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Week 1 and 2--lecture slides Flashcards

1
Q

what is type I diabetes

A

autoimmune disease leading to pancreatic islet cell destruction

ABSOLUTE insulin deficiency

*these patients always need insulin even if they are not eating

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2
Q

what is type II diabetes

A

insulin resistance and relative insulin deficiency

may have worsening insulin deficiency over time

may be diet controlled, on oral agents, on insulin, or a combination

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3
Q

who should be on insulin

A

all patient with DM1

those who DM2 who:

  1. are on max oral agents and the A1c is still above 7%
  2. have a new diagnosis and A1c is above 10%
  3. have metabolic decompensation (i.e weight loss, polyuria, HHS)
  4. renal or liver failure
  5. pre-pregnancy or during pregnancy
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4
Q

name the rapid acting insulins

A

Lispo

Aspart

glulisine

(a couple hours)

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5
Q

name the short acting insulins

A

human regular

around 6-7 hours

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6
Q

name the intermediate acting insulins

A

NPH

18-20 hours

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7
Q

name the long acting insulins

A

detemir

glargine

(about 24 hours)

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8
Q

when do you use rapid acting insulins

A

for bolus insulin–> for glucose elevations related to meals/carb intake or to correct high BG

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9
Q

when do you use short acting insulins

A

bolus insulin or insulin infusions

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10
Q

when do you use intermediate insulins

A

basal insulin–> for glucose elevations related to hepatic glucose production in the fasting state

peak can cover lunch

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11
Q

when do you use long acting insulins

A

basal insulin

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12
Q

if you are using an insulin mix (in one pen) when do you give it

A

before breakfast and before dinner

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13
Q

what kind of insulin of insulin pumps use

A

rapid acting

given as continuous infusion through a SQ catheter which acts as basal insulin

boluses are given through the same catheter for meals and corrections

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14
Q

how do you decide on an insulin dose

A

can use weight based approach–> 0.5 units / kg for Total Daily Dose

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15
Q

how do you split total daily dose of insulin between bolus and basal

A

50/50

for the bolus 50%, divide that by 3 to get the bolus dose for each meal

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16
Q

for mixed insulin, how do you divide dosing

A

2/3 of total daily dose with breakfast, 1/3 with dinner

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17
Q

if your patient is going to be counting carbs to get a personalized insulin dose, what is a good insulin:carb ratio to start with (for insulin sensitive patient)

A

1:20

1 unit of insulin for every 20 g of carbs

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18
Q

how do you calculate the insulin sensitivity factor

A

100/TDD

i.e if TDD is 50, ISF = 2–> every 1 unit of insulin lowers glucose by 2 mmol/L

if BG is high, calculate current BG-ideal BG. Then divide that number by ISF

i.e
BG 12, goal is 6.
12-6=6
6/2 (ISF from above) = 3 units to give to correct

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19
Q

is a sliding scale enough on its own

A

no–corrects hyperglycemia after the fact but does not prevent it

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20
Q

what are BG and A1c targets for the outpatient

A

pre prandial glucose 4-7

2h after meal 5-10

A1c less than 7%

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21
Q

what are the BG targets for the critically ill

A

8-10

allow higher

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22
Q

how do you manage hypoglycemia acutely (patient is conscious)

A

ingest 15g CHO

retest in 15 min–> retreat is BG still below 4

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23
Q

how do you treat BG acutely (patient is unconscious)

A

glucagon 1 mg IM if no IV

D50W 10-25 g IV over 1-3 minutes

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24
Q

define delirium

A

disturbance in consciousness, reduced ability to focus, or to sustain or shift attention

change in cognition such as memory, disorientation, speech or the development of perceptual disturbance

disturbance develops over hours to days and FLUCTUATES in severity

result of a GENERAL MEDICAL CONDITION

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25
Q

how does delirium compare to dementia with regard to:

onset

A

delirium–acute or subacute

dementia–insidious

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26
Q

how does delirium compare to dementia with regard to:

course

A

delirium–fluctuating

dementia–progressive

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27
Q

how does delirium compare to dementia with regard to:

conscious level

A

delirium–impaired, fluctuating

dementia–clear initially

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28
Q

how does delirium compare to dementia with regard to:

cognitive defects

A

delirium–poor attention, poor short term memory

dementia–attention PRESERVED, also poor short term memory

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29
Q

how does delirium compare to dementia with regard to:

hallucinations

A

delirium–common (usually visual)

dementia–often absent

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30
Q

how does delirium compare to dementia with regard to:

delusions

A

delirium–fleeting, non systematized

dementia–often absent

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31
Q

how does delirium compare to dementia with regard to:

psychomotor

A

delirium–increased or reduced

dementia–can be normal

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32
Q

what % of hospitalized and community populations over age 65 experience superimposed dementia

