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*Crozer-Keystone > 5. Medicine > Flashcards

5. Medicine Flashcards

1
Q

what are reasons/time/examples

for post-op fever?

A

wind (12-24 h)

  • Atelectasis (from muscle relaxers)
  • Post-op hyperthermia

water (~24 h)

  • UTI

walk (~48 h)

  • DVT
  • PE

wound (~72 h)

  • Post-op infection

wonder drug (anytime)

  • Drug fever
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2
Q

causes of post-op fever: Wind (12-24 hr)

causes / treatment

A

causes:

  • Atelectasis (from muscle relaxers)
  • Post-op hyperthermia

treatment:

  • Encourage incentive spirometer
  • Chest x-ray
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3
Q

causes of post-op fever: Water

causes / treatment

A

causes:

  • UTI

treatments:

  • Straight catheter
  • Urine analysis (UA) with Gram stain, culture and sensitivity
  • Treat with antibiotics if necessary
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4
Q

causes of post-op fever: Walk

causes / treatment

A

causes:

  • DVT
  • PE

treatments:

  • Heparin or Lovenox protocol
  • Use SCDs, TEDs, or get patient out of bed
  • (SCD: sequential compression device;*
  • TED stockings: thromboembolism-deterrent)*
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5
Q

causes of post-op fever: Wound

causes / treatment

A

causes:

  • Post-op infection

treatments:

  • X-ray, Gram stain, culture and sensitivity, blood cultures
  • Begin antibiotic
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6
Q

causes of post-op fever: Wonder drug

causes / treatment

A

causes:

  • drug fever

treatments:

  • discontinue drug
  • give reversal drug if necessary
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7
Q

When do fever peaks occur?

A

Between 4-8 pm

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8
Q

What part of the brain regulates the body’s temperature?

A

Hypothalamus

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9
Q

malignant hyperthermia: definition

A

A side effect of general anesthesia

Sxs include: tachycardia, hypertension, acid-base and electrolyte
abnormalities, muscle rigidity, hyperthermia

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10
Q

malignant hyperthermia: treatment

A
  • Dantrolene (for muscle relaxation) 2.5mg/kg IV x l,
  • then 1 mg/kg IV rapid push q6h until
    symptoms subside or until max dose of l0 mg/kg
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11
Q

If a risk of malignant hyperthermia is suspected,

what pre-operative test may be performed?

A

Creatine phosphokinase (CPK)

CPK is elevated in 79% of patients with malignant hyperthermia

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12
Q

MOA of local anesthetics

A

Block Na+ channels and conduction of action potentials along sensory nerves

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13
Q

toxic dose of lidocaine (Xylocaine)

A
  • 300 mg plain (4.5 mg/kg)
  • 500 mg with epi (7.0 mg/kg)
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14
Q

toxic dose of bupivacaine (Marcaine)

A
  • 175 mg plain (2.5 mg/kg)
  • 225 mg with epi (3.2 mg/kg)
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15
Q

How to convert the percentage of solution to mg/mL?

A

Move the decimal point of percentage one place to the right

(e.g. 1% solution has 10 mg/mL)

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16
Q

side effects of lidocaine and bupivacaine

associated with systemic exposure

A
  • CNS effects –
    • initial excitation (dizziness, blurred vision, tremor, seizures)
    • followed by depression (respiratory depression, loss of consciousness)
  • Cardiovascular effects –
    • hypotension,
    • bradycardia,
    • arrhythmias,
    • cardiac arrest
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17
Q

What can be given to help reverse

local anesthetic-induced cardiovascular collapse?

A

Intravenous fat emulsion (Intralipid)

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18
Q

Is there a risk with intra-articular injections of bupivacaine?

A

Yes,

studies have shown chondrocyte death following prolonged exposure to bupivacaine

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19
Q

In what age group should bupivicaine be avoided?

A

Children <12 years of age

should avoid bupivicaine

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20
Q

How are amides (lidocaine and bupivacaine) metabolized?

A

Liver

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21
Q

How are esters (Novocain) metabolized?

A

Plasma pseudocholinesterase

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22
Q

What is the only local anesthetic with vasoconstriction?

A

Cocaine

cocaine is the only local anesthetic with vasoconstriction

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23
Q

How is cocaine metabolized?

A

Plasma pseudocholinesterase

(just like other esters)

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24
Q

Can local anesthetics cross the placental barrier?

A

Yes,

local anesthetics cross the placental membrane

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25
Q

What does MAC (as in MAC with local) stand for?

A

Monitored anesthesia care

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26
Q

For anesthesia,

what cannot be given to a patient with an eggshell injury?

A

propofol (Diprivan)

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27
Q

pain management options for patient

with a codeine allergy?

A

(STUD or STTUUDDD-N)

  • S - Stadol
  • T - Toradol
  • T - Talwin
  • U - Ultram
  • D - Darvon
  • D - Darvocet
  • D - Demerol
  • N - Nubain
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28
Q

First choice for oral pain management

for patient with codeine allergy?

A

Darvocet N-100 one tab PO q4-6h prn pain

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29
Q

First choice for non-narcotic oral pain mgmt

for patient with codeine allergy?

