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3
Q

Breast feeding contraindications?

A 
Women who do illicits ie PCP cannabis cocaine etc. should BE GAILIC
Bromocriptine
Ergots
G?
Antithyroid 
Isoniazid
Lithium
Infx: ie hiv, tb, herpes
Chemo and Breast ca
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4
Q

Dental care- what should be done until teeth erupt?

How About after?

A

Wipe gums w soft warm cloth
W erupted teeth:
< 3: toothpaste smear
> 3: pea size amount

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5
Q

Sleeping hygiene
Can blankets or pillows be used initially?
When can rooming-in be recommended?

A

No!

Rooming in can happen from 6 m to 1 yr.

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6
Q

What are risks for sids?

A

Prone child

Smoking in home.

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7
Q

Car seats

What is initial orientation for car seat and how long should this happen for?

A

Rear facing car seat until 1 yr.

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8
Q

An infant seat should be used til what weight?

A

10 kg (22 lbs)

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9
Q

What should be done if a baby has outgrown the infant seat bc > 10 kg or head within 2.5 cm of top seat edge.

A

Use forward-facing convertible seat, w buckle at armpit level and harness at or below shoulders. 10-18 kg.

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10
Q

When to use a forward facing child seat til?

A

18 kg

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11
Q

When to use a booster seat?

A

Until 8 yo, 18 until 30 kg or 145 cm.

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12
Q

When can sit in front seat?

A

After 12 yo

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13
Q

How far to have everyone when bathing?

A

Within arms reach.

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14
Q

How much water does it take children to drown in?

A

2 inches

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15
Q

Should you use soaps on the body? What is max temp? How to position child relative to faucet?

A

No. 49 Celsius. Opposite end of tub.

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16
Q

If exclusively Breast fed how many BMs can occur daily?

A

Up to 10

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17
Q

What are risk factors for developmental dysplasia of the hip? What is NOT a RF?

A

Female, Breech, family history, swaddling

Prematurity is NOT a RF

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18
Q

At what age does dx lead to prognosis that is more optimal?

What are findings if after 3 mos?

A

Best before 6 mos.

If after 3 mos may see limited abduction, shortened leg and asymmetric creases.

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19
Q

What dot the 2 maneuvers do?

A
  • ortolani is for if they are OUT
  • flex hips and knees and adduct w anterior pressure

Barlow is that they are dislocatable… Abduct And put posterior pressure

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20
Q

What do do if O and B tests are pos?

Equivocal?

A

To ped ortho surgeon

If equiv-refer to U/S IF 4 mos then do xray.

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21
Q

What are the options for vitamin K and why is it given?

A

1 mg im within 6 hr of birth or oral Vit K at birth then 2x more over 4-8 wks.
Vit K supplementation helps to prevent hemorrhagic do of the newborn.

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22
Q

How long is one able to hold off from giving erythromycin eye ointment after birth? Why is it given?

A

Can wait up to 1 hr. Primary purpose is to prevent N gonorrhea. Can also provide benefit towards chlamydia.

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23
Q

How long to wait to do newborn screen?

A

Wait at least 24 hr- baby needs to have seen a protein load in order to detect high levels of phenylalanine. This accumulates in PKU.

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24
Q

What is the ideal timeframe for newborn screen?

A

Preferably within 48 hours- 72 hours.

Can be up to 7-14 days.

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25
Q

Name 4 / 18 of the newborn screen tests that are run.

A

PKU
Galactosemia
Congenital hypothyroidism
MCAD

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26
Q

When does fever in an infant become a medical emergency?

A

If < 3 mo … Risk of serious bacterial infx.

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27
Q

What temp is the gold stnd? After which age is tympanic temp less contreversial?

A

Rectal is gold.

If less than two years tympanic is controversial.

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28
Q

How to approach fever in the infant <28 days?

A

Full septic w/u with antibiotics.

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29
Q

How to manage the infant btwn 30-90 days?

A

If sending home, full septic w/u + antibiotics.

If keeping in hospital, partial septic workup + antibiotics.

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30
Q

Re medicine what can be provided for the febrile infant?

A

Tylenol 15 mg/kg/dose, max 75 mg/ kg/ day (5 doses)

Advil 10 mg/ kg/ dose (first choice for < 6 mos)

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31
Q

Are febrile seizures related to the rate of risk of temperature or peak temperature?

A

Rate of risk of temp

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32
Q

After which age is OTC cough medicine ok to use?

A

> 6 yr

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33
Q

What are vit D supplementation recommendations?

A

400 IU per day and 800 IU per day if live N of the 55th parallel

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34
Q

How long to remain on vitamin D supp?

A

Until at least 1000 mL / day of formula or complete adult table food.

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35
Q

What dz is due to vit D deficiency and what are the s and s?

What labs to order?

A

Rickets
Long bone bowing, widened joint space, rickettsial rosary.

Order vit D level. Ca, PO4, Cr.

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36
Q

How to visualize abnormalities of the back of the eye and opacities in the visual field?

A

Red reflex.

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37
Q

Is lead screening routine? What are reasons to screen?

A

No.

Recommended is house built before 1950, family hx of lead poisoning, eating paint chips.

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38
Q

What are the breastfeeding. Recommendations by the WHO/CPS?

A

Exclusive Breast feeding up to 6 months of age, with continued Breast feeding alongside complementary foods up to 2 yrs.

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39
Q

What should be encouraged in high risk atopic babies?

A

Exclusively br feeding until 4 m is beneficial

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40
Q

What should not be consumed in the first year?

A

Egg whites, nuts
Cows milk
Honey

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41
Q

When can yogurt and other dairy be consumed?

A

After 6 mos.

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42
Q

What is a reasonable nurse–> cows milk transition?

A

Br milk or formula til 1 yr.
the. Homo milk from 1-2 yr.
Then 2% milk when > 2 yr.

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43
Q

What are risk factors for adolescent drug and alcohol use?

A

Family: family hx esp for alcohol, anti-social, criminality, drug use norms, absent parenting.
Youth: low connection to adults, schools, mental illness, low achievement/ hope.
Peer norms
Early drug use.

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44
Q

What are useful screeninging tools for adolescent drug use assessment and health in general?

A

HEADSS: home, education/ employment, activities, drugs, safety/ sex/ suicidality.

CRAFFFT: do you use drugs in a car? To relax? Alone? To forget? Are friends and family asking you to cut down?Are you in trouble or has it gotten you into trouble in the past?

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45
Q

Is there evidence supporting utility for the use of drug screening?

A

No

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46
Q

What are the stages of motivation?

A

Precontemplative, contemplative, preparation, action, maintenance, relapse

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47
Q

What is a key consideration in motivational interviewing?

A

Aim for patient to describe only their next stage of motivation.

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48
Q

What are treatment considerations alongside substance use?

A

Treat coinciding mental health problems.
Consider methadone use.
Naltrexone?

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49
Q

Does ADHD inc drug use?

A

No!

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50
Q

What are important considerations for substance use harm reduction?

A

Hygiene: food and drink, sleep, exercise.
Use regularly vs binging.
Oral > snort > smoke > inject due to time to onset.
Choose safer drugs, places and people.

