Wk 5 Flashcards

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1
Q

What are changes of the kidney w aging

A

Glom changes…. Sclerosis obsolescence (can vanish)
Interstitial fibrosis
Tubular atrophy secondary to reduced tubular volume and length.
Thickening of basement membranes
Arteriolar hyaline sis, fibro elastic hyperplasia.

Too much red!

Grossly:
Cortical thinning, smaller kidney size

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2
Q

Changes in fcn of kidney w age

A

Dec renal blood flow, grr, tubular NA reabsorption, K excretion (ie because less Na getting to distal tubule, also bc in part due to low renin and aldosterone levels)…. Edema, HTN,
Urineary concentration and dilution.

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3
Q

Kidney status dictated by

A

Urine sedimentation. Urinalysis w urine protein and casts etc. eGFR and serum Cr (not just function, which is via eGFR and Cr)

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4
Q

New eGFR categories? For chronic kidney dz

New albumin categories?

A

G1, G2, G3a and G3b, G4, G5

It is important to remember is pt in steady state or not… GFR is applicable to CKD.

A1-A3.. Low grade to high grade.

Use CKD epi formula

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5
Q

What are the main causes of CKD in the elderly ? 10% of population, most is mild or mod,

A

Primarily HTN +/- ischemic nephrosclerosis

  • diabetic nephropathy, cardio renal syndrome
  • renal vasculitis syndromes also more common.
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6
Q

Mgmt of CKD in elderly

A

Treat BP, DM, underlying conditions…. Don’t necesaRily want to be aggressive though. Bc ortho hypotn risk. Hypoglycemia risk, renal artery stenosis.

Minimize risk for AKI… Harm reduction
- w/d or with holding aceis and arbs.
Avoid NSAIDS
Avoid ECFV depletion (present early if volume depleting illness!

Serial lab monitoring: serum Cr, eGFR, electrolytes, Hgb, minerals, PTH, U/A, urine ACR.

adjust really eliminate medications. Risk of metformin due to lactic acidosis…. Don’t give if

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7
Q

Insults on kidney?

A

Dec pressure on outgoing side by blocking angio tension 2 At efferent.
Prostaglandin inhibitor ie NSAID or cox2 inhib reduces renal blood flow and GFR
DiureticS And dec volume status…
Triple whammy to kidney

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8
Q

NSAIDS effect on kidney

A

Sodium retention and htn
AKI, hemodynamically mediated.
- Ranges from reversible to necrosis

Acute or chronic interstitial nephritis (analgesic nephropathy)
Concentration in papilla… Die, slow, painful gross hematuria. Papillary necrosis.
Glomerulonephritis

Hyperkalemia

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9
Q

What are reversible factors

A

Acute illness, CHF, I’m, pna, ce
Lolita’s, gout flare, gastroenteritis, food poisoning
Vol- dep,eating diuretics

Meds: NSAIDS, ace ARB, aminoglycosides, uv contrast dye, Otis.

Obstruction- abdo ultrasound indicated if

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10
Q

What is mortality in hospital if dialysis started?

A

RRT up to 50% in hospital, not ,ugh diff in younger ppl.

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11
Q

What are components of high morbidity in dialysis?

A

Hypotension, falls, access, infections.

Candidacy probably best based on baseline fcn status / comorbid it’s burden.

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12
Q

Gfr declines with as due to

A

Neohrosclerosis

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13
Q

When to stop the ACEi when it becomes effective and changes to detrimental

A

No set value, depends on clinical picture. Some benefit up to gfr of 15

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14
Q

What does it mean for a drug like phenytoin to be a zero order drug?

A

Zero order drug means half life changes with dose and will be about 85% of steady state at 7 days. Draw within first couple days to get an idea of if you are in therapeutic window. set amount cleared over time independent of amount in body. Therefore half life is always changing depending on how much drug is in there. So if you give high amounts that saturTe tissues, then small dosage apchange wpcan sky rocket.

Vs 1st order…. Eliminated based on fraction (ie percentage per unit time) in body. This is how we get half life…. Think usually 5-6 half lives will eliminate from body.

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15
Q

Why must phenytoin be given at 50 mg/min max?

A

Risk of faster infusion is hypotension and cardiovascular collapse because of propylene glycol.

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16
Q

Why does albumin level matter with phenytoin?

A

Phenytoin is hig,y protein bound, as are most meds.
Usually is 90% bound to proteins so 10% is free and active.

If low albumin ie 44, then not enough binding. Total concentration is same (think its happy because in range), but if albumin super low then may actually be toxic and therefore must correct for amount of free drug.

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17
Q

What is the difference between high dosing extended interval HDEI vs traditional?

A

Aminoglycosides are concentration-dependent killing drugs. So giving more bang for buck. (As is Fluoroquinolones… Therefore can dose adjust to 500 once a day instead of 250 bid)

Vs traditional which is less at higher freq.

With huge peak, killing more
Also post-antibiotic effect … High conc penetrates inside cell and this can’t measure in plasma but is still acting while giving …. So eliminates quickly because 1st order kinetics…. Therefore by 18 renal has cleared out and now toxicity- free period for organs to rest while ears and kidney relax.

Saturable uptake…. Constant bathing of cells in gentamycin. Vs high peak which eliminates and gives free period w no bathing kidneys and ear.

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18
Q

Why is CKD a contra to gentamyinc HDEI? Ie exclusion Criteria

A

Bc doesn’t eliminate fast enough and builds to way higher levels over time.
Therefore majority of time don’t give to elderly bc inherent true fcn of kidneys not as good (even if Cr looks pretty good, half life is still going to be higher.)
(>75 yo)

Always want to have measurable trough level so organ is always bathed in antibiotic,.
Abn body comp ie burns, morbid obesity.
Neutropenia, meningitis. Endocarditis etc.
Ascite cf, cirrhosis,

Surgical prophylaxis…. Use conventional dosing.
When used for synergy ie endocarditis.

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19
Q

Should you do a post level for aminoglycosides?

A

No, just do pre-level if you are to measure anything. Should be 0 in blood for 18-24 hours but dont actually need to measure this. Bc if you think they are accumulating then just switch to traditional. If higher, then swap to traditional dosing. If you think renal function is suspect, just switch to traditional dosing

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20
Q

What is aminoglycoside dosed based on?

A

Lean of ideal body weight…. Extra body weight metabolizes drug differently.
This is aminoglycosides- specific.
Must compare IBW w actual BW.

Need to use dosing body weight (IBW + (0.4 x (adjusted body wt - IBW)

Multiply DBW x dose (6 mg per kg)

Round to administerable dose.

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21
Q

Conventional ordering of aminoglycosides

A

Pre and post 3rd.
When > 5 days
Elderly, 65-74 yrs.

Don’t need to orde routine serum peak and trough concentrations in HDEI

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22
Q

What to monitor patient for?

A

Vertigo, tinnitus, pressure fullness in ear, diplopia, pain, new onset hearing loss. Esp if > 5-7 days. Ie 4 wks for osteomyelitis.

Therapeutic drug monitoring and keeping in target range can still cause oto/vestibular toxicity.

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23
Q

What are constipation get meds?