A

tramadol (Ultram) 50 mg

one to two tabs PO q4-6h prn pain,

max daily dose of 400 mg per day

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30
Q

First choice for non-narcotic IV pain mgmt

for patient with codeine allergy?

A

Toradol 30-60 mg IV

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31
Q

Choice narcotic IV pain med?

(for patient with codeine allergy)

A
  • *Demerol**
  • Note: many hospitals, including our own, do not use Demerol due to its side effects*

Side effects:

lightheadedness, dizziness, sedation, nausea, vomiting, sweating, constipation, loss of appetite, headache, weakness, dry mouth, itching, urinating less than usual, flushing, drowsiness

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32
Q

Name two non-narcotic analgesics

A

ketoralac (Toradol),

tramadol (Ultram)

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33
Q

what schedule is this drug:

percocet

A

Class II

high potential for abuse – requires narcotic script

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34
Q

what schedule is this drug:

vicodin

A

Class III

moderate potential for abuse

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35
Q

what schedule is this drug:

Tylenol #3

A

Class III

moderate potential for abuse

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36
Q

what schedule is this drug:

Darvocet

A

Class IV

low potential for abuse

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37
Q

Percocet 5/325

(components and schedule)

A

oxycodone/acetaminophen (5 mg/325 mg)
1-2 tabs PO q4-6h prn pain

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38
Q

Roxicet

(components and schedule)

A

oxycodone/acetaminophen (5 mg/325 mg/5 mL)

*Essentially a liquid form of Percocet that is good for pediatric patients

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39
Q

What is the difference between
Percocet and Percodan?

A
  • Percocet has 325 mg of acetaminophen
  • Percodan has 325 mg of ASA
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40
Q

Vicodin 5/500

(components and scheduling)

A

hydrocodone/acetaminophen (5 mg/500 mg)
1-2 tabs PO q4-6h prn pain

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41
Q

Tylenol #3

(components and scheduling)

A

codeine/acetaminophen (30 mg/300 mg)
1-2 tabs PO q4-6h

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42
Q

Darvocet-N 100

(components and scheduling)

A

propoxyphene/acetaminophen (100 mg/650 mg)
1 tab PO q4h prn pain

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43
Q

Ultram

(components and scheduling)

A

tramadol 50 mg
1-2 tabs PO q4-6h prn pain

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44
Q

Toradol

(components and scheduling)

A

ketorolac 10 mg
30 mg IV q6h
1 tab PO q4-6h prn pain

*An NSAID not to be used more than 5 days due to possible significant side effects

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45
Q

Darvon

(components and scheduling)

A

propoxyphene
1 tab PO q4h prn pain

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46
Q

OxyContin

(generic name)

A

oxycodone extended-release

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47
Q

Morphine sulphate

(components and scheduling)

A

2-4 mg IV q2-6h prn mod-severe pain
For very painful dressing change or bedside debridement – 2 mg IV x one dose

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48
Q

MS Contin

(components and scheduling)

A

morphine sulfate extended-release (15-30 mg)
1 tab PO q8-12h prn pain

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49
Q

Dilaudid

(generic name, and scheduling)

A

hydromorphone
2-8 mg PO q3-4h prn severe pain
1-4 mg IV q4-6h prn severe pain

*This drug is very strong

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50
Q

Demerol

(generic name, note)

A

meperidine

*Our hospitals do not use this due to its side effects

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51
Q

What therapeutic effects are seen with acetaminophen

A

analgesic and anti-pyretic

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52
Q

maximum daily dose of acetaminophen

A

4 grams

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53
Q

what therapeutic effects are seen with most NSAIDs?

A
  • analgesic,
  • anti-pyretic,
  • anti-inflammatory
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54
Q

on which pathway do NSAIDs work?

A

Cyclooxygenase (COX)

NSAIDs nonselectively inhibit both COX-1 and COX-2 pathways

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55
Q

most common side effect of NSAIDs

A

GI disturbance

*(except with COX-2 inhibitors, because COX-1 protects the stomach lining)

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56
Q

only FDA-approved COX-2 inhibitor

A

celecoxib (Celebrex)

*Others were withdrawn due to increased risk of heart attack and stroke

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57
Q

NSAIDs with ONLY anti-inflammatory effects

A
  • indomethacin
  • tolmetin
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58
Q

Do NSAIDs decrease joint destruction?

A

NO, they only decrease inflammation

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59
Q

Do NSAIDs affect bone healing?

A

Yes

NSAIDs and COX-2 inhibitors may inhibit bone healing via their anti-inflammatory effects

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60
Q

NSAID causing irreversible inhibition of platelet aggregation

A

Aspirin

*(Think: AspIR-in is Ir-reversible)

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61
Q

NSAID that does NOT inhibit platelet aggregation

A

The COX-2 inhibitor, Celebrex

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62
Q

Only IV NSAID

A

ketorolac (Toradol)

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63
Q

Which NSAID is often given:

during surgery or immediately post-op

to decrease pain and inflammation?