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51
Q

What must every “drunk” person be assessed for?

A

Head trauma, CNS infx, co-ingestants

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52
Q

What has a similar intoxication presentation to alcohol?

A

GHB

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53
Q

What is the W/D pattern of alcohol w/d?

A

Have Me Some Drank

5-10 hr: alcoholic Hallucinosis, then
Metabolic increase ie tachycardia, HTN, Hyperthermia, tremor.
6-48 hrs- generalized seizures, typically isolated or occurring in brief flurry.
> 48 hr delirium tremens… Confusion, hallucinations, extreme agitation, hyperthermia, tachycardia, tachypnia, unstable BP

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54
Q

How does sedative hypnotic w.d present as compared to that of alcohol?

A

Similar manifestations but with a different time course.

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55
Q

What is opiate withdrawal characterized by?

A

Nausea, vomiting, Abdo cramps, diarrhea, generalized pain, mydriatics, piloerection, bowel sounds, yawning, rhinorrhea.

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56
Q

What is the half life of cocaine?

A

90 min

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57
Q

What differentiates cocAine vs methamphetamine re neuronal MOA.?

A

Cocaine is action potential dependent whole methamphetamine releases neurotransmitters independently of action potential.

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58
Q

What is the MOA of cocaine and how is this pertinent to chronic use and then abstinence?

A

Blocks DA reuptake and upreg a alpha 2 receptor.
Also blocks Na K ATPase and depletes glutaminergic neurons in the CNS ie aspartate and glutamate.

Because of upreg’d alpha 2 receptor there is a depression after ceasing chronic use. Therefore watch for suicide.

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59
Q

What does chasing the high mean w cocaine use?

A

Downregulate posts ymptom DA receptors and therefore need more to get same effects of previously highs.

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60
Q

MOA of methamphetamine?

A

Potent NA and DA release. This is AP independent.

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61
Q

What is the most efficient drug delivery route for meth?

A

When smoked.

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62
Q

What are longer lastingly? The psychogenic effects or the pharmacologic t1/2?

A

Psychogenic effects

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63
Q

What is true reverse tolerance, and what substance does this apply to?

A

True reverse tolerance is when there is a dec in unwanted s/Es but no equivalent loss of stimulant properties.
Meth

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64
Q

Why are MDA, MDMA, and 5-HT less addictive? MOA.?

A

NA, DA, 5-HT.

PO intake makes less addictive.

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65
Q

What is MOA of hallucinogens? S/Es? Tx?

A

Inhibition of inhibitory systems.
S/Es are largely GI upset
Tx is supportive w reassurance and Benzos if required for anxiety.

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66
Q

What is an interesting OD characteristic of benzo and non benzo sedative-hypnotics?

A

OD is characterized by sedation or coma w relatively normal VS, unless congestant like alcohol.

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67
Q

What is the t1/2 of THC/ marijuana? Does it exhibit reverse tolerance?

A

32 h, very lipid soluble. Yes, exhibits reverse tolerance.

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68
Q

What is more carcinogenic, tobacco or marijuana.

A

Marijuana.

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69
Q

Who does the Infants Act apply to?

A

Anyone < 19yo

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70
Q

Can children refuse tx to care if capable? Who can if they aren’t capable.m

A

Yes.

Parents can refuse tx if child is not capable.

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71
Q

If a child’s health and safety is compromised a parent making decision for child, what can happen?

A

Govt can intercede if determined by 2 physicians that a child’s safety and health is compromised.

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72
Q

Can can children be involved in medical research?

A

If it is determined to be in their bust interest

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73
Q

What is strength of recommendation based on a body of evidence graded? CEBM

A 
A-D.
The strength (or grade) of a recommendation for clinical practice is based on a body of evidence (typically more than one study). This approach takes into account the level of evidence of individ- ual studies, the type of outcomes measured by these studies (patient-oriented or disease-oriented), the number, consistency, and coherence of the evi- dence as a whole, and the relationship between benefits, harms, and costs.
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74
Q

How is level of evidence based on a study graded? CEBM

A

I- V.
The validity of an individual study is based on an assessment of its study design. According to some methodologies,6 levels of evidence can refer not only to individual studies but also to the quality of evidencefrommultiplestudiesaboutaspecific question or the quality of evidence supporting a clinical intervention.

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75
Q

What is strength of recommendation based on a body of evidence graded? CEBM

A 
A-D.
The strength (or grade) of a recommendation for clinical practice is based on a body of evidence (typically more than one study). This approach takes into account the level of evidence of individ- ual studies, the type of outcomes measured by these studies (patient-oriented or disease-oriented), the number, consistency, and coherence of the evi- dence as a whole, and the relationship between benefits, harms, and costs.
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76
Q

How is level of evidence based on a study graded? CEBM

A

I- V.
The validity of an individual study is based on an assessment of its study design. According to some methodologies,6 levels of evidence can refer not only to individual studies but also to the quality of evidencefrommultiplestudiesaboutaspecific question or the quality of evidence supporting a clinical intervention.

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77
Q

What is the A strength of recommendation?

A

Consistent randomized, controlled trial, cohort, all or none, clinical decision rule validated in different populations.

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78
Q

What is level B strength of recommendation?

A

Consistent, retrospective cohort, exploratory cohort, ecological study, outcomes research, case-control study, or extrapolations from Level A studies

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79
Q

What is level C strength of recommendation?

A

Case series or extrapolations from level B studies.

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80
Q

What is level D strength of recommendation??

A

Expert opinion without explicit critical appraisal, OR based on physiology, bench research or first principles.

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81
Q

What is Level I evidence?

A

Evidence is based on randomized control trials, or meta analysis of such trials, of adequate size to ensure a low risk of incorporating false-pos or self-Neg results.

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82
Q

What is level II evidence?

A

Based on randomized controlled trials that are too small to provide Level I evidence…. May show either positive trends that are not statistically significant, or no trends and are associated with a high risk of false-negative results.

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83
Q

What is level III evidence?

A

Evidence that us based in non randomized controlled or cohort studies, cAse series, case-control studies or cross-sectional studies.

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84
Q

What is type IV evidence?

A

Evidence that is based on the opinions of respected authorities or expert committees as indicated in the public consensus, conferees, kr guidelines.

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85
Q

What is type V evidence?

A

Evidence based on the opinions of those who have written and reviewed the guidelines, based on their experience, knowledge of the relevant literature and discussion w their peers.

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86
Q

What are the two types of study designs?

A

Experimental vs observational.

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87
Q

What are features that characterize an experimental study design?

A

Randomized controlled trial that such that randomization equalizes confounders.
Can include meta analyses and systematic reviews.

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88
Q

Do observational studies answer cause and effect questions?

A

No, they do show associations though.

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89
Q

Are experimental or observational studies more prone to bias? What are biases?

A

Observational… Biases are any systematic errors in the design, conduct, or analysis of a study that results in a mistaken estimate of an exposure’s effect on the risk of disease. I’d selection bias, information bias, confounding.

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90
Q

What does a cohort study observe?