A

22-89%

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33
Q

what % of terminally ill patients experience delirium

A

80%

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34
Q

wha % of medically ill hospitalized patients under 65 experience delirium

A

10-30%

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35
Q

wha % of medically ill hospitalized patients over 65 exprience delirium

A

10-40%

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36
Q

list the common causes/etiologies of delirium

A

DIMS FU

drugs–intox or withdrawal

Infections–chest, GU, SSTI

Metabolic–endocrinipathy (NA, Ca, K, diabetes, thyroid), renal failure, liver failure

Structural–stroke, hemorrhage, seizure, neopllasm

Fecal impaction

Urinary retention

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37
Q

how do you diagnose delirium

A
  1. confusion assessment method
  2. MMSE
  3. psych consult
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38
Q

what is the gold standard for diagnosing delirium

A

psych consult

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39
Q

how does a confusion assessment method assess delirium

A

two part screening instrument for both cognitive impairment and delirium

delirium screen is positive when:

  • acute onset, fluctuating course..AND..
  • inattention..AND..
  • disorganized thinking..AND..
  • altered LOC

*an acceptable screening instrument but dx should be ensured according to the formal criteria for delirium

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40
Q

what are the cutoff scores for the MMSE

A

27 or above is normal

less than 24 is abnormal

*does NOT clearly distinguish delirium from dementia

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41
Q

is delirium always reversible

A

not always

*up to 82% of people have residual deficits 6 m post discharge

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42
Q

how do you prevent delirium

A

multiple components

orientation–cognitive exercises, clues

mobilize early

minimize psychoactive drugs

prevent sleep deprivation

use eyeglasses and hearing aides

intervene with volume depletion early

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43
Q

how do you manage delirium

A

ID and treat reversible causes

supportive care–> protect airway, maintain hydration and nutrition, prevent pressure ulcers, avoid physical restraints

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44
Q

list non pharma methods of managing delirium

A

create calm, comfy enviro

use orienting influences

regular reorienting communication with staff

involve family members in supportive care

limit room and staff changes

coordinate schedule to allow uninterrupted sleep at night

encourage normal sleep-wake cycles

close clinical f/u

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45
Q

list pharma approached to delirium

A

consider if delirium sx put patient or others at risk or interrupt essential therapy

can use haldol or loxapine

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46
Q

how do clinical ethics differ from medical ethics

A

clinical–case based, based on patient in front of you

medical ethics–issue based (i.e abortion, euthanasia)

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47
Q

what is one way of addressing a clinical ethical issue

A

ID the conflict

name the principles involved

and then FORMULATE A QUESTION that addresses the scenario (i.e is it clinically permissible to…)

decide which principle should have priority in this particular case (and recognize that different priorities) OR find an alternative that avoids the dilemma

could there be more info that would help resolve the dilemma? (i.e prognosis etc)

evaluate your decision–is this what a consensus of exemplary doctors would do?

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48
Q

what are the top 4 principles of medical ethics

A
  1. autonomy
  2. beneficence
  3. non-maleficence
  4. justice
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49
Q

medical ethics: define autonomy

A

the respect for patients wishes, and the ability of a capable individual to make an informed decision about accepting or refusing a treatment

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50
Q

medical ethics: define non-maleficence

A

first, do no harm (primum no nocere)

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51
Q

medical ethics: define justice

A

equal distribution of resources

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52
Q

medical ethics: beneficence

A

doing what is in the best interest of your patient

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53
Q

what to clinical practice guidelines do?

A

clarify areas of management uncertainty

standardized medical care

raises the quality of care

achieve maximum benefit for each dollar spent

pass your exams! great for studying!