A

Toradol 30 mg IV

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64
Q

NSAIDs with the least nephrotoxicity

A
  • Celebrex,
  • Relafen,
  • Lodine
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65
Q

effect of NSAIDs on asthma

A

NSAIDs can increase/exacerbate symptoms of asthma

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66
Q

safest NSAIDs for a patient with asthma

A
  • Diclofenac
  • ketoprofen
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67
Q

NSAIDs that treat collagen vascular disease

A

“SIT”

  • sulindac
  • Ibuprofen
  • tolmetin
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68
Q

NSAIDs that are NOT renally cleared

A

Indomethacin and Sulindac

excreted in urine, less effect on renal function

  • Indomethacin
    • ~60% of an oral dose is excreted in the urine (predominantly in glucuronidated form)
    • ~40% is excreted in the faeces after biliary secretion (a large amount of the dose undergoes biliary recycling)
  • Sulindac
    • ~50% of dose is excreted in the urine (predominantly the conjugated sulfone metabolite)
    • <1% of dose appears in the urine as the sulfide metabolite.
    • ~25% is found in the feces, primarily as the sulfone and sulfide metabolites.
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69
Q

NSAIDs:

cardiovascular effects

A

Can cause vasoconstriction and increase blood pressure

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70
Q

NSAIDs with LEAST cardiovascular effects

A

Diclofenac & Ketoprofen

*(these are also the same 2 drugs that are safest for asthmatic patients)

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71
Q

NSAIDs:

most hepatotoxic

A

“DIN”

diclofenac, Ibuprofen, naproxen

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72
Q

Tx for Indomethacin overdose

A

Benadryl

Benadryl decreases serotonin and histamine release

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73
Q

Arthrotec

(components and use)

A

diclofenac/misoprostol –

use: an NSAID with protection for the stomach

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74
Q

anti-inflammatory dose of ibuprofen

A

1200-3200 mg/day in divided doses

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75
Q

which NSAIDS work on both the

lipooxygenase and cyclooxygenase pathways

A

Diclofenac and Ketoprofen

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76
Q

difference between Cataflam and Voltaren

A
  • Cataflam is diclofenac potassium and has an immediate-release
  • Voltaren is diclofenac sodium and has a delayed-release
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77
Q

Pro-drugs for NSAIDs

A

nabumetone and sulindac

Recall: a _pro-drug_ is a medication or compound that, after administration, is metabolized into a pharmacologically active drug. Instead of administering a drug directly, a corresponding prodrug can be used to improve how the drug is absorbed, distributed, metabolized, and excreted

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78
Q

Non-acidic NSAID

A

nabumetone

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79
Q

NSAIDs with fewer pulmonary problems

A

Diclofenac and Ketoprofen

(fewer pulmonary, cardiovascular, and issues with asthma)

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80
Q

Once-a-day NSAIDs

A

Think: “One Pill Cada Noche”

  • oxaprozin (Daypro)
  • piroxicam (Feldene)
  • celecoxib (Celebrex)
  • nabumetone (Relafen)
  • others
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81
Q

drugs that interact with NSAIDs

A
  • Anti-epileptics
  • Anti-hypertensives
  • Corticosteroids
  • Coumadin
  • Digoxin
  • Lithium
  • Methotrexate
  • Probenecid
  • Sulfonylureas
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82
Q

Effect of NSAIDs with:

Coumadin

A

increases action of Coumadin

(aka Warfarin - blood thinner)

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83
Q

Effect of NSAIDs with:

Sulfonylureas

A

increases action of sulfonylureas

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84
Q

Effect of NSAIDs with:

Corticosteroids

A

increases GI risk

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85
Q

Effect of NSAIDs with:

Anti-epileptics

A

increases anti-epileptic toxicity

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86
Q

Effect of NSAIDs with:

Antihypertensives

A

antagonizes antihypertensive meds

(recall: NSAIDs induce an increase in blood pressure (BP) and may potentially reduce the efficacy of several antihypertensive drugs)

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87
Q

Effect of NSAIDs with:

Digoxin

A

increases digoxin’s effect

(NSAIDs can increase Digoxin levels in the body, causing nausea, loss of appetite, visual changes, slow pulse, or irregular heartbeats)

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88
Q

Effect of NSAIDs with:

Methotrexate

A

decreases methotrexate’s clearance

  • (by decreasing clearance, increases bioavailability, increasing effects of methotrexate;*
  • serious adverse events include liver toxicity, acute renal failure, and cytopenia)*

DOI: 10.1002/pds.4555

Svanström (2018)

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89
Q

Effect of NSAIDs with:

Lithium

A

NSAIDs decrease lithium’s clearance

  • (by decreasing clearance, increases lithium bioavailability, increased effects;*
  • resulting in an increased risk for serious adverse effects like confusion, tremor, slurred speech, and vomiting)*
  • Source: nami.org*
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90
Q

Effect of NSAIDs with:

Probenecid

A

increases concentration of NSAIDs;

enhanced anti-inflammatory effect can be expected when these 2 drugs are combined

(MOA: ibuprofen oral will increase the level or effect of probenecid oral by acidic (anionic) drug competition for renal tubular clearance)

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91
Q

causes of acute arterial occlusion

A
  • Embolism – detached thrombus, air, fat, or tumor
  • Thrombus – occlusion of vessel by plaque or thickened wall
  • Extrinsic occlusion – traumatic, blunt, penetrating
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92
Q

triad of pulmonary embolism

(definition)

A
  • Dyspnea
  • Chest pain
  • Hemoptysis (although tachycardia is more common)
93
Q

Diagnostic tests:

Pulmonary Embolism

A
  • Chest X-ray
  • Ventilation perfusion scan
  • Pulmonary angiography
94
Q

Virchows triad

A
  • Venous stasis – tourniquet, immobilization
  • Endothelial wall damage/abnormality – surgical manipulation, trauma, smoking
  • Hypercoagulability – birth control, coagulopathy, history of DVT
95
Q

what does Virchow triad predict?