A

Exposure leading to disease.
Two or more groups are assembled that differ based on exposure. This follows individuals and monitors outcomes.
Think COED

Relative risk is calc’d according to abs exp/ abs nonexp

Think CORED

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91
Q

How does a cohort study compare to an ecological study?

A

a cohort study follows INDIVIDUALS and monitors outcomes whereas an ecological study studies GROUP level exposure and outcomes its schools, factories.

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92
Q

What does a case control study look at?

A

How a disease is associated with an exposure
Ie identify people w a disease and look for exposure … Uses OR.

Think CACODE
Case-control disease ass’d w exposure

Ie do all individuals with cancer (case) have the same exposure as those without cancer (control)?

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93
Q

What is a cross sectional study?

A

Exposure and disease are measure TOGETHER at one point in time in a group…
Informs PREVALENCE.

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94
Q

What is a case series?

A

This is when multiple cases are reported on and means to inform regarding a disease and exposure… Ie SARS.

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95
Q

What is a case report?

A

A case report describes a single case of a disease.

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96
Q

What are the two measures of effect?

A

Experimental and observational measures of effect.

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97
Q

What is the purpose of the experimental measure of effect?

A

Experimental is meant to realize cause and effect.

R TS are tests of significance and meta-analyses are combinations of odds ratios and relative risks.

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98
Q

What does the observational measure of effect describe?

A

The observational measure of effect describes ASSOCIATIONS.
Case control relates diseases leading to an exposure and uses ODDS RATIO whereas cohort describes exposures associated w a disease and uses relative risk.

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99
Q

How do you go about evaluating diagnostic tests and therapeutic interventions?

A

To assess diagnostic tests, new diagnostic tests need to be mentioned against the gold standard.
Create 2x2 table of results from the gold test (top) and new test (side).

Sensitivity and specificity then give info about the test.

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100
Q

How is sensitivity defined in reference with gold standard results?

A

Sensitivity describes the proportion of those WITH disease (gold stnd pos), how many tested positive w the new test.

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101
Q

What does Specificity describe in relation to the gold stnd?

A

Specificity describes the proportion of those without dz (gold stnd neg), who had a negative result on the new test.

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102
Q

What is the formula for prevalence?

A

a+C / a + b+ c + d

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103
Q

What is the definition of a pos likelihood ratio?

A

The positive likelihood ratio tells you how much the odds of having the disease increases when a test is positive.
Formula is sens / 1- spec

In general, tests with positive LRs higher than about 5 are useful in ruling in a disease.

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104
Q

What is the negative likelihood ratio?

A

Tells you what the odds are that you don’t have a disease if the test is employed and found to be neg.
1-sens/ spec

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105
Q

What is the Pretest odds formula?

A

Pretest prob / 1- Pretest prob

Prevalence is approx equal to pre test probability if rare dz in pop.

The odds that the patient has the target disorder before the test is carried out.

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106
Q

What is the pretest probability?

A

Pretest probability is the probability that a person has a disease after all patient historical, physical exam, and demographic data have been taken into consideration. For example, a person who is of Latino dissent who is in the office and as a chief complaint of numbness in the feet and impaired soft touch sensation bilaterally has a 60% chance of having diabetic foot neuropathy.
For rare diseases, the pretest probability is often equal to the prevalence of the disease.

The proportion of people with the target disorder in the population at risk at a specific time (point prevalence) or time interval (period prevalence). Prevalence may depend on how a disorder is diagnosed. A good example is dementia.

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107
Q

What is the post test odds formula?

A

Post test odds = Pretest odds x LR

The odds that the patient has the target disorder after the test is carried out (pre-test odds x likelihood ratio).

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108
Q

What is the post test probability formula?

A

Post-test probability = post-test odds/ post test odds + 1

The proportion of patients with that particular test result who have the target disorder

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109
Q

What else can be used to determine Pretest and post test probabilities?

A

A likelihood ratio nomogram

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110
Q

How are therapeutic interventions evaluated?

A

Therapies/interventions are evaluated using relative risk (RR), relative risk reduction (RRR), absolute risk reduction (ARR), and number needed to treat (NNT)

A table with the outcome (+ … Good; and - … Bad ) along the top vs therapy (control & treatment) along the side is built.

111
Q

What is absolute risk reduction?

A

Risk in control - risk in tx group

112
Q

What is relative risk formula?

A

Risk in tx group/ risk in cntl group

30%/40% = 0.75 so the outcome is 0.75 times as likely in the treatment group as compared to control

113
Q

What is number needed to treat formula?

A

1/absolute risk reduction

Ie 1/0.10= 10 and therefore we need to treat 10 people for two years to prevent one death

114
Q

What is absolute risk reduction?

A

Risk in control - risk in tx group

114
Q

What is relative risk formula?

A

Risk in tx group/ risk in cntl group

30%/40% = 0.75 so the outcome is 0.75 times as likely in the treatment group as compared to control

115
Q

What is relative risk reduction formula? What is an important consideration in looking at relative risk reduction?

A

Absolute risk reduction /Risk in control group
Ie 10%/40% = 25%
Treatment reduce risk of death by 25% relative to control.

An important to note is that. The lower the event rate in the control group, the larger the difference between the relative risk reduction and absolute risk

116
Q

What is number needed to treat formula?

A

1/absolute risk reduction

Ie 1/0.10= 10 and therefore we need to treat 10 people for two years to prevent one death

118
Q

What is relative risk reduction formula? What is an important consideration in looking at relative risk reduction?

A

Absolute risk reduction /Risk in control group
Ie 10%/40% = 25%
Treatment reduce risk of death by 25% relative to control.

An important to note is that. The lower the event rate in the control group, the larger the difference between the relative risk reduction and absolute risk

119
Q

How to traditionally Approach the febrile infant without a source?

A

Dependant on age of child.
Neonate is 0-28 days
Young infant is 1-3 mos
Older infant is 3-36 mos

120
Q

Who has the highest risk of bacterial infx, and what are the prime pathogens?

A

Neonates… E. coli, GBS, HSV and listeria

121
Q

What should be done in the neonate for workup/ mgmt?

A

ADMIT for antibiotics
CBC diff,
Blood cultures
Catheter urine for culture, urinalysis R + M
Lumbar puncture: little CHAPS… Cell count, HSV PCR, Agar (culture), Protein, Sugar

122
Q

What is tx for the neonate?

Should cephalosporins be used? Any that should not?

A

GAGA
Gentamycin has broad coverage. GET GENTAMYCIN LEVELS PRE AND POST 3rd DOSE! 7.5 mg/kg/ d
Ampicillin covers Listeria 200 mg/kg/ d
Acyclovir for HSV if high risk infant
Tylenol 50 mg po q4h prn for fever, max 5 doses per day.

Optional: 3rd gen cephalosporin but do t use ceftriaxone bc leads to increased bilirubin.

123
Q

What are important considerations to include for writing orders?

A

Name and unit no.
Allergy status
We
Dose (mg/kg/d)

124
Q

How to approach the well looking child w a soar throat?
Is clinical exam high yield?
What is the aim in treating strep? What does it not address adequately?