A

Opioid (senekot is first line, this is a stimulant so reversing opioid action) anticholinergics, ondansetron, iron.
Osmotics : use PEG 3350
Rwctal tx: docolax

Also can use: peripheral mu receptor antagonists…. Methylnaltrexone. Don’t use if obstructed, is expensive,

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24
Q

How to treat n and v?

A

Target the pathophys that feed to the integrative vomiting centre.

  1. Drugs (chemo, opioids, dig), biochemical ie uremia, electrolytes, hyperCa, toxic (radiation, emetogenic peptides)
  2. GI tract vagal - distension… Over eating gastric stasis, mass, obstruction, constipation, chemical irritants (blood, drugs)
  3. Cerebral- high CNS..l.msensory,
  4. CHECK OUT SLIDES!!!!
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25
Q

What is integrative vomiting centre stim’d by?

A

N predom, not relieved by vomiting.
Common in pall care.

Vomiting:
Chemoreceptor trigger zones
GI tract…. Vagal

Nausea:
Cerebral- high CNS
Vestibular
Inc ICP

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26
Q

What are clues that the chemoreceptor zone is predominantly being stimulated?

A

It is nausea predominant, and not relieved by vomiting. Sights and smells may aggravate.
Chemical/metabolic causes is majority.

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27
Q

What are drugs of choice for sx modification of dyspnea?

A

Opioids.
At appropriate doses, does not affect oxygen nor carbon dioxide levels.
If severe or in crisis, sc

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28
Q

Incident dyspnea:

A

Ultra short acting opioids pre activity ie fentanyl sufentanil if opis tolerance
TDropper under tongue.

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29
Q

When to use Benzos for end of life suspension?

A

Anxiety or panic crisis. SL, sc.

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30
Q

What is ddx for delirium

A

I WATCH DEATH
infection i.e. UTI, sepsis, ammonia
Withdrawal i.e. alcohol, benzodiazepine
Acute metabolic i.e. hypercalcemia, paraneoplastic disorder, electrolyte disturbance, hepatic failure and renal failure
, I.e. closed head injury, heatstroke, Severe burns
CNS apology by the tumors, Mets, abscess, syphilis, enkephalin just come in meningitis
Hypoxia IT anemia, hypertension, pulmonary or cardiac failure
Deficiencies I even be 12, fully, niacin, diamond
Discomfort i.e. pain, constipation, urinary retention dehydration
Endocrine up with these i.e. hyper or hypoadrenocorticalism, hyper hypo glycemia, thyroid, parathyroid disorders
Acute vascular i.e. hemorrhage, stroke
Toxins drugs i.e. benzo’s, opioids, anticholinergics, steroids in line heavy metals I eat lead

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31
Q

Treatment of delirium

A

Methotrimeprozine or Seroquel for Lewy body or Parkinson…. Don’t use haldol.
Rest can get antipsych and benzos (Note that benzodiazepines may aggravate especially in the elderly… Also can use midaz infusion when severe and end-of-life
Phenobarbital if end of life and refractory

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32
Q

What are end of life care orders to anticipate?

A

PPS 20 or Less
PRN antipsychotic for delirium, restlessness
Prn benzo for refractor ry restlessness.
Check out rest of slide!

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33
Q

Kidney biopsy assess what?

A

Glomeruli, interstitium, tubules, blood vessels.

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34
Q

How to treat resp secretions? Primary

A

Atropine (crosses BBB)
glycopyrrolate, buscopam (don’t cross BBB)

Don’t do suction, irritates.

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35
Q

For secondary resp secretions?

A

Ie don’t

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36
Q

Why use qduitiapine, nozinan, olanzapine as these are dirtier , less da selective.

A

Bc will be mild and easier on elderly vs eps stimulating.

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37
Q

What is a key rule of cmpa?

A

Relationship of trust based on fiduciary relationship. Docs must act in good faith and demonstrate loyalty toward the patient, never placing their personal interest ahead of the patient’s.

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38
Q

What does pharmacokinetic mean?

A

What body does to drug…. ADME. Absorption,

Metabolism systems that are important:
Cytochrome P450
Transport proteins

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39
Q

Pharmacodynamic means?

A

What drugs do to body. More common. 3/4s of interactions

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40
Q

What CYP 450 system isoenzyme has many polymorphisms?

A

2D6… Therefore can have a lot of variability in how people metabolize this.

LOOK UP SLide!,

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41
Q

What re most common transport protein systems?

A

P-glycoprotein

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42
Q

What is febrile neutropenia in the ped pop considered? What is the defn

A

Medical emergency

> 38.5 once or > 38 twice

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43
Q

What is the defn of opioid experienced?

A

equivalent of 60 mg per day.

co2 inc a bit, resp rate Down a bit. Tidal volume inc though so oxygenation is unchanged.

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44
Q

What are the two types of adverse drug events

A

Type a: most common, dose-dependent, predictable as it follows pathophysiology

Type b: less common, not dose-dependent, and less predictable. Hypersensitivity and idiosyncratic

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45
Q

What are 4 categories of pharmacokinetics w aging

A

1)
Absorption (minor)
- inc gastric ph
- dec SA

Distribution

  • rescued total body water… Decreased Vd for hydrophilic drugs and increased free blood levels.
  • reduced lean body mass (increased fat)- increased Vd for lipophilic drugs and inc T1/2.

Diazepam is very lipophilic and therefore residu effect lingers on. Vd inc w aging thus inc T1/2

2) SLIDE

3) metabolism
- dec hepatic mass
- reduced metabolism (phase 1 only; phase 2 unchanged)

4)

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46
Q

How is phenytoin handled differently in older people that predisposed them to toxicity?

A

Dec phase 1 metabolism in liver

(Redox) which is less efficient imaging.

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47
Q

What is albumin effect in aging?

A

Albumin dec w age, or if acute phase reaction leads to inc in unbound phenytoin.

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48
Q

Why does metoprolol not effectively lower bp in elderly.

A

Down reg of beta receptors and or reduced post receptor effect hence dec sens to beta blockers w aging.

Consider switching to another hypertensive.

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49
Q

What is an atypical presentation of ADR dddx?

A
dementia 
Delirium 
Depression
Drugs
DiZZY
FALLS AND immobility
Incontinence
Homeostatic disturbance
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50
Q

What are drugs that interact w digoxin?

A
Amitrip + dig = delirium
Amitrip + codeine = constipation
Naproxen + ibuprofen = htn
Tylenol + amitrop = hepatitox 
NSAID + dig = renal tox and reduced dig clearance
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51
Q

What does the prescribing cascade entail?

A

Drug is given to manage the s/e of another drug.

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52
Q
Alzheimer's + lorazepam = 
Alzheimer's + ranitidine = 
AD + risperidone = 
Copd + lorazepam
Pud + NSAIDs
A
Delirium
Delirium
Minor eps 
Profound co2 retention bc resp dep. blunts drive to breath long term 
Bleed
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53
Q

What is entacopone

A

Prevents NT breakdown… Inhances is DA levels. Is in Sinemet

Can augment l dopa

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54
Q

If there is one intervention to inc med compliance in elderly, what is it?

A

Telephone call. NNT 16

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55
Q

What is pseudohypertension?