A
  • Risk of DVT
  • Previous DVT is #1 risk factor for having another DVT
96
Q

DVT:

risk factors

A

(I AM CLOTTED)

  • I – immobilization
  • A – arrhythmia
  • M – MI (past history)
  • C – coagulable states
  • L – longevity (old age)
  • O – obesity
  • T – tumor
  • T – trauma
  • T – tobacco
  • E – estrogen
  • D – DVT (past history)
97
Q

DVT

clinical diagnosis

A
  • Pain, heat, swelling, erythema of unilateral limb
  • Positive Pratt sign – squeezing of posterior calf causes pain
  • Positive Homan sign – abrupt dorsiflexion of foot causes calf pain
  • Pulmonary embolism
98
Q

Diagnostic tests:

DVT

A
  • Doppler ultrasound
  • Venogram
  • D-Dimer
99
Q

drugs for long-term DVT prophylaxis

why?

A
  • Heparin – works right away
  • Coumadin – takes 3-5 days and causes an initial transient hypercoagulable state
100
Q

DVT treatments

A
  • Thrombolytic agents
  • Heparin
    • 5000 Units IV bolus,
    • then 1000 Units IV q1h and monitor PTT
101
Q

dosing Heparin for perioperative DVT prophylaxis

A
  • 5000 units SC 2h prior to surgery
  • 5000 units SC q12h until patient ambulates
102
Q

Heparin:

half-life

A

1.5 hours

103
Q

Heparin: MOA

A
  • Intrinsic pathway
  • Potentiates antithrombin III 100-fold –> inhibits the serine protease in the clotting cascade
104
Q

Heparin: reversal

A

Protamine sulfate 1 mg per 100 units of heparin

105
Q

what is enoxaparin (Lovenox)?

A

Low molecular weight heparin (LMWH)

106
Q

dosing Lovenox for perioperative DVT prophylaxis

A

30 mg SC q12h for 7-10 days

(adjust dose to q24h for renal patients)

107
Q

Lovenox: half-life

A

4.5 hours

108
Q

+/- of using Lovenox vs. regular Heparin

A
  • Advantages – Lovenox has longer plasma half-life with significant anticoagulation in trough
  • Disadvantages – increased post-op complications when used with spinal/epidural anesthesia
109
Q

How to check Lovenox?

A

*there is NO TEST for the effects of Lovenox*

110
Q

Lovenox: reversal

A

Recombinant Factor VII

111
Q

Coumadin: dosing

A

5-10 mg PO daily for 3-4 days then adjust for INR

112
Q

Coumadin: half-life

A

20-60 hours

113
Q

how long before Coumadin is therapeutic?

A

3-5 days

before Coumadin becomes therapeutic

114
Q

Coumadin: MOA

A
  • Extrinsic pathway
  • Interferes with clotting factors II, VII, IX, X
115
Q

Coumadin: reversal

A
  • Vitamin K
  • Fresh frozen plasma
116
Q

INR values:

  • normal
  • intense anticoagulation
A
  • Normal: 1
  • Intense anticoagulation: 2-3
117
Q

levels of Heparin and Coumadin for

DVT/anticoagulation prophylaxis

A
  • Heparin – maintain 2-3 times normal PTT
  • Coumadin – maintain 2 times normal INR
118
Q

perioperative DVT prophylaxis:

nonpharmacologic measures

A
  • Early ambulation – most important
  • TEDs – thromboembolic deterrent stockings
  • SCDs – sequential compression devices
119
Q

surgical treatment for a patient

with prior DVTs or recurrent PEs

A

Greenfield filter

*gold standard for inferior vena cava (IVC) filters;

purpose is to trap clinically significant emboli

120
Q

Greenfield filter is inserted at what level of the body?

A

Inferior vena cava below the renal veins;

(femoral IVC to prevent DVTs)

121
Q

Pletal

(generic name, use)

A
  • Generic: Cilostazol
  • Use: vasodilator
    • used to reduce the symptoms of intermittent claudication and can increase your ability to walk further distances
122
Q

Trental

(generic name, use)

A
  • Generic: Pentoxifylline
  • Use: Anti-inflammatory and Vasodilator
    • can treat poor blood circulation by improving the flow of blood through the vessels
123
Q

Indications for Pletal or Trental

A

Intermittent claudication

124
Q

CRPS: define

A

Complex regional pain syndrome

  • (previously known as RSD – reflex sympathetic dystrophy)*
  • A progressive disease of the autonomic nervous system causing constant, extreme pain that is out of proportion to the original injury
125
Q

CRPS:

types

A
  • CRPS Type I (reflex sympathetic dystrophy)
  • CRPS Type II (causalgia)
126
Q

CRPS Type I

(define, causes)

A

(reflex sympathetic dystrophy)

  • Nerve injury cannot be immediately identified
  • Spontaneous pain not limited to single nerve distribution
  • Abnormal response in sympathetic nervous system
  • Abnormal reflex leading to vasomotor instability and pain
127
Q

CRPS Type II

(define, causes)

A

(causalgia)

  • Distinct, “major” nerve injury has occurred
    • o Trauma
    • o Peripheral nerve injury
    • o Drugs – anti-TB, barbiturates, cyclosporine
  • Continued pain not necessarily limited to injured nerve distribution
128
Q

what are the stages of CRPS?