A

Clinical exam is poor at distinguishing bacterial vs viral etiologies…

Want to do throat swab and do no prescribe initially…. WAIT FOR
SWAB!
If pos swab for GAS, Rx Pencillin V 37.5 mg/kg/day broken into tid for 10 d.

The reason for treating strep is to prevent rheumatic fever, but it will not prevent PSGN renal failure
M

125
Q

How to approach the teen girl w dysuria?

A

HEADSS, as UTI suggests sexual activity
Urine R and m, c and s.
Septra - trimethoprim sulfamethoxizole (80 mg tmp/ 400 smx) 2 tabs PO daily x 3 days OR nitrofurantoin

126
Q

How does body composition change over childhood?

A

Extra cellular fluid decreases, fat increases

127
Q

How does renal function change over childhood and what are the ramifications of this?

A

GFR is low at birth (proportional to adult renal failure), doubles by wk 1, adult values by 6-12 months

128
Q

What are features of the phase I metabolism enzymes of the liver in children?

A

Phase I metabolism enzymes are involved in redox reactions and hydrolysis.
They are low at birth, mature at variable levels and the hepatic activity of kids may actually exceed adult levels.

129
Q

Are sensitivity and specificity more epidemiological or clinically relevant? Defn? Also known as what?

A

Epidemiological. Answers the question, of all who have disease, how many are revealed in this test as positive? Or of all without disease, how many tested as negative.

sensitivity is the proportion of all persons at high risk for the disease who have a positive test result. Also known as true positive rate of a test. SnNOut and PID… positive in disease

Specificity is the proportion of all persons at low risk for the dz who have a negative test result. Also known as the true negative rate. Because a test w high specificity has low false positive rate, then if someone if positive, can rule in the disease w high certainty (SPIN) and NIH … Negative in health

So do want good sp sn in order to have a sense of if it a good test to utilize in clinic in the first place, but then once that decision is made one must depend on predictive values so as to gauge the utility in their practice population.

130
Q

Who are screening tests used for?

A

Developing screener is based in the need to ID higher risk patients for a particular disease in a population, and who appear healthy.

131
Q

What values are more useful for physicians? What are they also known as?

A

Positive predictive value and negative predictive value… Bc only when a test is positive do patients or docs get interested.

PPV: of all those with a positive test, how many actually have the disease? This is also called precision or yield. True positives of all positives

NPV: the opposite… Of all those w a negative test result, how many actually do not have the disease? True negatives of all negatives.

132
Q

What values are influenced by prevalence?

A

Positive and negative predictive values.
Ie if low prevalence, then relatively more false positives. Bc false positives are a function of the test and not the disease.

133
Q

The sum of what two values equalling 150 can indicate an excellent screening test?

A

Sum of PPV and sensitivity.

134
Q

If we don’t have prevalence data available what can be used instead?

A

We can use incidence x duration (average duration of dz)

135
Q

What type of studies are often used to determine sensitivity and specificty?

A

Case-control. Compare results of the screening test to a gold standard to determine the true positive (positive result in a person at high risk for disease (can’t say they actually have it because it is a screener) and false negative (negative result in a person at high risk for the disease who has

136
Q

What is the defn of accuracy?

A

TP + TN / TP + FP + FN + TN

137
Q

For screening tests, are PPV and NPV influenced by specificity and sensitivity, in addition to prevalence?

A

Yes! Positive predictive value is influenced by specificity as both include false positives in their denominators (B) of their formulae and by sensitivity as both include true positives in their formulae.

Similarly, NPV is influenced by sensitivity as both have false negative in their denominators and by specificity as both include true negatives In Their formulae.

Note that predictive values are influenced by prevalence whereas sens and spec are not.

138
Q

If a screening test has a low PPV and many false positives, why might it still be used? Ie cervical ca and pap.

A

Bc inexpensive, convenient, safe, picks up ca precursors, ie low grade squamous epi lesions, which require less invasive treatment and prevent advancement.
These benefits outweigh the harms of further investigations and treatment of false pos.

Also, it has a HIGH POSITIVE LIKELIHOOD RATIO. Therefore in the presence of. Pos test, likelihood for developing cerv ca is high. These pts thus require follow up.

Also has a low negative likelihood ratio, so a single pap is not sufficient to conclude that likelihood of developing cerv ca is low enough to d/c follow up.

139
Q

Are predictive values useful in determining the usefulness of a screening test?
What about LRs?

A

No- influenced by prevalence or incidence so not particularly useful in determining usefulness of a screening test.
LRs are better bc they are NOT Affected by PREV or inc.

140
Q

What are mnemonics for a diagnostic test that allows one to rule out and in a Dz?
Why can you actually rule in and out with diagnostic test?

A

SnNOut. Sensitive test w Negative result rules Out dz.
SpPIn. Specific test w Pos result rules In.

More specific for the disease and higher yield, costly, etc. but firm dz. Versus a screener where you could not apply these mnemonics.

141
Q

Do screening tests indicate absence or presence of the disease?

A

NO- they identify those who need further testing

142
Q

What are the features that characterize and strengthen the case for inference of causation?

A

BBE CCASST
Biological gradient- dose-response…. Dose not rule out causality though because could be threshold exposure value
Biological plausibility- The association agrees with currently accepted understanding of pathological processes.
Experiment- The condition can be altered (prevented or ameliorated) by an appropriate experimental regimen.

Coherence- The association should be compatible with existing. Knowledge. In other words, it is necessary to evaluate claims of causality within the context of the current state of knowledge within a given field and in related fields. What do we have to sacrifice about what we currently know in order to except a particular claim of causality? Sometimes Orthodox he needs to be challenged and Advance society forward.
Consistency- across studies results are replicated in different settings using different methods.
Analogy - similar agent has led to similar outcome.
Strength of association- all w dz were exposed to presume causal agent, and those who are not were not exposed. Is quantified as relative risk. This is defined by the size of the association as measured by appropriate statistical tests. The stronger the association, the more likely it is that the relation of “A” to “B” is causal. For example, the more highly correlated hypertension is with a high sodium diet, the stronger is the relation between sodium and hypertension.
Specificity- agent or risk factor is found that consistently relates only to this disease. This is established when a single putative cause produces a specific effect.- A waek criterion that does not undermine causality. Because outcomes are likely to have multiple factors influencing them, it is highly unlikely that we will find a one-to-one cause-and-effect relationship between two phenomena .causality is often multiple. Therefore it is necessary to examine specific causal relationships within a larger systemic perspective.
Temporality- dz predates exposure

143
Q

What are the roles of public health in Canada?

A 
Population health assessment
Health surveillance
Health promotion 
Health protection
Disease and injury prevention
Aboriginal health
144
Q

Who addresses public health at the federal level?

A

1 the public health agency of Canada. PHAC.
Est 2006 after the 2003 SARS crisis.

2 health canada …

145
Q

Who directs the PHAC and who does this person report to?

A

Chief public health officer, who reports to the federal minister of health.

146
Q

Who directs health Canada?

A

Under the direction of the deputy and associate deputy ministers of health

147
Q

What are the 3 branches of health Canada that are involved with public health?