*peer reviewed, peer developed and help counter effects of marketing

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54
Q

in what ways are BC guidelines tailored to BC practice

A

MSP

condition-based incentive fees

rural and remote availability of tests, treatment and consults –> reflects the reality of BC practice

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55
Q

target audience for BC guidelines

A

BC physicians, NPs, residents, med students

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56
Q

how may guidelines are there currently

A

58

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57
Q

what are the 5 criteria for the development of BC guidelines

A
  1. address areas of care that are COMMON
  2. address areas of significant health system cost, whether financial or social
  3. focus on areas where there IS evidence
  4. areas where there may be variation or confusion in practice
  5. areas where there can be objective measurement of the effectiveness of the guideline
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58
Q

in what ways are guidelines used in clinical practice

A
  1. flow sheets for chronic disease care
  2. lab requisitions
  3. patient guides
  4. algorithms
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59
Q

name one area where the BC guidelines differ from the international and canadian guidelines

A

osteoporosis-

de-emphasized bone scans for everyone –> increased clinical assessment of risk before the ordering of scans

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60
Q

what are some of the things that the upcoming BC guidelines for opioid use disorder indicate? (designed for rural and remote physicians)

A

focused on suboxone as a first line therapy which can be prescribed without a methadone exemption

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61
Q

name the pairs of size/shape in dermatology

A

macule–patch

papule–plaque

nodule–tumour (cyst)

vesicle–bullae (pustule)

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62
Q

name the 3 mild topical steroids and what they are used for

A

for sensitive areas or mild disease

  1. hydrocortisone 0.5-2.5%
  2. desonide 0.05%
  3. flucinolone acetonide 0.01%
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63
Q

name the 3 medium potency topical steroids and what they are used for

A

for most parts of the body and extremities

  1. betamethasone valerate 0.05-0.1%
  2. mometasone furoate 0.1%
  3. beclomethasone diproprionate 0.025%
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64
Q

name three strong potency topical steroids

A

betamethasone diproprionate 0.05%

clobetasol proprionate 0.05%

halobetasol proprionate 0.05%

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65
Q

list 4 signs of a life threatening drug eruption

A
  1. oropharyngeal erosions
  2. blister formation
  3. skin pain
  4. facial swelling
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66
Q

name 7 types of drug eruptions/reactions

A
  1. exanthematous (“maculopapular/measles like”)
  2. urticarial/angioedema
  3. vasculitis
  4. serum sickness/serum sickness-like
  5. drug induced lupus
  6. pigmentation
  7. pseudolymphoma
  8. photosensitivity

a bunch of others

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67
Q

what is TEN/SJS

A

rare, life threatening drug induced skin reaction

consists of mucocutaneous involvement with associated skin tenderness, redness and exfoliation

*MUST HAVE MUCOMEMBRANE INVOLVEMENT (check vaginal pain, urination pain)

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68
Q

what is the difference between SJS and TEN

A

SJS is less than 10% of the body’s surface is involved whereas TEN is over 30% involvement

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69
Q

what are common culprits causing TEN/SJS

A

sulfonamides

anticonvulsants

allopurinol (especially in Asians)

NSAIDs

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70
Q

how do you manage TEN/SJS

A
  1. ID offending drug
  2. stop offending drug
  3. specialized supportive care–with SPECIALIZED NURSING (i.e burn unit or ICU care)
  4. consult derm, IM/ICU/burns
  5. can consult others if needed given presentation
  6. maintain fluid/electrolyte/ protein balacne
  7. maintain thermoregulation
  8. prevent sepsis
  9. minimize tapes
  10. meds are controversial–most are offered cyclosporine as first line
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71
Q

in terms of timeline, how can you ID the drug that may be causing a TEN/SJS reaction

A

started 7-21 days prior to reaction–> NEVER shorter than this, takes at least 7 days to appear

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72
Q

should you debride SJS affected skin?

A

NO

but nursing should be aware of what to do if and when it sloughs off by itself

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73
Q

what med is often offered first line in SJS/TEN

A

cyclosporine

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74
Q

what is DHS/DRESS

A

another possibly life threatening drug eruption

measles-like–> due to altered drug metabolism which leads to build up of toxic metabolites

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75
Q

how do you manage DHS/DRESS

A

ID and stop offending drug

corticosteroids may need to be considered depending on specific organ involvement-> order end organ function tests–> LIVER, KIDNEY

check TSH after 3-4 months

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76
Q

in terms of timeline, how can you ID the drug that may be causing a DHS/DRESS reaction

A

usually started 2-6 weeks before reaction develops

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77
Q

what is the natural course of DHS/DRESS

A

may have multiple relapses before eventually settling but typically do very well overall and eventually recover

may have delayed thyroiditis (check TSH 3-4 months)