A
  • Acute – early (0 to 8-20 weeks)
  • Dystrophic – mid (2-6 months, possibly up to 1 year)
  • Atrophic – late (over 6-12 months)
129
Q

Acute CRPS

(timing, characteristics)

A

Acute – early (0 to 8-20 weeks)

  • Constant pain out of proportion (intense burning)
  • Possible edema, muscle wasting
  • Hyperhidrosis
  • Pain increased by light touch, movement, emotion
130
Q

Dystrophic CRPS

(timing, characteristics)

A

Dystrophic – mid (2-6 months, possibly up to 1 year)

  • Increased edema that is indurated (brawny edema)
  • Constant pain by any stimulus
  • Skin is cool pale and discolored
  • X-ray shows diffuse osteoporosis
131
Q

Atrophic CRPS

(timing, characteristics)

A

Atrophic – late (over 6-12 months)

  • Intractable pain spreads proximally to involve entire limb
  • Decreased dermal blood flow causing cool, thin shiny skin
  • Fat pat atrophy
  • Joint stiffen, may proceed to ankylosis
132
Q

CRPS:

radiographic findings

A

On X-ray:

  • Periarticular,
  • mottled,
  • irregular bony demineralization (30-60% of cases) and
  • cortical thinning

Per Radiopaedia:

  • severe patchy osteopenia, particularly in the periarticular region
  • soft tissue swelling, with eventual soft tissue atrophy
  • subperiosteal bone resorption
  • preservation of joint space
133
Q

CRPS: bone scan

usefulness, sensitivity and specificity

A

The 3-phase bone scan has sensitivity of 96% and specificity of 98%.

  • A normal scan does not exclude the diagnosis.
  • The findings of the bone scan are based on the phase.
134
Q

CRPS bone scan findings:

acute, dystrophic, atrophic

A
  1. Acute
  • Increased flow and blood pool activity in the affected extremity
  • Increased activity particularly in a periarticular distribution on delayed images
  1. Dystrophic
  • Flow and blood pool abnormalities begin to normalize
  • Increased activity on delayed images persists
  1. Atrophic
  • Flow and blood pool activity can be normal or decreased (in about 1/3 of patients)
  • Normal or decreased activity is commonly seen on delayed images, however, persistent increased delayed activity has been reported (up to 40%)
  • Decreased flow in advanced stage smay be related to disuse, which is a common feature of post-hemiplegic CRPS
135
Q

CRPS: treatments

A
  • anti-inflammatory drugs
  • antidepressant drugs
  • local peripheral nerve blocks
  • paravertebral sympathetic ganglion blocks
  • physical therapy
136
Q

diabetic ketoacidosis (DKA)

which DM type?

A

Type I

(IDDM)

137
Q

diabetic coma

which DM type?

A

Type II

(NIDDM)

138
Q

hypoglycemia: signs

A
  • nervousness
  • tachycardia (fast HR)
  • diaphoresis (sweating)
  • nausea
  • headache
  • confusion
  • tremor
  • seizures
  • coma
139
Q

hyperglycemia: signs

A
  • polyuria (excess urination)
  • polydipsia (excess thirst)
  • weight loss
140
Q

biguanide: function

A

anti-hyperglycemic

(but NOT hypoclygemic)

141
Q

what is a typical supplemental insulin scale?

A
142
Q

FDA-approved drugs for

treating diabetic neuropathy

A
  • duloxetine (Cymbalta)
  • pregabalin (Lyrica)
143
Q

osteoarthritis (OA):

clinical findings

A
  • Pain relieved with rest
  • Stiffness aggravated with activity
  • Crepitus with motion
  • Asymmetric joint swelling
144
Q

osteoarthritis (OA):

radiographic findings

A
  • Asymmetric joint space narrowing
  • Broadening and flattening of articular surfaces
  • Osteophytes at joint margins
  • Subchondral sclerosis
145
Q

MC inflammatory arthritis in men over 30?

A

Gout

146
Q

gout:

stages

A
  1. Asymptomatic hyperuricemia
  2. Acute gouty arthritis
  3. Intercritical gout
  4. Chronic tophaceous gout
147
Q

gout:

clinical findings

A
  • Asymmetrical, monoarticular arthritis
  • Sudden onset of red, hot, and swollen joint
  • Excruciating pain with acute attack
  • Tophaceous deposits
  • Most commonly affects 1st MPJ
148
Q

gout:

radiographic findings

A
  • Radiographic findings appear late in the disease after multiple attacks
  • Bone lysis in acute stages
  • Periarticular swelling with preserved joint space
  • Tophi at joint margins
  • Rat bite – punched-out, periarticular erosions
  • Cloud sign – tophaceous material
  • Martel sign – periarticular overhanging shelves of bone
149
Q

gout:

laboratory tests

A
  • Uric acid:
    • males >7 mg/dL,
    • females >6 mg/dL,
    • *though may be normal during attack
  • Synovial fluid analysis provides a more accurate diagnosis
150
Q

gout:

what would a joint aspirate show?