A
  1. Health products and food branch
  2. Health environment and consumer safety branch
  3. First Nations and Inuit branch
148
Q

Who finds public health and who is responsible for most the public health jurisdiction?

A

Feds fund, prov and terr respons

149
Q

What are three situations that the federal govt would intervene for public health issues?

A
  1. Criminal law ie legalizing marijuana
  2. When public health issues affect POGG (peace, order, and good government) of the nation.
  3. Public health risks involving international borders. Ie quarantine at entry into or exit from Canada under the quarantine act.
150
Q

What is the organization of public health at prov terr level?

A

1 minister of health and his/her deputies (ie deputy minister)
2 office of the chief medical officer (or chief public health officer)
3 provincial or territorial public health agency
4 branches of ministry of health… Respons for Provincial policy and legislation
5 regional health authorities.
… In some provs, separate prov lab services and / or health surveillance Office.. Ie BC Centre for disease control.

151
Q

What are provs and terrs respons for?

A 
1 health surveillance
2 outbreak investigations
3 quarantine, isolation, and mandatory tx
4 drug addiction
5 mental health
6 health profession regulation
7 workplace health and safety
8 food regulation for health reasons
9 safety and security of patients and hospitals
152
Q

What statute enables a prov or terr to intervene during public health emergencies? What does this describe provisions for?

A

Each prov terr has its own emergency health powers act. Describes provisions for:
1 who must report
2 what events trigger a report
3 what are reportable dzs
4 when a report must be made ( w/in 24 hrs)
5 to whom a report must be made
6 what info must be reported
7 what info is shareable w other jurisdictions

153
Q

What’s the defn of a Public health emergency?

A

1 An occurrence or imminent threat caused by any of the following:
- bioterrorism
- appearance of a novel or prev controlled or eradicated Infx agent or biological toxin
- natural disaster
- chemical attack or accidental release
- nuclear attack or accident
2 poses a high probability of any of the following harms:
- large number of deaths in pop affected
- Lg no. Serious or long term disability
- widespread exposure to an infectious agent that poses signif risk of substantial Harm to a large no. Ppl

154
Q

What are the two types of communicable Dz lists?

A

Lists all individuals must report and lists all labs must report.

155
Q

Who maintains the national list?

A

The Canadian notifiable disease surveillance system

156
Q

Where is the list maintained in bc?

A

The health act communicable disease regulation

157
Q

How can communicable dzs be organized?

A

1 Enteric, food and waterborne
2 resp transmission
3 direct contact transmission and thru healthcare provision
4 those preventable by routine vaccination
5 Sexually transmitted and bloodborne
6 vectorborne and zoonotic
7 potential bioterrorism agents

Any nonlisted dz that becomes epidemic or unusual features

158
Q

Who do docs report dzs to and w/in what timeframe?

A

Local public health officer, otherwise known as Medical health Officer within 24 hrs.

159
Q

What must a report submitted to the local public health officer entail?

A
  1. Name of dz
  2. Name, age, and sex with address of pt.
  3. Details if epidemic or unusual presentation
  4. Any other info requested by medical health officer
160
Q

What are he rules around isolation / quarantine on the docs part?

A

Can put individual there but no legal authority to enforce it.

161
Q

Who represents the first level of public health response and what are responsibilities?

A

Local Medical health officer verifies event and initiates infx control measures initially.

If serious, must report to appropriate national public health agencies within 24 hours.

162
Q

How long do national public health agencies have to report to WHO.

A

24 hr

163
Q

What is the attack rate?

A

The proportion of exposed individuals who contract the disease over a specific period of time, expressed as percent or number per 100000.

164
Q

What makes a good screening test?

A 
Valid, especially high sensitivity... B/c want to pick up as many as possible, even false positives, and then further work up and rule out fps later.
Safe
Cheap
Easy to use
Quick
165
Q

What are the principles of causation?

A

BBE CCASST

Biological gradient (dose-response) : if those w the most intense or longest exposure to the agent have the greatest freq or severity while those w less ensure are not as sick, more likely causal.
Biological plausibility- explanation available?
Experiment- evidence from exp animal studies

Coherence: is this plausible? …. Limited by our current scientific understandings
Consistency: confirmed by several studies
Analogy: analogous effects created by analogous agents in past
Specificity: if an agent or RF is found that relates consistently to only this dz
Strength of association: if all those w the Dx were exposed to the presumed causal agent, but very few in the comparison healthy group were exposed, the stronger the association. Ie high relative risk.
Temporality: exposure to presumed cause predates Dz onset

More likely causation and less so association

166
Q

What are particularly poor tasting medicines?

A

FACS

Flagyl, augmentin (amox-clav), cloxacillin, steroids,

167
Q

What are particularly good tasting medicines?

A

ZAC tastes good

Zithromax, amoxicillin, cefprozil (2nd gen ceph)

168
Q

How many pregnancies are unplanned?

A

49%

169
Q

What is an optimal website to investigate medicine safety in pregnancy?

A

Motherisk.org

170
Q

What is optimal for pain and fever control in kids?

A

Tylenol 15 mg/ kg/ dose q4h max 5 dose per day

Advil 10 mg/ kg / dose q6h prn.

171
Q

Why should codeine be avoided in peds?

A

Effect depends on rate of metabolism into morphine… So of slow metabolized will get no effect/ pain relief.
Fast metabolizes can become toxic.

172
Q

What is dosing for morphone oral soln in kids?

A

0.15-0.6 mg/kg/dose q3-4 h prn. (Start at Lower end and titrated up)

173
Q

What is a very important caution for treating actively seizing pediatrics?

A

DO NOT underdose this patient…stacking lower doses does not work to abolish seizure, and as increasing accum, can get toxic levels leading to respiratory depression.

174
Q

What is benzo dose for a seizing child?

A

Lorazepam 0.1 mg/kg/dose SL IV
Or
Diazepam 0.5 mg/kg/dose PR q10 min prn.

175
Q

How effective are puffers w spacers as compared to nebs?

A

As if not more effective.

176
Q

What is a mandatory investigation for all children presenting with suspected asthma attack?

A

CXR r/o other pathology.

177
Q

What are ventolin and Flovent, w dosing?

A

Ventolin is salbutamol, a short acting beta agonist and Flovent is fluticasone, a corticosteroid.

Ventolin 100 mcg / puff 1-2 puffs via spacer q4h prn.
Flovent 50 mcg/puff and 125 mcg/ puff. 50-100 mcg bid

178
Q

What are some atopic dermatitis medications?

A

1% hydrocortisone ointment, NOT cream, bid to rash until clears.
If not responding, 0.1% betamethasone ointment.

Moisturizers: glaxal base, Vaseline

Inform parents of chronic its of this dz.

179
Q

If possible meningitis in an infant, what is the approach?

A

Do lp and cover at meningitis doses until CSF cx neg.

if child sick enough for hospital, go to upper end of range at 180 mg/ kg/ day

180
Q

What does the evidence say about antigen load in contemporary times?

A

There is no evidence of inc sA/e w inc # of vaccines given at one time. Antigen load has decreased since the 1990s

181
Q

What does staggering vaccine schedules put children at risk for?