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78
Q

what is bullous pemphigoid

A

most common AUTOIMMUNE subepidermal BLISTERING disorder

usually affects older adults

can start as a generalized itchy eruption, may be non specific itch for months with occasional urticarial plaques and blistering

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79
Q

how do you diagnose bullous pemphigoid

A

high index of suspicion in pruritic elderly patients

usually tense bullae, if blisters are already present

take a skin biopsy to check for immune factors

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80
Q

how do you manage bullous pemphigoid

A

super potent topical corticosteroid or immunomodulator

if systemic required–> tetracycline abx with or without nicotinamide

*if need rapid control use systemic steroids

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81
Q

name steroid sparing treatments for bullous pemphigoid

A

azathioprine

methotrexate

mycophenolate

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82
Q

what is the natural course of bullous pemphigoid

A

most patients eventually go into remission–morbidity depends on when the diagnosis is made and if systemic therapy is used

mortality can relate to both coexisting medical disorders and treatment choices–can also get secondary infections

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83
Q

what is atopic dermatitis

A

inherited EPIDERMAL barrier defect with bacteria occasionally acting as a super-antigen

a chronic, recurrent, inflammatory disorder of the skin –> dont really have a cure, just management

84
Q

when should you think possible atopic dermatitis

A

if you see a vesicular rash–> likely acute eczema

chronic– ill defined erythema with scale

85
Q

what is the atopic triad

A

atopic dermatitis

allergic rhinitis

asthma

86
Q

what is the pathophysiology of atopic dermatitis

A

defective epidermal layr

FILAGGRIN defect–> missing ceramids

“leaky” skin barrier leads to increase in trans epidermal water loss

*subclinical skin inslammation–> normal appearing skin is still abnormal on histologic examination with T cell mediated changes

87
Q

what can patients do to manage atopic dermatitis

A

no role for diet–> but can try a dairy log to see if foods are associated with flares if they are really bothered by it

minimize irritants like clothing

can try silver impregnated clothing

skin care with soaps, cleansers, not too hot water

88
Q

how can the physician treat atopic dermatitis

A
  1. topicals–> corticosteroids (1% hydrocortisone for the face)
  2. topical calcineurin inhibitors
  3. phototherapy
  4. systemics–> azathioprine, cyclosporine, methotrexate, mycophenolate, dupilumab (anti IL4 alpha receptor antagonist)
89
Q

what med should you avoid in atopic dermatitis

A

systemic corticosteroids

90
Q

list examples of secondary skin changes

A 
crust
scale
lichenification
erosion
ulceration
excoriation
91
Q

when should you refer to derm

A

vesicular and bullous lesions get their attention

skin pain or if patient looks ill–> red flags

treatment failing

it urgent, call derm

92
Q

what should you include in derm referrals

A

description–as much primary morphology as possible

what has been tried and for how long

past medical hx, other meds, allergies, bleeding risk, infectious risk

93
Q

what type of topical works best

A

ointment

94
Q

how much of a cream covers the entire body of an adult male once

A

20-30 g

95
Q

what is psoriasis

A

chronic, inflammatory skin disorder with a strong genetic basis

1-2% of general pop, all races, bimodal age distribution

96
Q

what are the classic psoriatic lesions

A

well demarcated geographic erythematous plaques with overlying scale

look for nail changes

97
Q

what are some other disease associated with psoriasis

A

IBD

psoriatic arthritis

98
Q

what is the ddx of red, well circumscribed lesions with overlying scale

A

tinea corporis

pytiriasis rosea

nummular ezcema

lichen planus

lupus

secondary syphillis

neoplastic (cutaneous T cell lymphoma)

99
Q

where is psoriasis usually distributed

A 
scalp
knees
hands
palms
feet
lumbosacral
100
Q

non pharmacologic treatment of psoriasis

A

PHOTOTHERAPY

minimize triggers (stress, trauma, lack of sun, infections)

moisturizers, emollients

weight loss and diet

alcohol consumption

counselling

101
Q

pharmacologic treatments for psoriasis

A

topicals–> corticosteroids, vitamin D analogues, calcineurin inhibitors, vit A analogues, coal tar, anthralin

systemic–> acitretin, methotrexate, cyclosporin, apremilast, biologicals (etanercept, infliximab)

102
Q

what is urticaria

A

chronic, spontaneous urticaria is defined by spontaneous eruption of wheals, angioedema or both for greater than or equal to 6 weeks

103
Q

how do you dx spontaneous urticaria

A

history–> transient (less than 24 hours), erythematous, pruritic plaques with central pallor

can have both acute lasting less than 6 weeks, and chronic, lasting more than 6 weeks.