A

Needle-shaped monosodium urate crystals that are negatively birefringent (yellow) under polarized light

151
Q

What is CPPD?

A

Calcium Pyrophosphate Dihydrate Deposition Disease,

aka Pseudogout

152
Q

Pseudogout (CPPD):

what would joint aspirate show?

A

rhomboid-shaped and positively birefringent (blue)

under polarized light

153
Q

what is a “Martini sign” and what is it associated with?

A

Histology showing a PMNC engulfing a crystal

(associated with pseudogout)

154
Q

if gout is suspected, what should a specimen be sent in?

A
  • One in formaldehyde (dissolves gouty tophi), AND
  • one in alcohol (does NOT dissolve gouty tophi)
155
Q

acute gout: treatment

A
  • Colchicine
  • NSAIDS – indomethacin
  • Corticosteroids
  • ACTH
156
Q

chronic gout: treatment

A
  • Colchicine (prophylactically)
  • Allopurinol
  • Uricosurics – probenecid, sulfinpyrazone
157
Q

Colchicine: dosage

A
  • 0.6 mg PO q1h until symptoms resolve,
  • GI side effects occur, or max dose of 6 mg reached
158
Q

Colchicine: max daily dose

A

6 mg

159
Q

Can allopurinol, probenecid or sulfinpyrazone

be used for acute gout?

A

No, because they may cause an initial hyperuremia

160
Q

how to determine if patient is an

overproducer or underextretor?

A

Take a 24 hour uninalysis

161
Q

which is more common with gout:

overproducer or underexcretor

A

*Underexcretors make up approx 90%

162
Q

What medication for OVERPRODUCER of gout?

Medication for UNDEREXCRETOR of gout?

A

(“Over-Achieving, Under-Paid”)

  • Overproducer → Allopurinol
  • Underexcretor → Probenecid
163
Q

rheumatoid arthritis (RA):

clinical findings

A
  • Symmetric, progressive, polyarticular, and degenerative inflammatory arthritis
  • Pain first thing in morning
  • Stiffness after rest and reduced with activity
  • Rheumatoid nodules (25%)
  • Nail fold infarcts, splinter hemorrhages
  • Swan neck deformities – flexed DIPJ and extended PIPJ
  • Boutonniere deformities – extended DIPJ and flexed PIPJ
  • Other – bullous dermatosis, Raynaud phenomenon, vasculitis
164
Q

rheumatoid arthritis (RA):

epidemiology

A
  • Age of onset between 3-4th decades
  • Females > males
165
Q

rheumatoid arthritis (RA):

laboratory findings

A
  • Rheumatoid factor – positive
  • RBC – slight to moderate anemia
  • WBC – elevated in acute cases and normal to decreased in chronic
  • ESR & CRP – moderate to marked elevation
  • Synovial fluid analysis – elevated WBCs with cloudy fluid
166
Q

rheumatoid arthritis (RA):

radiographic findings

A
  • Clinical symptoms may present several years prior to radiographic findings
  • Peri-articular edema
  • Periosteal elevation and ossification
  • Marginal erosions
  • Subluxation and contractures (Swan neck deformities)
  • Fibular deviation of digits
  • Osteoporosis
  • Symmetric joint space narrowing and destruction (late stage finding)
167
Q

what causes fibular deviation of digits

associated with Rheumatoid arthritis?

A

Erosive changes of medial plantar metatarsal heads compromise the integrity of medial
collateral ligaments leading to lateral deviation of digits

168
Q

pannus: define

what disease is it associated with

A
  • Granulation tissue that secretes chondrolytic enzymes which break down articular cartilage
  • *Associated with Rheumatoid arthritis
169
Q

psoriatic arthritis:

clinical findings

A
  • Polyarthritis including DIPJ involvement
  • Sausage digits
  • Psoriatic skin changes
  • Nail lesions
170
Q

psoriatic arthritis (PA):

laboratory findings

A
  • HLA-27 – positive
  • Rheumatoid factor – negative
171
Q

psoriatic arthritis:

radiographic findings

A
  • Erosions with bony proliferation
  • Symmetric narrowing of joint space
  • Increased periosteal activity
  • Pencil-in-cup appearance
  • Osteopenic changes
172
Q

reiter syndrome:

clinical findings

A
  • Polyarticular, asymmetric arthritis of lower extremity (mostly affects small bones of feet, ankle, knee, SI joint)
  • Most affects males
  • Capsulitis with digital edema
  • Bony erosions
  • Reiter Syndrome Triad (can’t see, can’t pee, can’t climb a tree)
    • Conjunctivitis
    • Urethritis
    • Arthritis
    • Also keratoderma blenorrhagicum
173
Q

what is the Reiter Syndrome Triad?