A

The blood vessel wall becomes more rigid and less elastic with aging because of hyaline degeneration and endothelial hyperplasia. Hemodynamically this increases the impedance to bloodflow. This phenomenon is for the exaggerated by the presence of atherosclerosis. As a result blood pressure measurements in the elderly maybe overestimated . clinical detection supported by positive oslers sign

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56
Q

What is Oslers sign?

A

Palpable brachial artery wall when blood pressure cuff inflated above systolic blood pressure with disappearance of korotokoff 1 sounds

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57
Q

Is orthostatic hypotension a normal part of aging?

A

Very common but not normal

Done immediately after and 3 mins after

Do routinely after 65.

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58
Q

What is sequence to dec meds of lorazepam, citalopram, diltiazam and metoprolol?

A

Do it with littlest use and greatest potential dec in effect of hypotn.
L then d then m then c

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59
Q

Which is most predictive of aortic valvular stenosis?

A

d answer. Inc aortic vent pressure gradient.
Gold stand echo or Angio inc pressure grad
Dec x sec ao valve area

Other: narrow pulse pressure
Pulses parvus et tardus- uncommon in elderly due to rigid carotid artery wall.
- intensity and pattern of radiation of murmur not helpful

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60
Q

What aging process can inc the likelihood of chf?

A

Inc oxidative stress in myocytes, dec cell renewal capacity, accumulation of wastes in myocytes increases risk of apoptosis.

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61
Q

What happens to beta receptors and post receptor effects in aging?

A

Down regd and reduced

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62
Q

What is the picture of thyrotoxicpsis in elderly?

A

They look hypo…. Apathetic thyrotoxicosis

Palpa, tremor, diarrhea, depression anxiety, delirium, fall

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63
Q

What can be a complication of spironolactone use in elderly?

A

Hyperkalemia. Potassium sparing diuretic
Negates aldosterone effect
Has show survival benefit i class iv : refractory heart failure. Usual dose 25-50 mgbid
Each: qrs lengthens pr lengthen tenting of t waves. Then sinusoidal. Then vf.

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64
Q

What does calcium gluconate do in hyperK?

A

Nothing to K, stabilizes the heart

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65
Q

Normal axis on ecg?

A

Two thumbs up of major qs In V1 and V2

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66
Q

Qt interval rule

A

Look up

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67
Q

Early repolarization on v1 and v2

A

Look up

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68
Q

What to use for Lewy body dementia delirium

A

Quetiapine

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69
Q

Look up bs benzos vs antipsychotic

A

Mao benzos exacerbate delirium?

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70
Q

What are 2nd line for end of life dyspnea?

A

Benzo ie Midaz

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71
Q

What is black box warning above 12 wks of maxeran?

A

Tardive dyskinesia black box warning.

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72
Q

What is the moa of zofran?

A

Serotonin

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73
Q

At end of life what to do to get Ng tube out?

A

Octreotide and steroids.

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74
Q

At end of life in home, what is logistical?

A

Bc no cpr form
Home care nurse- call them. Pronounced .
Notification of expected death… Person who takes responsibility for body post mortem. SIgns on later. Then 24 7 funeral home will come.

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75
Q

What are organic etiologies that can lead to. Picture of MDD and should be ruled out?

A

v: stroke
n: neoplasm
D: beta blockers, levodopa, corticosteroids.
Degen: Parkinson’s
Intox: alcohol
E: hypothyroidism and Cushing dz

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76
Q

In the acls adult tachycardia algorithm, with a wide QRS (>.12) when to use adenosine?

A

Only if regular and monomorphic ecg
- can also use if regular narrow and there are signs and symptoms of instability including hypotension, acutely altered mental status, signs of shock, ISCHEMIC chest discomfort, or acute heart failure.
Dosing: first dose 6 mg rapid IV bolus, follow w NS flush.

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77
Q

What are options for treatment if stable wide-QRS tachycardia?

A

Consider adenosine only if regular and monomorphic. Otherwise:
PAS
1. Procainamide: 25-50 mg/ min until arrythmia suppressed, hypotension ensues, QRS inc > 50%, or max dose 17 mg/ kg reached.
Maintenance infusion 1-4 mg per min
2. Amiodarone IV
1st dose: 150 mg over 10 min
Repeat as needed por if VT occurs.
Maintenance infusion of 1 mg/min for first 6 hours.
3. Sotalol
IV dose 100 mg over 5 min

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78
Q

What is initial and maintenance procainamide dosing?

A

25-50 mg/ min until arrythmia suppressed, hypotension ensues, QRS inc > 50%, or max dose 17 mg/ kg reached.

Maintenance infusion 1-4 mg per min

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79
Q

When to avoid using procainamide?

A

Avoid if prolonged QT or CHF.

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80
Q

What is amiodarone dosing?

A

1st dose: 150 mg over 10 min
Repeat as needed por if VT occurs.
Maintenance infusion of 1 mg/min for first 6 hours.

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81
Q

What is sotalol dosing?

A

Sotalol IV 100 mg over 5 min

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82
Q

When should Sotalol be avoided?

A

If long QT.

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83
Q

For adult bradycardia that is persistent and causes hypotension, acutely altered mental status, signs of shock, ischemic chest discomfort, and acute heart failure, what can be administered?

A
1.Atropine first dose 0.5 mg bolus repeat q3-5 min to max of 3 mg.
If atropine ineffective, 
2. Transcutaneous pacing, or
3. Dopamine infusion IV
2-10 mcg / kg per min, or
4. Epinephrine infusion IV
2-10 mcg per min

And consult cardio to consider transvenous pacing.

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84
Q

What is atropine dosing for Bradycardia

A

Atropine first dose 0.5 mg bolus repeat q3-5 min to max of 3 mg.

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85
Q

What is dopamine dosing for bradycardia refractory to atropine w no transcutaneous availabke?

A

Dopamine infusion IV

2-10 mcg / kg per min

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86
Q

What is epi dosing for Bradycardia?

A

Epinephrine infusion IV

2-10 mcg per min

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87
Q

What do acls guidelines recommend re precordial thump?

A

Precordial thump should not be used for unwitnessed out of hospital cardiac arrest.

May be considered in its w witnessed, monitored, unstable VT, including pulse less vt if a defib is not immediately available for use.

Should not delay cpr and shock delivery.
NNT 20
NNH 2-10

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88
Q

What proportion of the population have asymptomatic disc protrusion?

A

50%

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89
Q

What needs to be done to distinguish star from disc material on spinal MRI?

A

Contrast

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90
Q

What does the MRI signal so on degenerated disc disease?

A

Decreased signal

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91
Q

What are reasons for failed back surgery?

A

Post op scarring, recurring herniation, missed free disc fragments, infections

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92
Q

With regards to contour abnormalities of the spinal cord, what is a significant cause of back injury?

A

Annular tear. This shows increased MRI signal at periphery T2

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93
Q

What are the two types of nerves that are found at each disc space?

A

Each disc space has traversing and exiting nerve root.
Two nerves run across each disc level and only one exits the spine through the foramen at that level.

The exiting nerve root is the nerve root that exit the spine at the particular level. For example the L4 nerve root exits the spine at the L4 L5 level.
The traversing nerve root is another route that goes across the desk and exits the spine at the next level below. This is called the traversing nerve root. For example the L5 nerve root is the traversing never did at the L4 five level and is exiting the nerve root at the L5 S1 level

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94
Q

Explain what happens when the traversing nerve root is affected.