104
Q

major causes of acute urticaria

A

drugs
food
infectious (URTIs)
no good explanation

105
Q

major causes of chronic urticaria

A

no good explanation or inducible (reaction to vibration, exposure to cold, aquagenic, dermatographism)

106
Q

are labs helpful in dx of urticaria

A

not really

107
Q

when should you refer patient with urticaria

A

individual lesions are lasting more than 24 hours or leave discolorations –> bruise-like is urticaria vasculitis, may indicate underlying lupus disorder

suspect drug or food cause

if associated arthritis or arthralgia

fevers

not responding to tx

108
Q

treatment for urticaria

A

first line–> ANTIHISTAMINES

omalizumab

cyslosporine

monelukast

methotrexate

caution systemic corticosteroids in urticaria

109
Q

what is dermatophytosis

A

fungi in skin

3 genera of fungi–> trichophyton, epidermophyton, microsporum

110
Q

treatment of tinea corporis

A

terbinafine 1% daily for 14 days or terbinafine 250 mg po daily for 28 days

111
Q

appearance of tinea corporis

A

plaques with central sparing with scale

112
Q

how are the dermatophytoses names

A

by location:

capitis
faceie
corporis
cruris
pedis
ungium
incognito
113
Q

management of dermatophytosis

A
  1. confirm presence of dermatophyte before tx
  2. keep area clean and dry
  3. look for potential sources
  4. topical antifungals
  5. systemic antifungals (rarely needed)
114
Q

what should you avoid in the treatment of dermatophytes

A

corticosteroids

lotriderm

kenacomb

triacomb

viaderm KC

115
Q

treatment for scabies

A

5% permethrin cream applied from the neck down covering entire body, then again in 7 days

116
Q

can pregnant women use permethrin to treat scabies

A

yes

117
Q

why do people with scabies get itchy

A

delayed type (2-6 weeks later) hypersensitivity reaction

can control with corticosteroid cream after treatment

118
Q

what should you use to treat a 15 year old with scattered comedones

A

0.01% tretinoin cream applied to entire affected area at bedtime

119
Q

what should you use for 25 year old male with inflamed papules, scattered comedones but no scars

A

minocycline 100 mg x 6 weeks + 0.01% tretinoin cream to face at night

120
Q

what to look for when assessing melanoma

A

ABCDE

asymmetry
border 
color 
diamete
evolution/enlargement

*look for the ugly duckling that is different from the rest of the moles

121
Q

risk factors for melanoma

A

personal history of melanoma

family history of melanoma or atypical nevi or pancreatic cancer

increased number of typical or atypical nevi

blistering sunburns

tanning bed use

fair skin

blue or green eyes

red or blond hair

122
Q

what is the most important prognostic factor for melanoma

A

bresslow’s depth

123
Q

which radiographic tests have NO radiation

A

U/S

MRI

124
Q

which radiographic tests have very very little radiation

A

CXR, rand xray

125
Q

which radiographic tests have middle amount of radiation

A

pelvis xray
mammography
abdo CT
nuclear med bone scan

126
Q

which radiographic tests have moderate to high radiation

A

abdo CT without and with contrast

whole body PET

127
Q

which radiographic tests have the highest radiation

A

CTA chest, abdo, pelvis with contrast

transjugular intrahepatic portosystemic shunt placement

128
Q

is xray one of the recommended imaging modalities for aortic dissection to rule out other etiologies?

A

yes–because you can get it quickly, as long as it wont cause delay in CT or MRI. wont necessarily dx aortic dissection but may ID other things causing the pain

129
Q

what is the definitive test to dx aortic dissection

A

CT angio

130
Q

what is the most appropriate radiographic test for PE?