A

Under vaccination due to missed doses.

182
Q

What does gardasil vaccinate against? What about cervarix?

A

Quadravalent, against 6, 11, 16, 18

Cervarix is bivAlent against 16 and 18.

183
Q

What are adverse events ass’d w hpv vaccine?

Any assn w GBS, thromboembolism, or death?

A

Local pain, syncope.

No.

184
Q

What is the rotavirus vaccine?

A

A live attenuated vaccine of 3 PO doses

185
Q

What is the GATC project?

A

A hypothesis that genetic polymorphisms can be ass’d w adverse drug reactions.

186
Q

What does it mean when there are blasts and pancytopeni on a peripheral smear?

A

Acute leukemia… > 25% blasts

187
Q

What are diagnostic emergencies?

A

These are when definitive laboratory diagnosis is required immediately, so immediate treatment can begin.
- pt must be in imminent danger of complications.
Call pathologist to discuss if off hours.

188
Q

What is turnaround time for acute leukemia? Solid tumors? Cytogenetics?

A

Hours, 1-2 days, 1-3 days.

189
Q

What is the standard trauma screen in the pediatric pt?

A

Cerv xray, CXR, pelvic xray

190
Q

What are radiation considerations for the pediatric pt?

A

Children are more radio sensitive than adults. Ie with abdo ct inc risk of mortality of 1/1000 over lifetime.

191
Q

What is the imaging modality of choice for hypertrophic pyloric stenosis?

A

Ultrasound. Shows pyloric muscle thickness > 3 mm, length of pyloric canal > 14 mm.

192
Q

What is the imaging modality of choice for appendicitis in the ped?

A

Ultrasound. Sens and spec 70-80% and more dep on user.

Reserve CT for problem cases.

193
Q

What is the preferred imaging modality for mal rotation and volvulus?

A

Upper GI series w contrast +/- ultrasound

194
Q

What is the preferred imaging modality for intussusception? Where does this typically occur in the bowels?

A

Typically ileum into cecum. U/s for imaging and tx w inflation.

195
Q

Outside of what age range should a pathological lead point be considered in intussusception?

A

Outside 18 mo to 4 y

196
Q

What are the majority of leukemia types diagnosed in children?

How do aml and all differ in tx?

A

Lymphoid.

Aml: inpt at bcch, 6-8 mos intensive tx w strict isolation for 28-69 days at a time, ICU common.

All: shorter admit, only 7-14 d.
Mostly outpt. First 7-9 mo intensive then next 18-30 mo qD po meds q monthly IV chemo and q3 mo intrathecal

197
Q

What to do upon new Dx?

What are immediate concerns? (5)

A

Call bc children hospital pediatric oncology
Invesitigations: Bloodwork, chem 7 extended uric acid, ldh, PTT inr, d dimer, fibrinogen.
Blood cx if febrile
CXR: mediastinal mass?
Immediate management:
Arrange Infant transport team via peds ICU to nicu/picu at bc children’s
- there they recieve Dxic marrow and lumbar puncture, central line placed by peds gen surgeon,n
Immediate concerns:
1) tumor lysis syndrome
- metabolic consequences of spontaneous or tx-related tumor necrosis.
2) hyperleukocytosis
- highest risk in AML w WBC > 200; ALL w WBC > 300
3) DIC
- uncontrolled activation of coagulation and fibrinolysis. Highest risk are aml pts.
4) mediastinal mass
- potential SVC syndrome.
5) febrile neutropenia- medical emergency

198
Q

What is one to follow in tumor lysis syndrome?

What are consequences of tumor lysis syndrome?

A

Increasing uric acid, K+, phosphate and decreasing Ca.
Consequences:
1) acute renal failure secondary to uric acid and calcium phosphate deposition in the microvasculature and renal tubules.
- esp Tumor infiltration into the kidney, ureter, or renal vessel obstruction.
– Cardiac arrhythmias

199
Q

When does Tumor lysis syndrome typically start?

A

Usually within 1 to 5 days of starting treatment in tumors that are rapidly growing. Examples include Burkitt’s lymphoma, T cell lymphoblastic leukemia/lymphoma, ALL with many blasts

200
Q

What are signs and symptoms of tumor lysis syndrome?

A

Abdominal pain, back pain, decreased urine output.
Electrolyte anomalies:
– Calcium decrease leads to anorexia, vomiting, cramps, carpopedal spasm, tetany, seizures.
– Increased potassium leads to G.I. symptoms, weakness, ECG changes including QRS widening and T waves, ventricular arrhythmias, death.

201
Q

What does management of tumor lysis syndrome?

A
  • Fluids at 2 to 3 times maintenance dose.
  • Alkalinize urine with sodium bicarb 50 to 100 mEq to keep urine pH from 6.5 to 7.5
  • inhibit xanthene oxidase and thereby decreasing uric acid production with using allopurinol
  • use urate oxidase to convert uric acidwater-soluble allantoin
  • treat hyperK w Ca gluc, insulin and glucose, ventolin, kalxylate, dialysis.
202
Q

What is a critical value in pathology terms?

A

Implies a pathologic finding wich requires urgent contract between pathologist and clinician.
Therefore in biopsy pathology, would be something unexpected or would require an urgent change to pt mgmt.
ex: a unexpected malignancy in a tissue expected to be benign.
Other: unexpected infection ie fungal or mycobacterial on cyto pathology specimen from lung.
Non-malignant but potentially rapidly injurious dx ie granulomas on temporal artery biopsy suggesting temporal arteritis.

203
Q

What are high dose extended interval aminoglycosides?

A

They are less toxic.

Don’t use for burns, ascites, crcl 120, preg

204
Q

What can leukemia in the child leading to hyperleukocytosis cause?

A

This can cause high viscosity leading to respiratory dysfunction, CNS bleeds and strokes.

High risk numbers include AML w CBC count > 200
ALL w WBC count > 300

205
Q

What to look for when the pediatric leukemia case has bruising, bleeding, shock, intracranial bleed, and death.
Pathophys?

A

This is DIC, due to uncontrolled activation of clotting factors and platelets. As such, clotting factors and platelets consumed.

206
Q

What criteria are used for serotonin syndrome?

A

Hunter Criteria

207
Q

What types of pts are prone to DIC?

A

Those w severe illness/ septic shock, pts w AML.

208
Q

What are the bloodwork findings w DIC?

A

Inc pt, ptt, d-dimer,

Dec platelets, fibrinogen, clotting factors.

209
Q

What is the management of DIC?

A

1) treat underlying cause

2) treat numbers: FFP, cryoprecipitate/ platelets, pRBCs.

210
Q

When to use heparin in DIC?

A

This is controversial. Only use when aggressive therapy fails to correct a dangerous coagulopathy.

211
Q

What is a classic appearing drug induced torsade?

A

PAC w long QTc, sinus driven, into short run of VT, then sinus beat w atypical qrs, then fulminant vt

212
Q

How to risk stratify someone for QTc prolongation?

A

LOOK AT SLIDE!