A

Lumbar radiculopathy. In the lumbar spine, there is a weak spot in the disk space that’s wise right in front of the traversing nerve root, so lumbar discs tend to herniate or leak out and impinge on the traversing air route. For example, a typical posterior lateral behind the disc into the side lumbar disc herniation at the 45 level often affects the nerves that traverses that level and exits at the L5 level.

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95
Q

When the exiting nerve root is affected, discuss what happens.

A

For example, cervical radiculopathy. The opposite is true in the neck. In the cervical spine, disc tends to her need to the side, laterally, rather than toward the back and side, post her laterally. If the disc material her needs to the side, it would likely compress the exiting nerve root. For example the C6 nerve root would be affected at the C-5 6 level because in the neck the exiting nerve root is named for the level below it.

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96
Q

Describe the four stages of herniation.

A

1) degeneration: disks begin to we can.
2) prolapse/protrusion: focal outpouching of nucleus pulposis
3) extrusion: implies disruption of posterior longitudinal ligament.
4) sequestration: free disk fragment, disruption of posterior longitudinal ligament

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97
Q

Name three causes of a tethered cord.

A

Scarring, lipoma, ependymoma.

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98
Q

What is the differential diagnosis of degenerative back pain.

A

Spondylosis: a bony defect in the pars interarticularis. This is due to separation of the lamina and inferior facet joints from the vertebral body
Disc herniation
spinal stenosis: abnormal narrowing of the spinal column
Foraminae stenosis: narrowing of the spinal foramen through which the spinal nerve exits

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99
Q

What is the theoretical belief behind cause of spinal spondylosis?
Where is this most common and who is it most common in?

A

It is believed to be due to chronic stress fractures.m common in L4/L5 in adolescents

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100
Q

Describe the approach to back pain regarding imaging

A

1 initially assessed nonspecific back pain with AP and lateral graphs.
2 CT or MRI if symptoms consistent with herniation.
3 CT for bony fractures, spinal canal compromise, disc herniation, fractures, osteomyelitis, local metastases.

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101
Q

What is the approach for lateral lumbar x-ray?

A

Three column model approach: this states that if any two columns are injured then the injury is unstable.
1 anterior: anterior longitudinal ligament – the anterior two thirds of the vertebral body.
2posterior longitudinal ligament – Posterior one third of vertebral body (middle column)
3 ligamentum flavum – posterior bone arch (posterior column) entailing the spinous processes and the interspinous ligament that connect them superiorly and inferiorly

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102
Q

What are key findings to look for on the lateral?

A

Height of vertebral bodies
Fragments of bone detach from
disc spaces for osteophytes

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103
Q

What is the approach for the AP view?

A

Owls head…each vertebra in the thoracolumbar column looks like an owl’s head. Eye represents pedicle, the beak represents sponge process

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104
Q

If there is greatly increased space between the pedicles, what does this signify?

A

The distance between the pedicles becomes gradually wider apart but if it is greatly increased then this is the burst fracture.

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105
Q

What does a winking Eye mean?

A

If there is a missing eye, so called the winking owl, this represents destruction of a pedicle and can represent metastasis.

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106
Q

What does a cracked eye represent on ap?

A

Chance fracture

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107
Q

What is the main purpose for the oblique view?

A

The oblique view of the spinal x-Ray is mainly used for evaluation of the pars interarticularis. This literally means space in between the joints.
The vertebra is described by appearance of the “ Scottie dog” You like the outline is formed by the vertebral arch is of the L spine

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108
Q

Do the parts of the Scottie dog represent?

A

Nose is the transverse process (ie going away from you behind the body), ear is the superior articular process, Eye is the pedicle, neck is the pars interarticularis (and very importantly, if there is a collar on the neck this implies pars interarticularis fracture), Front leg is the inferior articular process, the body is the lamina, the tail is the contralateral superior articular process, the rear leg is the contralateral inferior articular process.

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109
Q

Where would one find most fractures and disc related pathologies?

A

Fractures and disc related pathologies are more common in the lower thoracic and lumbar spine compare to the upper thoracic spine.… Most fractures occur at the junction between the immobile thoracic spine and the mobile lumbar spine

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110
Q

What is a chance fracture?

A

This is a severing of the vertebra horizontally.
It is characterized by transverse splitting of the vertebra and spinous process, often with associated rupture of the intravertebral disc. All three columns are involved.

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111
Q

What is the chance fracture usually due to?

Lateral and ap findings?

A

Typically it is because of hyperflexion/flexion-distraction injury. Often caused by’s lapbelt injury in MVA. these are associated with high force deceleration injury center most common at the thoracolumbar junction. They are unstable and carry a high risk of neurologic deficit and abdominal organ injury
It is also associated with intra-abdominal pathology.

The fracture line may pass through the disc rather than the vertebral body and therefore may not be visible bone injury on anterior column.

The AP view me show fractured pedicle on both sides of the vertebra, and also an increased interspinous distance between the spinous processes.

112
Q

What is a wedge fracture? Where Is it best seen?

A

This is a compression fracture of the enter vertebral body. Best seen on the lateral view

113
Q

What is a common mechanism behind the wedge fracture?

A

Typically due to anterior or lateral flexion.it is usually stable and not associated with neurologic injury.

114
Q

How many C-spine traumas are fatal percentagewise. How many are associated with spinal cord injury? What is the most common cause?

A

20%. Half Are associated with spinal cord injury. Motor vehicle accident is most common cause.

115
Q

What are the most common sites of trauma in C-spine?

A

C1-c2 and C5 to C7.

116
Q

What are the three standard views for C-spine plain radiography?

A

Lateral, AP, Odontoid- peg

117
Q

What warrants an inadequate study?

A

If any of the seventh cervical vertebra or the C7 to T1 junction is missing on the lateral and AP views

118
Q

What are the four lines that are drawn when interpreting cervical spine x-rays?

A

Anterior vertebral, posterior vertebral, spinolaminar, posterior spinous line. Any malalignment should be considered evidence of ligamentous injury or occult fracture and therefore C-spine immobilization must be maintained.

119
Q

What is the approach for the cervical neck spine x-ray

A

Abcs
Adequacy and alignment… The anterior line is the line of the anterior longitudinal ligament, the posterior line is the line of the posterior longitudinal ligament, the spinolaminar line is the line formed by the end of the spinous processes which extends from the inner edge of the skull
Bones… Vertebral bodies, facet joints if they are perched versus locked, the Harris ring (ring of corticated bone). Assess a odontoid peg for fracture.
Cartilaginous disc spaces… Each intravertebral disk space should be roughly equal anteriorly and posteriorly and widening so just vertebral compression.
Soft tissue : assess Prevertebral soft tissues

120
Q

What is a perched facet joint?

A

A perched facet joint is vertebral facet joint who is inferior articular process on one side appears to sit perched on the superior articular process of the vertebra below.
- any further anterior subluxation will result in this location… With one facet “dumping” over the other end becoming locked in this position. A locked facet joint is also known as a jumped facet joint.

121
Q

What are the maximum allowable prevertebral soft tissue distances?