A

CXR is good for quick screening study

CT angiogram is definitive study

(VQ scan still appropriate and well rated, depending on the circumstances, ie those with impaired renal function or allergy to IV contrast)

131
Q

what if a patient with suspected PE is pregnant–what radiographic tests do you do

A

CXR + doppler U/S of legs

**may be an initial test prior to CTA that may prevent the need for ionizing radiation in the appropriate clinical setting

*if doppler was negative, may have to consider whether to do CTA or VQ–if positive, DVT tx is the same at PE so treating anyway

132
Q

what are the most appropriate radiographic tests in the setting of trauma with a patient who is STABLE

A

CT abdo and pelvis with contrast

CT chest with contrast

133
Q

what are the most appropriate radiographic tests in the setting of trauma with a patient who is UNSTABLE

A

CXR

Abdo XR

US FAST scan

  • because they can be done faster usually
  • will depend on location–> local pattern of practice at VGH etc is to do CT for both stable and unstable patients
134
Q

most appropriate radiographic test for head trauma, GCS 8

A

non con CT head

135
Q

when should you give contrast in head CTs

A

to look at/for:

vascular structures
tumours
sites of infection

136
Q

common indications for head CT

A
  1. cranial facial trauma
  2. acute stroke
  3. suspected subarachnoid or intracranial hemorrhage
  4. evaluation of headache with any kind of sensory or motor function loss
  5. evaluation of sensory or motor function loss
  6. evaluation of sinuses
137
Q

what 3 windows are commonly used in CT head

A

brain

bone

subdural

138
Q

what should you think when you see a midline shift on CT head

A

mass effect

139
Q

what are signs of acute infarct on head CT (less than 3 hours)

A

hyperdense MCA sign

loss of grey-white differentiation (because cells start to swell without blood supply) –> FIRST CT SIGN OF ACUTE INFARCT

**CT not best modality for acute infarct but in BC we depend mostly on CT

140
Q

what is the best imaging method of acute brain infarct

A

MRI

141
Q

what are the signs of chronic infarct on CT

A

retractment of parenchyma from skull due to atrophy

focal area of hypodensity indicates encephalomalacia

mild midline shift TOWARDS the lesion might occur due to atrophy

142
Q

what vessels are implicated in subdural hematoma

A

tearing of bridging veins

143
Q

in what context do you see subdural and epidural hematoma

A

TRAUMA only

epidural–> skull fractures

144
Q

what does subdural hematoma look like on head CT

A

crescent shape along brain surface

CAN extend across suture lined

145
Q

what vessels are implicated in epidural hematoma

A

rupture of middle meningeal artery

146
Q

what does epidural hematoma look like on head CT

A

bi-convex, lenticular shape

does NOT cross suture lines

147
Q

in what context does a subarachnoid hematoma occur

A

in trauma AND spontaneously (thunderclap headache from ruptured aneurysm)

148
Q

what does subarachnoid hematoma look like on head CT

A

look for evidence of convexity in the sulci, blood in the ventricles and blood in the cisterns

radiologist must comment on where the blood is to help the neurosurgeon

149
Q

complications from subarachnoid bleed

A

hydrocephalus–> blood blocks drainage of CSF

infarction–> constriction of blood vessels from mass effect

herniation–> from mass effect

150
Q

when do you start folic acid supplementation in pregnancy and how much do you give

A

1 g standard

high dose (4-5 g) for those women with pre existing med conditions or who are on other meds

start 1-2 months before conception

151
Q

what potential genetic problem might you anticipate in a chinese mom/dad

A

hemoglobinopathy

152
Q

are most vaccines safe to give in pregnancy

A

yes

**except for live vaccines like rubella and varicella, which you should do before pregnancy

153
Q

what needs to be addressed at the first prenatal visit

A
  1. age at EDD–> for abnormality screening
  2. ethnic origin–>this of genetic screening for conditions
  3. past obstetric history
  4. confirm dates (early dating U/S and date all pregnancies by first U/S)
  5. general med history
  6. specific questions–> STIs (ask about genital herpes specifically because of congenital infection), chicken pox (if unsure, order serology)
  7. history of mental illness
  8. pre pregnant BMI (height and weight)
  9. general physical exam including BP!!! and swabs/cervix cytology
  10. referral to prenatal genetic screening (i.e down syndrome)–check guidelines because they change a lot
  11. standard pre natal lab work
154
Q

what populations are at high risk for thalassemias (beta type)

A

mediterranean

african

155
Q

what populations are at high risk for thalassemias (alpha type)

A

chinese

156
Q

who are the only people NOT at risk for hemoglobinopathies

A

japanese

koreans

caucasians of northern european ancestry

first nations

inuit

  • means that most women should be screened with a hemoglobin electrophoresis because of mixed ancestry etc
  • if moms is normal then can stop there–if hers is abnormal, screen dad –> if both carriers, refer to medical genetics
157
Q

if mom has history of herpes, what should you do in pregnancy

A

start prophylactic acyclovir in third trimester to protect baby

158
Q

what is the standard pre natal lab work

A

CBC

group and screen

antibody titres

Urine cx

serology rubella/varicella

HIV test

syphillis

hep B

159
Q

what is the most important investigation done at every pre natal visit

A

BP

160
Q

what is important about symphyseal-fundal height measurements?