213
Q

In those w lymphoid leukemia, what do mediastinal masses predispose to?

A

SVC syndrome

Assess this w CXR, do not intubatr.

214
Q

How do methadone, fluoxetine and trazodone effect qtc?

A

Methadone does it inherently.
Fluoxetine does it inherently and blocks methadone metab.
Trazodone Does it inherently and blocks CYP

In addition to modifying doses, if slow hr and on metoprolol, dec dose so as to dec risk for further prolongation due to bradycardia..

215
Q

How are the outcome rate of the control and outcome rate of the tx compared?

A

Outcome rate of control is a/a+b
Outcome rate of tx is c/c+d

The RRR is athe difference in outcomes between the treatment and control groups.. This is expressed as a proportion of the outcome rate in the control

Outcome rate tx - outcome rate cntrl / outcome rate cntrl. CHECK!

The ARR is outcome rate control - outcome rate tx.

NNT is 1/ARR

216
Q

What are absolute neutrophil counts that can be of concern?

A
217
Q

What are the signs and sx of febrile neutropenia in a child?

A 
Septic shock- CAN OCCUR QUICK!
Fever or hypothermia
Hypotension, tachycardia
Dec perfusion
Resp distress, grunting
Edema
218
Q

What is the management of a febrile neutropenia cSe?

A

Empiric broad spec antibiotics asap: Vanco and cefotaxime which are good coverage in the non onc pt.m
IVF, inotropes, CXR O2

219
Q

What to never do if mediastinal mass in pediTric?

A

DONT INTUBATE!

W airway mgmt in the pediatric pt, don’t need to INTUBATE, can just do bag mask

220
Q

Why do we use irradiated product in transfusion?

A

To prevent transfusion ass’d graft vs host dz.

221
Q

What are indications for irradiated pediatric blood transfusions?

A

Intrauterine
Neonatal exchange
Low body weight

222
Q

How is cmv transmission lowered in transfusions?

A

Leukoreduction

There is a list of cmv status in apheresis platelet donors. Keeping a list of cmv negative donors.

223
Q

What patients are cmv negative transfusion candidates?

A 
Cmv negative transfusions are used in cmv negative AFE for high risk candidates: 
Pregnancy
Intrauterine transfusions
Stem cell/solid organ transplants
Possibly hiv pos subjects.
224
Q

How long does a group and screen last?

A

96 hrs. Could be building an allo-Ab reaction

225
Q

What are the most risky transfusion products?

A

Platelets

226
Q

What are the numbers for the following acute reactions?

Minor: allergies, hives.

A

1/100

227
Q

Fever

A

1/300

228
Q

Anaphylaxis to platelets

What to tx anaphylaxis w?

A

1/1600

Epi 0.01 ml/kg/dose of 1:1000 strength sub q. Up to 0.5 mL
Benadryl and hydrocortisone
Admit and observe
Inform blood bank

229
Q

What is the clinical picture of an acute hemolytic transfusion reaction?
Pathophys and usual trigger?
Cause?
Workup

A

Anxiety, impending doo , pain ie chest lung, red urine…
DO NOT IGNORE ANXIETY
Can be mild w hemolysis and some mild Inflamm response sx, or very Severe.
Pathophys: pts Abs mount response against Ag on transfused RBCs.
Most commonly caused by ABO incompTibility. … Anti a and anti b antibodies fix complement (vs non ABO which do not and so clinical picture is rarely significant)
Complement cascade activation.
–> donor red cells lose and disseminate the anaphylotoxins C3a and C5a . These generate inflammatory cytokines and histamine release, leading to vascular dilation, inc permeability, and hypotension.
If systemic coag cascade activation…. DIC
… The fragments of red lysis leads to immune complex formation and microthrombi formation. The can obstruct capillaries.

Autonomic response is mounted which entails can lead to vasoconstriction of some vessels ie the renal arteries leading to renal failure.

Can die acutely from shock or DIC.

Usually is a clerical error.

Workup: confirm dx w DAT, rpt G and S, cbc w smear, serum haptoglobin, coags inc fibrinogen and d dimer, bun/ cr
CXR, ecg

Mgmt: stop transfusion, IVF, 02, cryo if in doc, diuretics to consider.
ICU, call lab.

230
Q

If pt had a fever , should you ever restart a transfusion?

A

NO! Admin Tylenol.

231
Q

What are signs and symptoms of TACO?

A

Non prod cough
Tachycardia
Orthopnea
Pulm Edema

232
Q

Who. Are at risk of TACO

A 
Osce who are vulnerable to cardiac overload
Chf, copd, severe asthma
Peevious taco 
Unstable 
Elderly and peds
233
Q

If suspect pulmonary edema, what is differential and what is workup?

A

TRALI, ARDS, TACO.
for TRALI must prove that the pt was noti n prev heart failure w cv exam and if no overload, neg bnp
- new episode of hypoxemia
- b/l infiltrates

234
Q

What is the overall risk of any reaction in transfusing? RBC, plt

A

0.6%, 11%

235
Q

What is the overall risk for severe rxn in transfusing? RBC, plts

A

0.04%, 0.1%

236
Q

What is the most common transfusion reaction?

A

Febrile nonhemolytic transfusion reaction

237
Q

What is the clinical picture of a febrile nonhemolytic transfusion reaction?

A

The patient develops a fever greater than 38°C which or an increase of greater than 1°C over pre transfusion temperature.
Maybe accompanied by chills and rigors.
This is clinically of no consequence except that severe chance you can also presents with fever
Tylenol

238
Q

What does the pathophysiology of a acute hemolytic transfusion reaction entail?

A

Patients anti-body recognize antigens on the transfused red blood cells
- A EO is the clinically pertinent reaction because anti a anti B abs can mount a response that fixes compliment because they are IgM
The complement cascade is activated and this leads to lysis of donor cells and anaphylotoxins C3a and C5a.

239
Q

In an acute hemolytic transfusion reaction, what types of reactions are clinically concerning?

A

ABO because these can fix compliment. This activates The complement cascade and triggers donor red cell lysis in addition to releasing c3a and c5a anaphylotoxins

240
Q

In acute hemolytic transfusion reactions, what does the lysis of red donor cells lead to?

A

Circulating fragments lead to the formation of immune complex and this subsequently causes micro thrombi. As such, capillaries can become thrombosed.

241
Q

In acute hemolytic transfusion reactions, what does the release of anaphylatoxin lead to?

A

This generates inflammatory send to clients and other mediators like history. As such vascular dilation, increased permeability and hypertension results.
A reflex autonomic response is induced coma leaking to vasoconstriction of some vessels. The most susceptible are the renal arteries and this can lead to renal failure

242
Q

What are the possible outcomes in acute hemolytic transfusion reactions?

A

More common, is that the patients suffer a milder version with hemolysis And some mild symptoms of inflammatory response.
This can be lethal…There is a 4% risk for fatality due to shock or DIC.

243
Q

What is the most common cause for acute hemolytic transfusion reaction? AHTR

A

Clerical error. This most frequently happens in the OR.

244
Q

What do you do if you suspect an acute hemolytic transfusion reaction?