A

C1 to C-3 is the retropharyngeal space and must be less than 7 mm. You like C4 to C7 is the retro tracheal space and must be less than 22 mm. This does not matter if the person is intubated.

122
Q

What does widening of the atlanto-dental interval suggest?

Distances?

A

This is the space between the ant arch of the ring and the dens. The transverse ligament lies behind the dens, spamming the lateral masses and attaching to them b/l
Less than 3 mm and adults is normal and less than 5 mm and children is normal.
If the Atlantodental interval is widened (which you can see on the lateral x-ray anteriorly between the dens and the anterior arch of ring), this suggests disruption of the transverse ligament

123
Q

What is the Harris ring?

A

This is a ring like density of the central portion of the body of C2 in an important radiological landmark. This so-called Harris ring is actually confluence of radiographic shadows from the superior articular facet of C2 superiorly, the posterior vertebral body line posteriorly, the transverse foramen inferiorly, and the anterior vertebral body anteriorly.

This ring is often disrupted in fractures through the body of C2, with a step in the ring evident. This is a type III Odontoid fracture.

124
Q

If the lateral view does not show the vertebrae down to T1 what additional views may be necessary?

A

then a repeat view with the arms lowered or a swimmers view may be required

125
Q

What is the primary purpose of the open mouth view?

A

Primary purpose is to view the lateral mass (processes) alignment. Is between C1 and C2
The distance between the Peg and the lateral masses of C1 should be on each side less than 2 mm. > 2 mm abn.

126
Q

What is the shape of the spinous processes in the c-spine?

A

Bifid. These should be in a straight line Nd the distance between the processes equal at all levels.

127
Q

What are fractures to look for in odontoid/ open mouth view?

A

Jefferson burst fracture of C1, dens fracture, avulsion of lateral masses of C1.

128
Q

What is the differential for flexion injury w forward bending of the head and neck in mid-sagittal plane?

A

Simple wedge fracture
Flexion teardrop
Odontoid fracture
Clay shoveler’s fracture.

129
Q

What is the flexion teardrop fracture?

A

This is due to hyperflexion of cervical region ie diving into Shallow water
Usually at C5.
Paraplegia in greater than 80%, completely unstable.
- Anterior vertebral body avulsion # (teardrop fragment)
- posterior vertebral subluxation or displacement
– spinous process fracture
- widened facet joint
– Prevertebral hematoma
– cord compression from fracture fragments or vertebral body displacement

130
Q

What is more unstable, a extension teardrop fracture or a flexion teardrop fracture?

A

Flexion

131
Q

Odontoid fracture types?

A

Type I- fracture of the superior odontoid
Type II- fracture through the base of the odontoid
Type III- fracture through base of odontoid into body of axis.

132
Q

What are usually the stabilizes of types I- III fractures?

A

I: rare, stable
ii: unstable, highest risk of non-Union
Iii: usually stable.

133
Q

What are Clay shovellers fractures?

A

Avulsion injuries of spinous process, due to mechanism of repeated forceful flexion assoc w shovelling.

134
Q

What is the DDx for midsagittal plane bending of head posteriorly, which is an extension injury?

A

Extension teardrop fracture

hangman’s fracture.

135
Q

What is the extension teardrop fracture?

A

Hyperextension may result in avulsion of the anterior corner of the vertebral body, most commonly on c2.
The anterior longitudinal ligament remains attached to the bone fragment which is separated from the vertebral body.

136
Q

What is the hangman’s fracture?
Cause?
What is seen on film?

A

Results from a high force hyperextension injury.
Fracture Involves b/l # of pedicles of C2 and often results in anterior displacement (spondylolisthesis) of the body and peg of C2.

Seen with hanging and in MVA when chin strike dashboard.
B/l pars interarticularis #s of c2, ant dislocation of cr vertebral body, prevertebral soft body swelling.

137
Q

What is the ddx for a rotational injury, Turning/ pointing head and spinal segments on vertical axis.

A

Unilateral facet dislocation.

138
Q

What are the ddx that entail a force extended down a vertical axis, resulting in a compression (axial load)?

A

Jeffersons fracture

Burst fracture,

139
Q

What is a Jeffersons fracture?

What is the rule of spence?

A

Burst fracture of the bony ring of C1.
Due to compression of cerv region from axial force on head vertex ie dive.
On film:
Displacement of lateral masses of c1 beyond margins of C2 body.

Rule of spence: A + B > 7 mm

140
Q

Burst fracture?
Cause?
Film?

A

Collapse of an entire vertebral body, usually extending into posterior elements.
Axial load to spine ie fall from height.
Lateral view: heights of the anterior and posterior vertebral body dec
Ap: widened interpedicular distance

141
Q

What is the big concern in burst fractures?

A

Retro pulsing of fragments into spinal canal leading to spinal cord injury.

142
Q

What is an Atlanto-occipital dislocation?

Ass’d rule?

A

Skulls separates from spinal column during severe head injury.
12 mm rule: basion- dental interval should be less than 12 mm ….

(Basion is inferior portion of occiput)

Basion-axis interval is posterior axial line drawn up from dens and connected to basion. Should be

143
Q

In atlanto occipital dislocation what does a basion-internal interval > 12 mm mean?

A

Internal decapitation. Leads to high mortality and respiratory failure,

144
Q

What are valid consent exceptions

A

Emergencies
Preliminary examination and diagnosis
Mental health act
- ideally a second opinion

145
Q

What is the hierarchy in substitute decision makers?

A
Committee - from court
Representative or guardian
Temporary substitute decision maker: (19 yo, in contact within 1 yr, no disputes with the adult.)
- spouse
- adults child
- Parent
Sibling
Grandparent
Grandchild
Related by birth or adoption

A close friend
A person immediately related to the adult by marriAge
Public trustee as last resort.

146
Q

In BC can power of attorney make healthcare decisions?

A

No! Only are relevant for finance decisions.

147
Q

How many witnesses required for advanced directive?

A

2, unless notary or lawyer.

Those who are less than 19 or who are paid by personal services are excluded.

148
Q

What is a nomination of a committee?

A

A nomination is a legal doc in which a capable adult nominates a person or persons to be appointed committee

Nominee can turn it down.

149
Q

What is a representation agreement?

A

Act: an agreement where you act someone to be your representative and act on your behalf should you be incapable. Can be for finances, healthcare or personal care.

There are two types… Section 7s and 9s (enhanced… Wider scope for representative). Rel agreement is active as soon as signed or if a date is designated,

Can have different people in different areas is health and finance.

150
Q

What is the difference between a committee and a RA

A

Committee often sought out not by pt but, for example. By pts child, who seeks out committee … is court-designated, and two independent medical reports are needed to stipulate a person is not capable of managing their person. Then judge appoints someone… This is typically done when someone is incapable. More strenuous process for the legal proceedings of this.

151
Q

What is higher on hierarchy RA or advance directive

A

RA

152
Q

When does an RA end?

A

Slide!

153
Q

What is required to make an RA?

A

In writing, properly signed and witnessed.
Legal advice from lawyer or notary recommended but not required.
Access published forms from ministry of the attorney general.

154
Q

What personal care decisions ca. Be included under an RA9?