A

the trend over time (not individual measurements) –ie if baby stops growing

161
Q

in a pregnant woman (over 20 weeks), normal detailed U/S, presenting with pelvic pressure and a little bit of bleeding, what do you need to rule out

A

do speculum exam to rule out cervical insufficiency

*often these cases are misdiagnosed at UTIs based on abnormal urinalysis, but MOST pregnant women have abnormal UAs–> ALWAYS EXAMINE CERVIX

162
Q

what should you do in the case of cervical insufficiency

A

rule out chorioamnionitis and progressive labour

discuss with patient the high risk of losing the pregnancy/ delivering right now

refer immediately to OBSGYN or MFM specialist for consideration of an emergency cerclage

163
Q

what must you NOT do before doing the fetal fibronectin test

A

do NOT digitally examine the cervix–must have been nothing in the vagina for 24 hours prior to taking the fetal fibronectin sample

164
Q

define pre termlabour

A

regular contractions with

  1. cervix that is OPEN at 3 or more cm
    - or-
  2. progressive cervical changes
165
Q

how useful is the fetal fibronectin test

A

negative fFN has a NPV above 95% for delivery within the next 7-14 days (PPV only at 30%)–so a negative fFN helps rule OUT labour (but not rule it in)

should be sent once you know the membranes arent ruptured and cervix is not dilated

166
Q

what if a woman is in preterm labour–what do you do?

A
  1. steroids to enhance fetal lung maturity –> this has really improved fetal survival in preterm labour
  2. prophylactic antibiotic to prevent neonatal GBS infections (IV pen G)
  3. tocolysis with nifedipine or indomethacin (only helps us to get the steroid benefit, that little bit of extra time… or time for transfer to higher level of care/ acceptable nursery)
167
Q

woman at term pregnancy presents with a headache–most important thing to do?

A

BP–severe headache always worrisome for gestational hypertension and preeclampsia

*can present postpartum as well!!

168
Q

definition of gestational HTN

A

dBP above 90 based on 2 measurements taken using the same arm more than 15 min apart

HTN that developed at 20 weeks or later

severe HTN is sBP above 160 or dBP about 110–> MEDICAL EMERGENCY patient is at risk of stroke!!

169
Q

how to you dx. preeclampsia

A

NEW high BP and proteinuria or more than one other “bad thing”
-or-
if pre existing HTN existed, then it is resistant HTN, new or worsening proteinuria, or 1 or more other “bad things”

170
Q

maternal signs/sx of preeclampsia

A

persistent or new/unusual headache

visual disturbance

persistent abdo or RUQ pain

severe nausea or vomiting

chest pain

dyspnea

peripheral edema

labs:
increased Cr (normally around 50 in pregnant women)
increased ALT, AST or LDH
low platelets 
albumin under 20
171
Q

fetal signs/sx of preeclampsia

A

oligohydramnios
IUGR
absent or reversed end-diastolic flow on umbilical artery doppler
intrauterine fetal death

172
Q

how do you manage pre-eclampsia if 37 weeks or over

A

deliver baby (even if only mild preeclampsia)

173
Q

how do you manage preeclampsia if gestation under 37 weeks and: MILD preeclampsia

A

mild = no adverse conditions

consider conservative management with very close monitoring (NST 3x/week and blood work 2x/week)

174
Q

how do you manage preeclampsia if gestation over 34 weeks and severe

A

DELIVER

175
Q

how do you manage preeclampsia if gestation under 34 weeks and severe

A

conservative management with very close monitoring in hospital can be considered in certain circumstances

MFM consult recommended

176
Q

what is the most important/immediate issue in the management of eclampsia

A

it is crucial to stabilize the mother before proceeding to delivery

in a medical emergency in a pregnant woman, the most important thing you can do is LOOK AFTER THE WOMAN

even if maternal seizures are often accompanied by a fetal bradycardia due to maternal hypoxia, an immediate C section is inappropriate as it would be unsafe for the mother

177
Q

list good choices for anti-HTN therapy in pregnant women

A

labetalol

hydralazine

178
Q

what should you NOT use to manage HTN in pregnant women

A

ramipril (baby cant handle it)