A

(can’t see, can’t pee, can’t climb a tree)

  • Conjunctivitis
  • Urethritis
  • Arthritis
  • Also keratoderma blenorrhagicum
174
Q

reiter syndrome:

laboratory findings

A
  • HLA-27 – positive
  • Rheumatoid factor – negative
  • ESR – elevated
  • Synovial fluid analysis – Pekin cells
175
Q

What are Pekin cells?

(aka Reiter’s cells)

A

vacuolated macrophages with ingested neutrophils

176
Q

reiter syndrome:

radiographic findings

A
  • Fluffy periosteal reactions
  • Large, bilateral heel spur formation
  • Inflammation and widening of Achilles tendon insertion
  • Deossifications
177
Q

ankylosing spondylitis (AS):

clinical findings

A
  • Mostly males affected
  • Bilateral sacroiliitis – low back pain and stiffness
  • Heel pain
  • Peripheral joint pain
178
Q

ankylosing spondylitis (AS):

laboratory findings

A
  • HLA-27 – positive
  • Rheumatoid factor – negative
179
Q

ankylosing spondylitis (AS):

radiographic findings

A
  • Irregular joint widening with erosions
  • Reactive sclerosis
  • Bony ankylosis
  • Sacroiliac joint fusion
  • Bamboo spine
180
Q

septic arthritis:

clinical findings

A
  • Painful, hot, swollen joint
  • Systemic signs of fever, N/V, tachycardia, confusion
181
Q

septic arthritis:

laboratory findings

A
  • WBC – elevated with left shift
  • ESR – elevated
  • CRP – elevated
  • Blood cultures – positive
  • Synovial fluid analysis – elevated WBC with cloudy white or gray color
182
Q

septic arthritis:

radiographic findings

A
  • Normal in early stages
  • Joint effusion
  • Juxta-articular osteopenia
183
Q

septic arthritis:

etiologies

A
  • Contiguous,
  • hematogenous,
  • direct implantation,
  • surgical contamination
184
Q

septic arthritis:

most common offending organisms

A
  • All ages – Staphylococcus aureus
  • Neonates – Streptococcus and Gram negatives
  • Children – H. influenza
  • Teenagers – Neisseria gonorrhea
  • Puncture wounds – Pseudomonas aeruginosa
  • Adults with sickle-cell – Salmonella
185
Q

septic arthritis:

treatment

A
  • Needle drainage of joint
  • Open arthrotomy if osteomyelitis, joint implant, or chronic infection
  • Initial joint immobilization followed by passive ROM
  • Appropriate IV antibiotics for 2 weeks followed by 2-4 weeks of oral antibiotics
186
Q

brachymetatarsia:

define

A
  • Premature closure of epiphyseal plate of metatarsal resulting in a short metatarsal
  • Usually the 4th metatarsal is affected
187
Q

conditions associated with brachymetatarsia

A
  • Downs syndrome
  • Turners syndrome
  • Cri du chat
  • Pseudo- or pseudopseudohypoparathyroidism
  • May be idiopathic
188
Q

maximum length that a metatarsal may be acutely lengthened for correction of brachymetatarsia?

A

1 cm graft allows acceptable stretching of neurovascular structures

189
Q

If more than 1 cm of lengthening is required, what procedure may be performed?

A

Callus distraction with Mini-Rail fixation

190
Q

How much lengthening is typically achieved with

callus distraction?

A

1 mm per day (0.25 mm q6h)

191
Q

achondroplasia:

define

A

Dwarfism –

all bones short with tibia undergrowth and fibular overgrowth causing genu varum

192
Q

fibular hemimelia:

define

A

Aplasia or hypoplasia of the fibula

193
Q

DISH:

define

A

Diffuse Ideopathic Skeletal Hyperostosis (DISH) –

characterized by multiple ossifications at tendinous
or ligamentous insertions

194
Q

Apert syndrome:

define

A

multiple bony coalitions

People with Apert syndrome can have distinctive malformations of the skull, face, hands, and feet. Apert syndrome is characterized by craniosynostosis, a condition in which the fibrous joints (sutures) between bones of the skull close prematurely.

195
Q

paget disease:

define

A

Osteitis deformans –

  • abnormal bony architecture caused by increased osteoblastic and osteoclastic activity.
  • More common in elderly
196
Q

malignant bone degeneration that may be seen with

Paget disease

A

Osteosarcoma

197
Q

Paget disease:

stages

A
  1. Destructive – osteolytic
  2. Mixed – osteolytic and osteoblastic
  3. Sclerotic – osteoblastic
198
Q

Charcot:

stages

A
  1. Acute or destructive
  2. Coalescence
  3. Remodeling
199
Q

conditions with positive HLA-B27?

A
  • Ankylosing spondylitis (AS)
  • Reiter disease
  • psoriatic arthritis (PA)
  • reactive arthritis (RA)
  • enteropathic arthropathies
200
Q

CREST syndrome:

components

A
  • Calcinosis
  • Raynauds phenomenon
  • Esophageal dysmotility
  • Sclerodactyly
  • Telangiectasias
201
Q

CREST syndrome:

what is it?

A

limited cutaneous form of systemic sclerosis (lcSSc), is a multisystem connective tissue disorder.