A

Slide

155
Q

Other than major and minor health care, what does a RA 7 not have the authority to include?

A

Slide

156
Q

Check into slide before DUTIES AND TESPONSIBIKITES OD A REP

A

Ok

157
Q

What does the comiitteeship of person act fall under?

A

Slide!

158
Q

Does mental health act include ect?

A

Yes… In bc. In Nova Scotia though, need to seek out SDM

159
Q

Fetal fibronectin… When to do?

A

Via spec Before digital exam

160
Q

What is the definition of impairment?

A

Loss or abnormality of psychological, physiological, or anatomical function, this is observable.

161
Q

What is a disability?

A

Disabilities are caused by impairments, always relative to the task.

162
Q

What are the three types of factors influencing antibiotics election?

A

1) agent factors: i.e. type of bacteria suspected, suspected resistance patterns.
2) host factors: site of infection, antibiotics aimed at certain site, pregnancy, renal failure, allergy, immunocompromise.
3) environmental factors: nosocomial versus community acquired; travel, exposures, IV drug use.

163
Q

What’s the gram-positive have that make them distinct?

A

Large cell wall. This is target in most mechanisms of action.

164
Q

What is distinct about gram-negatives?

A

Inner and outer membrane. Therefore intracellular targets are also available.

165
Q

What are the cell wall synthesis inhibitors?

A

Have the Cell wall CC the GP so he’s on TIME
Cephalosporins
Carbapenems
Glycopeptides

  • Time dependent killing… Frequent dosing to keep around for sustained time.

– Inhibit cell wall synthesis
Cross-reactivity between classes

166
Q

What are the protein synthesis inhibitors?

A
C My (proteinaceous) LATs
Clindamycin
Macrolides
Linezolid
Aminoglycosides
Tetracyclines

Groups
AT MOL

AT- 30s ribosome
MOL- 50s ribosome

Aminoglycosides
Tetracyclines

Macrolides
Oxazolidinones
Lincosamides

167
Q

What are the DNA gyrate inhibitors?

A

Gyrating is for Queer Fag’s Rears
Quinolones
Flagyl
Rifampin

168
Q

Is the antimetabolite antibiotic?

A

Sulphonamide

169
Q

What is the main role for penicillin?

A

Treats gram-positive organisms including streptococcal species (GAS, strep viridans) and syphilis IM… IV f neurosyph

170
Q

What are the antistaphylococcal penicillins?

A

Cloxacillin, methicillin
- use for serious staph aureus infection, but it is narrow spectrum so do not use if one cannot differentiate between staph versus strep cellulitis

171
Q

What are the aminopenicillins?
What if it is ext spectrum?
What does adding clavulin do? what can it now cover for and what is it used for?

A

These are ampicillin and amoxicillin.
They cover gram-positive including, strep, enterococcus, listeria.
It extended spectrum, can include some gram-negative rods including E. coli, H influenza, Proteus
If combined with Clavulin this makes it broad-spectrum oral antibiotic. It can treat gram-positive, gram-negative, and anaerobes. This is used in sinus infections, otitis media, and URTI

172
Q

What is a ureidopenicillin?
What does it cover?
What is it combined with to make and extended spectrum antibiotic? What is it then used for?

A

Piperacillin
Gram-positive, gram-negative’s including Pseudomonas, and anaerobes.
When combined with tazobactam it becomes extended spectrum. PIP TAZ
Can then be used as an empirical treatment for polymicrobial/suspected resistant/unknown sources.

173
Q

What is the trend with cephalosporins?

A

As they progress from 1st to 3rd generation, they become less gram-positive and more gram- negative.

174
Q

What are two examples of first generation cephalosporins?

What do they cover?

A

Cefazolin (Ancef) IV and cephalexin (Keflex) po

Cover gram-positive, some ground negatives including PEcK (proteus, E. coli, klebsiella)

Therefore used for cellulitis, preop coverage, UTI.

175
Q

What is an example of a second generation cephalosporin?

What does it cover?

A

Cefuroxime PO/IV

Dec gram pos coverage, namely covers strep pneumo

Increased gram-negative coverage including HEN PEcK
- proteus, E. coli, Klebsiella, H influenza, enterobacter, Neisseria

Will cover for respiratory infections

176
Q

What are examples of third generation cephalosporins?
What do adults with gonorrhea get?
What are third-generation cephalosporins used for?

What does Ceftazadime cover for?

A

Ceftriaxone, cefotaxime, cefixime,

Adults with and gonorrhea get PO cefixime

Ikelea these drugs are used in community acquired pneumonia, meningitis, pyelonephritis

Ceftazadime covers for pseudomonas

177
Q

Why are there generation cephalosporins you need coverage for Neisseria in meningitis? How does the half-life play into this?

A

Third generation cephalosporins penetrate the blood brain barrier her. Therefore they can be used as empiric coverage for Neisseria in meningitis. Also they have long half lives and therefore once daily dosing is doable.

178
Q

What is an example of a fourth generation cephalosporin?

A

Cefepime… This is a very powerful broad spectrum antibiotic but it is less anaerobic than pip tazo.

179
Q

What are examples of the carbapenems?

Is the coverage? What are these for?

A

Imipenem and meropenem

The cargo pants are broad-spectrum with gram positive, gram-negative (Pseudomonas, ESBL), and anaerobes.
They are reserved for serious sepsis, musical meal infection where resistance is likely.

180
Q

What are the glycopeptides? Are the beta-lactam’s?

What is an example of a glycopeptide?

A

Like a peptides are not beta-lactam antibiotics.
The standard glycopeptide is vancomycin.
It is bacteriocidal, with gram-positive coverage for MRSA, coagulase negative staph aureus, enterococci.

It can be po used for C diff.

181
Q

What are adverse affects of vancomycin? Blood work is required for Vanco use?

A

Red man syndrome, nephrotoxicity, rare otototoxicity.

Need to measure levels at trough.

182
Q

What is the one type of cell membrane agent?
What is An example of the antibiotic?

What is the MOA and what does it act on?

A

Lipopeptide
- daptomycin

Cell membrane of gram positive only. MRSA, enterococcus (VRE)

183
Q

What are examples of aminoglycosides?

Best used against?

Is there a particular gram-positive infection that these are useful against?

A

Gentamicin, tobramycin, amikacin

Best used against gram negatives. Ie gram neg sepsis.

Can also provide synergy against gram-positive enterococcal endocarditis… Ampicillin – gentamicin: grandma positives punch holes to let aminoglycosides in.

This is concentration dependent killing and therefore you need peak and trough levels.

184
Q

What are adverse events secondary to aminoglycoside use? Therefore what must be done with regards to consent?

A

Nephrotoxicity, ototoxicity, vestibulotoxicity,

Therefore if cheating for 4 days must document patient consent

185
Q

What are examples of the tetracyclines?

What are these useful in treating? What type of spectrum are they?

A

Doxycycline and tetracycline.
They are fairly broad spectrum and treat atypical cell walls or intracellular organisms.
Ie spirochetes, like a plasma, chlamydia, Rickettsia.

186
Q

Are contraindication populations for tetracycline?

A

Children

Pregnant women

187
Q

What are examples of the macrolides? When do you use these specific ones/for what organisms?