179
Q

immediate management of eclampsie in women

A

ABCs

have mother lying on either side or wedged to the left side

padded bed rails to prevent taruma

supplemental oxygen

treat convulsions with IV MgSO4

treat HTN with IV labetalol (better) or IV hydralazine

180
Q

how do you treat seizures from eclampsie

A

MgSO4 IV

181
Q

which tests help you diagnose HELLP

A

CBC
liver enzymes
bilirubin
peripheral blood smear

182
Q

what is HELLP

A

a severe form of preeclampsia in which women present with:

Hemolysis
Elevated Liver enzymes
Low Platelets

pathogenesis unclear but may be related to abnormalities in placental development

up to 20% of patients do NOT have associated HTN or proteinuria

183
Q

what are the diagnostic criteria for HELLP

A

platelets 100 or lower

total bilirubin 20 or higher

AST 70 or higher

peripheral smear showing characteristics of microangiopathic hemolytic anemia (schistocytes)

184
Q

potential complications of HELLP

A

DIC

placental abruption

acutre renal failure

pulmonary edema

subcapsular liver hematoma

detached retinas

185
Q

what is the definitive treatment for HELLP

A

delivery

*NO role for expectant management in a pregnant woman with HELLP–patients require stabilization and delivery

186
Q

first test in bright red vaginal bleeding in 32 week pregnancy with NO PREVIOUS PRENATAL CARE

A

ultrasound –find out where the placenta is before doing digital exam

187
Q

how do you diagnose placenta previa

A

transvaginal U/S is gold standard

low lying placenta is less than 20 mm from internal cervical os

placenta previa is overlying the cervical os

188
Q

classic presentation of placenta previa

A

painless vaginal bleeding

189
Q

management of placenta previa with acute bleeding or contractions

A

ABCs

large bore IV access

CBC, type, G + S and cross match

coagulation profile

monitor FHR, maternal vitals

deliver via section if severe hemorrhage and/or abnormal FHR

190
Q

most common cause of third trimester bleeding

A

bloody show associated with labour

191
Q

what are the most IMPORTANT causes of third trimester bleeding

A

placenta previa

placenta abruption

192
Q

what are some other causes of third trimester bleeding

A

vasa previa

cervical polyp or ectropion

cervical cancer

genital tract trauma

193
Q

signs and symptoms of placental abruption

A

VAGINAL BLEEDING

ABDOMINAL PAIN

uterine tenderness

abnormal FHR

preterm labour

high frequency contractions

uterine hypertonus

IUFD

maternal hypovolemic shock

abnormal bleeding, DIC

194
Q

risk factors for placental abruption

A

previous abruption

HTN

trauma

cocaine

smoking

multiple gestation

PPROM

chorioamnionitis

195
Q

how do you diagnose abruption

A

CLINICALLY

no single diagnostic test

high index of suspicion in:

  • abdo pain and/or bleeding
  • trauma
  • otherwise unexplained pre term labour

external bleeding not necessary for diagnosis

lab findings may support dx

196
Q

potential complications from severe abruption

A

preterm delivery

severe hemorrhage

maternal shock

DIC

couvelaire’s uterus

need for blood transfusion

renal failure

hysterectomy

fetal or maternal death

197
Q

first stage of labour

A

onset until full cervical dilation

latent and active phases

198
Q

second stage of labour

A

full cervical dilation until delivery of infant

199
Q

third stage of labour

A

delivery of infant until delivery of placenta

200
Q

fourth stage of labour

A

delivery of placenta until 1 hour post partum

201
Q

possible complications of oxytocin use to augment delivery

A

uterine hyperstimulation

water intoxication

uterine rupture

202
Q

most important test in post menopausal bleeding

A

endometrial biopsy

203
Q

risk factors for endometrial cancer

A

obesity

DM

hx PCOS

late menopause

history of infertility

LYNCH syndrome

tamoxifen use

HRT with unopposed estrogen use

hx endometrial hyperplasia

204
Q

treatment for trichomonas

A

metronidazole 2 g PO single dose

same as BV… can also do 500 mg PO BID

205
Q

how does trichomonas appear on wet mount

A

multiple mobile flagellated organisms

206
Q

outpatient management of PID

A

ceftriazone 250 mg IM single dose PLUS doxycycline 100 mg PO BID for 14 days

-or-

oral cefixime 800 mg PLUS doxy

207
Q

what is the risk of infertility with PID

A

one episode–increased risk of infertility of about 15-20%

PMP (9 decks)

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