A

First confirm diagnosis with DAT, repeat group in screen, CBC with peripheral, serum haptoglobin, coagulation (fibrinogen, d dimer), bUN and creatinine.
Chest x-ray and ECG to rule out other causes

Management:
Stop transfusion, IV fluids, 02, consider cryoprecipitate it in D I C, consider diuretics.
Consider ICU
Talk to transfusion medicine lab

245
Q

What is a transfusion related acute lung injury? TRALI

A

This can be lethal…is an immune mediated acute severe noncardiogenic pulmonary Edema following transfusion of plasma containing blood products.

246
Q

What is the pathogenesis of TRALI?

A

It is not fully understood, but there is the to hit hypothesis:
1 certain clinical conditions such as surgery, trauma, sepsis, lead to neutrophil margination in the pulmonary circulation.
2 donor antineutrophil antibodies Target recipient granulocytes
- leads to degranulation and subsequent pulmonary vascular injury and massive pulmonary edema.

247
Q

Where is TRALI most common?

A

The OR and ICU

248
Q

What is the presentation of TRALI?

A

Shortness of breath, chest pain, cough, fever, hypo or hyper tension.

249
Q

What is important to differentiate TRALI from?

A

It is important to differentiate this from TACO or other causes of pulmonary Edema.
In TRALI there is no evidence of cardiogenic pulmonary edema or volume overload.

250
Q

What is the treatment for TRALI?

A

This can be lethal…Supportable only including O2 , fluids, consider ventilatory support.

251
Q

What is the role of diuresis in TRALI.

A

Often diuresis is contraindicated

252
Q

As opposed to immune mediated febrile nonhemolytic transfusion reaction, allergic/anaphylactic response, acute molybdic transfusion reaction, and TRALI, What are delayed (greater than 24 hour) immune mediated transfusion reactions?

A

Delayed reactions include a delayed hemolytic transfusion reaction and alloimmunization.

253
Q

What is an immune mediated delayed hemolytic transfusion reaction?

A

This is very similar to a AHTR, Except that there is no complement fixation.
As such, there is no intravascular hemolysis.
Antibody-labeled red blood cells are cleared by the spleen over several days.

254
Q

What is the presentation of a delayed hemolytic transfusion reaction?

A

Patients are typically not very ill except for their anemia. They developed jaundice as the clearing by the spleen occurs.
risk for patients is minimal

255
Q

What happens to the hemoglobin numbers upon delayed hemolytic transfusion reaction?

A

Hemoglobin falls to pre-transfusion levels

256
Q

What is alloimmunization?

A

This is a delayed immune mediated process entailing development of non-ABO antibodies against donor red blood cells, potentially affecting future transfusions

257
Q

What are some acute non- immune acute transfusion reactions?

A

v: Air embolism: accidental injection of large air bubble into vein
- volume overload= transfusion associated cardiac overload… TACO: congestive heart failure due to rapid increase in intravascular volume.
I: bacterial sepsis… The risk of this is one in 100,000. It is the most likely infectious risk of transfusion
E: electrolyte abnormality…
- Hyperkalemia due to leakage out of red blood cells.
- Hypocalcemia due to transfusion of calcium chelators

258
Q

What are some nonimmune delayed transfusion reactions?

A

Infectious: viral, parasitic, or prion.
– The highest risk is of viral infection with hepatitis B… 1 in 150,000.
Hiv…1 in 7.8 million

Iron overload: development of iatrogenic iron overload from repeated reply till 10 fusions over matter of years and

259
Q

In addition to taco, AHTR, and TRALI, what is another lethal transfusion reaction?

A

Anaphylactic reaction…. Severe dyspnea, cough, urticaria

260
Q

What is the purpose of the likelihood ratio?

A

I likelihood ratio combines sensitivity and specificity into a single figure that indicates by how much the test results will reduce the uncertainty of a given diagnosis. The likelihood ratio is the probability that a given test results would occur in a person with the target disorder divided by the probability that the same result would occur in a person without the disorder

261
Q

What are the two types of drug interactions?

A

Pharmacokinetic – what the body does to the truck or movement of drug throughout the body –ADME

Pharmacodynamic – what the drug does to the body or the effects of the drug.

262
Q

What is the mnemonic that pharmacokinetic action entails.?

A

ADME
1 absorption. Drug goes into systemic circulation
2 distribution. Drug is distributed throughout tissues.
In tandem with
3. Drug metabolism… Drug metabolized
4. Drug excretion… Drug exits body.

263
Q

What actions occur through pharmacodynamic processes?

A

Drug concentration at site of action leads to pharmacologic effect.
This leads to a clinical response.
Two possible outcomes of clinical response are 1) toxicity and 2) efficacy

264
Q

What are more common, pharmacodynamic or pharmacokinetic interactions?

A

Pharmacodynamic… 3/4 of interactions

265
Q

What are the possible outcomes following drug metabolism interactions, pertaining to substrate concentration and risk of toxicity?

1) cyp substrate + cyp inhibitor
2) cyp substrate + cyp inducer
3) cyp substrate + cyp substrate

A

1) increased substrate concentration and increased risk of toxicity.
2) decreased substrate concentration and decreased substrate efficacy
3) increased, decreased or equivocal substrate concentration and change in efficacy or toxicity

266
Q

What is the most widely studied transport protein?

A

P – glycoprotein

267
Q

Who is at highest risk for drug drug interactions?

A

Increased age,
Chronic conditions
Narrow therapeutic index drugs including your friend, anticoagulant, NSAID, ace i

268
Q 
What are clinical manifestations and severity of drug/drug class interactions of the following ?
1 NSAIDS and ACEi
A

By inhibition of vasodilating renal prostaglandins leads to renal impairment of minor/moderate severity

269
Q

2 omeprazole and clopidogrel

A

Inhibition of Clopidogrl metabolism to active metabolite leading to dec clopidogrel effectiveness. This is major severity

270
Q

3 warfarin and NSAIDS

A

Increased bleeding risk of major/moderate severity

271
Q

4 digoxin and clarithromycin

A

Inhibition of P-glycoprotein leading to increased digoxin levels and toxicity of moderate effect.

272
Q

5 ACEi and spironolactone

A

Enhanced hyperkalemic effects leading to hyperkalemia of major/moderate severity

273
Q

6 warfarin and ssri(esp fluoxetine and fluvoxamine)

A

Enhanced warfarin anticoagulation theorized to be due to CYP inhibition. Altered anticoagulation with start and stop of SSRI

274
Q

How do you risk stratified someone with QT prolongation?

A

Separate into high risk patient versus low to medium risk patient.

275
Q

What are high-risk patient factors for prolonged QT syndrome?

A

Congenital LQTS
Syncope of abrupt onset and abrupt offset.
Family history of syncope/spontaneous cardiac death
Cardiac arrest survival
QTC is greater than 500 ms

276
Q

Low to medium risk factors for prolonged QT

A 
Female
I'll delete
CHF or am I
Hypokalemia
Bradycardia less than 50
QTC greater than 450
Concurrent qt prolonging drugs

Preparation For Medical Practice (8 decks)

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