A

MACROLIDES ACE it

Azithromycin – respiratory tract infections, atypical, Moraxella, H influenza, Legionella.

Clarithromycin – community acquired pneumonia, sinusitis, h pylori, legionella

Erythromycin – used for penicillin allergy.

188
Q

What is an example of a lincosamide?
What is the moa?
Adverse events secondary to Climdamycin use?

A

Clindamycin po and iv
Climdamycin is bacteriostatic and leads to decreased toxin production.

Useful for gram positive and anaerobes

Treats cellulitis, abscess, some diabetic foot

Adverse event: high risk for c diff

189
Q

What is an example of an oxazolidinone?
What can this be used to treat?

How is the bioavailability of linezolid?

A

Linezolid

Treats staph including MRSA and coag neg staph aureus.
Treats enterococcus including VRE.

Bioavailability of linezolid is very good.m

190
Q

Are there particular adverse effects of linezolid?

A

Cutopeniss, ssri interaction, ? Neurotoxicity.

191
Q

What are example of the quinolones? What are they particularly good for Treating?

A

Ciprofloxacin, levofloxacin, moxifloxacin

  • often used in respiratory infections
  • treats INTRACELLULAR pathogens… Legionella, mycoplasma; and gram negative bacteria.
192
Q

What does Flagyl treat?

A

Anaerobes and parasites

193
Q

What does rifampin treat?

A

Mycobacteria (tb), MRSA w fusidic acid, listeria, Neisseria, h influenza, legionella.

194
Q

What is the anti metabolite sulphonamide moa?

A

Blocks bacterial folate synthesis

195
Q

What are anti pseudomonas antibiotics?

How are these admind?

A

CACAQ

Carbapenems: meropenem, imipenem
Aminoglycosides: gentamicin, amikacin, tobramycin.
Cephalosporins
Antipseudomonal penicillins: Piperacillin, ticarcillin
Quinolones: ciprofloxacin, levofloxacin, moxifloxacin.

All by injection, except aerosolized tobra and Fluoroquinolones

196
Q

For Odontoid fracture, can be subtle. What to look for?

A

Prevertebral Edema and offset of spinolaminar line. Loss of Harris ring.

197
Q

What are the three exogenous camnabinoids?

A

Thc- psychoactive… In flower of plant
Cannabinol- medicinal
Nabilone- synthetic. Not detected in urine. Oncology and chronic pain.

198
Q

What is synthetic thc?

A

Dronabinol

Synthetic Po capsule

Good for n v … And for anorexia

Hiv peripheral neuropathy NNT 3.6

199
Q

What sativex?

A

Rx spray of cannabidiol and thc.
Better absorption.

Dosing is highly variable. You need to get patients to self titrate.

Approved for ms neuropathic pain… Is actually the only true approved/ fill indication for pain.
Role in sleep and RA as well.

200
Q

Safety issues for marijuana

A

Tolerance- not major issue but can happen
Psychosis esp in adolescents
MI - tachycardia and vasodilation
Euphoria - non issue w rx
Paradoxical nausea
Decreased motivation…. “Amotivation syndrome”

201
Q

Two regulations

A

Medical marihuana access regulations
MMAR
Allowed for possession of marijuana as authorized by a physician and growth for personal use… Was repealed in 2014, no longer can do this.

Marijuana for medical purposes regulations
MMPR
- creates conditions for industry that is responsible to prod and distribution

202
Q

Max pot on person allowed

A

150 g or 30x authorized use, whatever less.

203
Q

Are pot shops legal in Vancouver?

A

No. But are low priority to VPD.

204
Q

What is prevalence of marijuana use in Canada?

A

2-5 percent in gen pop and higher in some chronic dz

205
Q

What does add marijuana rx mean?

A

If they get caught they will not go to jail.

206
Q

How many g in 1 joint?

A

0.25-1 g… 6-8 puffs

207
Q

How to approach different THC potencies?

A

Use lowest potency for effect… S/e worse but benefits unchanged at higher conc.

208
Q

What is the only way to use thru Hwalth Canada?

A

Smoked

209
Q

If going to be edible, what do you need to eat with?

A

Something fatty

210
Q

How long does health canada form last?

A

1 yr

211
Q

What is a scale to Measure sleep?

A

Epworth sleep scale…. Asks patient likelihood of falling asleep in certain everyday situations.
Max score of 24.

212
Q

Definition of OSAH syndrome

A

Slide

213
Q

Sleep definitions

A

In photos

214
Q

What defines an obstructive apnea on polysombography?

A

No ventilatory mvnt w persisting respiratory effort

215
Q

Ranges and degree?

A

30 severe

216
Q

Prevalence of OSAHS?

A

5 % of adult pop

25% > 5 events but may be asx

217
Q

To what degree will obstructing sleeper wake?

A

Not enough to be awake but enough neural input to break negative pressure w pharyngeal dilator muscle activation

218
Q

Outcomes

A

Tachy Brady alternations, hypoxemia, etc SLIDE

219
Q

What is a GI complication of OSAHS? (Think negative pressure)

A

GERD

220
Q

What is periodic limb movement disorder

A

SLIDE

221
Q

Presentation of osa in children ie due to large adenoids

A

Cognitive impairment/ poor school performance
SLIDE
Enuresis?

222
Q

What are alternative to expensive polysomnogrphy

A

Clinical prediction rules

Ambulatory sleep studies

223
Q

What is the adjusted neck circumference score.

A

Risk stratifies based on other risk factors. If >48 high pretest probability. Then could do overnight oximetry. Or ambulatory sleep study.
Then can do cpap trial and do study again, if improved then can presume OSA w/o doing the expensive and limited gold stnd of polysomnogrphy.
Limitations: assuming sleep but not guarunteed. More prone to technical failure and more difficult to interpret.

224
Q

What is an unusual endocrine cause of OSA?

A

Acromegaly

225
Q

Why is supine worse for OSA

A

Tongue pulled back w gravity.

226
Q

What does cpap provide?

A

Pneumatic splint.

227
Q

Other options to cpap?

A

Oral appliance…. Mandibuoar advacement applicance…. Progressive advancement of mandible w screw device to pull forward. Makes pharynx less liable to obstruct. Not as effective as cpap but more compliance. So similar outcomes w
Bc though cpap very effective, compliance only 60-70%.

228
Q

What is success rate of uvulopalatopharyngoplasty?

A

Low, 40% . Mot typically recommended.

229
Q

What is most common misinterpret of St elevation on a normal ecg otherwise.

A

j point elevation… If it is smiling then is j point vs inverse on St. If discrete vertex is less concerning than if gradual inc is more concerning.

230
Q

Tie breaker of lead 2. Axis

A

Check out tutorial!!! Optional online

231
Q

Should you ever call St elevation a reciprocal change?

A

no! Because that is mega dangerous. So if anything call the St depression the reciprocal changes

232
Q

What makes a significant q wave?

A

1 mm wide and 1/3 of the complex size.

233
Q

What makes atrial enlargement count?

A

3 X 3

234
Q

If hypertrophy, R wave v5 plus S wave v1 >35…. And St depression, must ask, is this due to ischemia or is it just STRAIN in setting of hypertrophy.?