202
Q

cutaneous larva migrans:

treatment

A

“Promethia under occlusion”;

  • Anthelmintics (tiabendazole, albendazole, mebendazole and ivermectin)
    • Topical thiabendazole is considered the treatment of choice for early, localised lesions.
    • Oral treatment is given when the cutaneous larva migrans is widespread or topical treatment has failed.
  • If these are unavailable, physical treatments (liquid nitrogen cryotherapy or carbon dioxide laser) may be used to destroy the larvae.
  • Antihistamines and topical corticosteroids may also be used w/ anthelminthics to provide symptomatic relief of itch.
203
Q

Lyme disease:

treatment

A

Doxycycline 100 mg PO daily, or

Rocephin l g IV daily

204
Q

necrotizing fasciitis:

drug of choice

A

Primaxin 250-1000 IV q6-8h

(most commonly 500 mg IV q8h)

205
Q

Felty syndrome:

define

A
  • Rheumatoid arthritis,
  • splenomegaly,
  • leukopenia
206
Q

mycosis fungoides:

define

A

Cutaneous T-cell lymphoma that can resemble eczematoid or psoriasis

207
Q

erythrasma:

define

A

Chronic, superficial infection of intertriginous skin caused by Corynebacterium minutissimum.

  • Interdigital lesions appear as maceration.
208
Q

ecthyma:

define

A
  • Ulcerative pyoderma of the skin
  • often caused by Streptococci.
  • Infection extends into dermis and is characterized by ulcers with overlying crusts.
209
Q

cellulitis:

define

A
  • Acute spreading infection of dermal and subcutaneous tissue
  • commonly caused by group A Strep or Staph aureus
  • Affected area is erythematous, warm, edematous, and tender.
210
Q

erysipelas:

define

A
  • Superficial infection that extends into the lymphatics.
  • Lesions are erythematous, indurated with sharply-demarcated margins, and have erythematous, ascending streaks.
211
Q

lymphangitis:

define

A

Inflammation of the lymphatics as a result of a distal infection

212
Q

psoriasis:

define

A
  • Hereditary disorder with chronic scaling papules and plaques in areas of body related to repeated minor trauma.
213
Q

psoriasis:

symptoms

A
  • Positive Koebner phenomenon and Auspitz sign.
    • Koebner phenomenon: formation of skin lesions on parts of the body where a person doesn’t typically experience lesions; “isomorphic response”
    • Auspitz sign: pinpoint bleeding that can occur when the surface of a scaling rash has been removed and capillaries just beneath the skin’s surface rupture
  • Other sxs:
    • joint pain
    • nail changes incl pitting, beau lines, oil spot, subungual hyperkeratosis, and discoloration
214
Q

lichen planus:

define

A
  • Inflammatory dermatosis involving skin or mucous membranes with pruritic, violaceous papules clustered into large, flat-topped lesions with distinct borders.
  • Lesions possibly covered with Wickham striae (white streaks).
  • Ridges, onycholysis, subungual hyperkeratosis, and discoloration.
215
Q

“6 P’s” of lichen planus

A
  • Planar (flat-topped)
  • Purple
  • Polygonal
  • Pruritic
  • Papules
  • Plaques
216
Q

another name for menopausal lipoma

A

juxtamalleolar lipoma

semi-fluctuant, irregular lobulated fatty mass anteroinferior to the lateral ​malleolus, commonly occurring bilaterally​

217
Q

main screening test if suspecting AIDS

A

ELISA (Enzyme Linked Immunosorbent Assay)

218
Q

What test should be performed to

confirm the diagnosis of AIDS?

A

Western blot

219
Q

effects of steroids

A

Anti-inflammatory

  • Decreases production of prostaglandins, cytokines, and interleukins
  • Decreases proliferation and migration of lymphocytes and macrophages

Metabolic

  • Decreases osteoblast activity
220
Q

difference between phosphate and acetate-based steroids

A

Phosphate-based – soluble with shorter half-life

  • Minimize inflammatory reaction and edema

Acetate-based – insoluble with longer half-life

  • May delay inflammatory process or healing and can mask infection
221
Q

common complication following steroid injection

A
  • Steroid flare – hypersensitivity reaction.
  • Apply ice.
222
Q

glucocorticoid metabolism

A
  • Metabolized in the liver
  • Secreted in urine
223
Q

diazepam:

use

A
  • Valium, a benzodiazepine
  • an anxiolytic/anticonvulsant/muscle relaxant
224
Q

diazepam: how to reverse

A
  • Flumazenil (Romazicon) for benzodiazepine reversal
  • Dosage
    • 0.2 mg IV over 15 seconds, then
    • 0.2 mg IV prn over 1 minute
    • (up to 1 gram total)
225
Q

insomnia: drugs

A

(BE HARD)

  • B – Benadryl
  • E – estazolam
  • H – Halcion
  • A – Ambien
  • R – Restoril
  • D – Dalmane

*Most commonly used are Benadryl 25 mg PO qhs or Ambien 5 mg PO qhs

226
Q

drugs causing metallic taste in the mouth

A
  • Flagyl
  • Lamisil
227
Q

treatment for Tylenol overdose

A

acetylcysteine (Mucomyst)

228
Q

Gray Baby Syndrome:

what causes it

A

Chloramphenicol

229
Q

what is chloramphenicol?

A

An antimicrobial

*Crozer-Keystone (14 decks)

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