A

Need to look at other leads across from these. Are there reciprocal changes? AND COMPARE TO OLD ECG.

235
Q

What is the mnemonic for BBB?

A

WiLLiaM MaRRoW…
Left bundle branch has relatively normal qrs progression. No nice bunny ears.
Once LBBB dz is made must stop…. Cannot distinguish ischemia or infarction on ST segments on a LBBB

236
Q

Are ST elevation in hyperkalemia ecg findings?

A

No

237
Q

What does a U Wave mean?

A

Hypokalemia or hypocalcemia

238
Q

I and aVF upright?

A

Normal axis

239
Q

Findings on hypokalemia/ cal emia?

A

U wave, long qt

If St depression consider ischemia

240
Q

If 1-3 p waves, sawtooth, what do you call it? 150 bpm.

A

Can call it a a flutter w variable block.

Try carotid massage to see if you can bring them out.

241
Q

How to remember time frames for insulin

A

Remember long is 24 hrs

Remember reg is Toronto and know it’s i fo. Then just deified by 2 To get rapid.

242
Q

What does basal bolus insulin entail

A

Night or am of basal single injection
Prandial insulin,

= multiple daily injections

243
Q

What is premixed?

A

One vial of rapid for breakfast…. Nph goes for 12 hours so get this to cover lunch. Then do again in evening.

Problem: no rapid acting at lunch so if big meal or not enough not well controlled.

70-30 70 Nph: rapid

There basal bolus is gold standard.

244
Q

Basal bolus vs premixed preference?

A

Basal bolus is better for dm1.

Premixed is not as ideal for dm1 … But is simpler.

245
Q

For 45 yo otherwise healthy on 3 meds including metformin who feels fine with uncontrolled Hba1c, what to do?

A

Consider insulin after 3 non insulin agents.
Nph (int) once daily or long acting qHS is glargine

Long acting or int once a day less weight gain

246
Q

For those in hospital w diabetes and acute illness ie infection, reduce home meds by 30-50 %. What to choose amongst low, med and hi targets on sliding scale.

A

Prescribe what you think they will need. Then Instead think of it as a correction scale… Where did I go wrong and where does it need adjusting.

Correction scale strength is proportional to home dose.
Correction factor CF = reduction in [glucose] given 1 unit of insulin = 100 / total daily dose.

I’ve 49 glargine lisp do 20 tid… Then 1 unit brings down glucose by 1 mmol.

247
Q

What is in hospital number to remember?

A

5-10

248
Q

Recommendations for sliding scale

A

Use formula to estimate starting point.
Closely monitor response and adjust dosing.
Being conservative is safer in hospital. Reduce doses by 30-50 percent.

249
Q

Are numbers checked before or after meals?

A

Before

250
Q

Simple approach to titration

A

1) What is the pattern of abnormal glucose?
2) too much or too little insulin?
3) how can we prevent this from happening again?

251
Q

Rules

A

1) Titrated by apply pharmacokinetics
2) to asses prandial (rapid) insulin effect, look at subsequent dose.
3) to assess the basal dose effect, Fasting (breakfast) glucose

With lows thru night, keep in mind that people do get rebound hyperglycemia in the morning.

252
Q

Do dm2 ever get their BG checked throught day?

A

No formal recommendation

253
Q

Diabetes f/u investigations

A

Hba1c can change w anemia…. Get cbc
ACr
+/- ecg
Lipid panel q3mo to start, q1 yr once stable

254
Q

Go straight to insulin once A1c > what value?

A

9

255
Q

Rosaglitizone still used?

A

Inc NNH, overall inc mortality

256
Q

CI. To metformin

A

Pregnancy

Stage 4-5 CKD (gfr

257
Q

Diabetic hierarchy

A
  1. Metformin sensitizer
  2. Sulfonurea (glyburide is cheaper but inc poor cv outcomes., glickizide is more expensive but can get covered if endocrinologist prescribes…. So can refer to get the script then step down back to GP) secretagogue…. Therefor high risk for hypoglycemia
    3 thiozidinediones/ ddp4 ???? etc, endo consult! Or insulin
258
Q

Insulin starting considerations?

A

Start low, Long acting ie 10 units lantus

Then consider prandial

259
Q

Insulin dosing….

A

0.5-1 unit/kg/day
Start at .5 for new users.
1:1:1:2
Tid ac x3 then hs

Divide total units by 5.
Is for 60 kg person starting…. 30 units per day. So 6:6:6:12

260
Q

Lipid targets for prevent

A

LDL

261
Q

If not doing prandial, and on non insulin oral agents, how to calculate basal?

A

Same calc just leave out tid.

262
Q

Treatment refractory HTN defn

A

3 meds at target dosing including one diuretic.

263
Q

Apnea defn

A

Pause > 10 sec

264
Q

Hypopnea defn
Apnea
A-h index

A

Dec 50 % minute ventilation
Dec spo2 > or = 3-4%

Apnea - hypopnea index n 0-4
Mild 5-14
Mod 15-29
Sev 30 or greater

Add up apneic intervals of at least 10 sec

265
Q

What is a great three part topical medication

A

Ketamine + lidocaine + morphine

266
Q

Treatment for neuropathic pain

A

1st SNRI (venlafaxine and dulox) TCA (amitriptyline) Anticonvulsant (only gabapentin has studies vs pregabalin which hasn’t been),

2nd opioids, tramadol, cannabinoids (sativex, not cannabinol)

3rd SSRI other anticonvulsants

267
Q

Trigeminal neuralgia 1st line

A

Carbamazapine

268
Q

What is cannabinoid-ass’d Hyperemesis syndrome..

A

Pathognomonic- hot shower to stop it

Thought to be due to deranged storage of cannabinoids in adipose and then dumping which goes for a few days and cycles…. Dangerous w ARF electrolyte derangement etc.

269
Q

What are clues that the G.I. tract/vagal input is the main mechanism for nausea and vomiting.?

A

Not yet worse with eating and relieved by vomiting; may include distended abdomen, hiccups, sluggish bowels
– Majority caused by impaired gastric emptying

270
Q

What are clues that mechanism for nausea and vomiting is vestibular?

A

Nausea and vomiting is aggravated by motion and is intermittent. There is a normal G.I. exam. There may be nystagmus.
I.e. cerebellar tumor

271
Q

What are clues that the mechanism for vomiting is raised ICP?

A

Early morning vomiting nausea associated with headache. There may also be neurologic signs and or symptoms.
Ie brain Mets.

272
Q

What are clues that the mechanism for nausea and vomiting is cerebral?

A

Usually anxious/anticipatory/emotional triggers with waves of nausea.
I.e. anxiety

273
Q

What are good medications and vomiting upon chemoreceptor trigger zone stimulation?

A

D2 antagonists i.e. antipsychotics, Maxeran

274
Q

What are good drugs to use for G.I. tract vagal vomiting?

A

D2 antagonists like Maxeran, 5 HT3 antagonists like Zofran, obstruction meds like octreotide or ranitidine plus dexamethasone

275
Q

What are good drugs for cerebral or high CNS causes of nausea?

A

GABA benzodiazepine complex drugs and cannabinoids

276
Q

What are good drugs for vestibule are causes of nausea?

A

H1 antagonists and anticholinergics like scopolamine and atropine