Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Board Exam > Common Problems in Acute Care > Flashcards

Common Problems in Acute Care Flashcards

1
Q

Amphetamines (e.g. MDMA): presentation

A

euphoria, elation
dilated pupils
agitation, anxiety, insomnia
tachycardia, hypertension
vomiting
decreased appetite
tremors, muscle twitching, bruxism
perspiration, chills, pallor

resolves 24-48 hours after ingestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pneumocystis jirovecii: CXR

A

bilateral interstitial infiltrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

pneumocystis jirovecii: treatment

A

TMX-SMZ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

malignant hyperthermia

A

Genetic disorder that causes a fast rise in body temperature and severe muscle contractions when someone receives general anesthesia with one or more of the following drugs: (DISH-Succ)
- desflurane
- isoflurane
- sevoflurane
- halothane
- succinylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

malignant hyperthermia: Dx

A

caffeine halothane contracture test

Usually based on clinical signs and symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

malignant hyperthermia: signs

A

Earliest indication: increased end-tidal CO2 that is resistant to increases in minute ventilation
Late sign: hyperthermia

tachyarrhythmias
tachypnea
acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

malignant hyperthermia: treatment

A

dantrolene - interferes with muscle contraction by inhibiting calcium ion release from the sarcoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

malignant hyperthermia: ABG

A

respiratory acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

malignant hyperthermia: SVO2

A

decreased d/t significantly increased O2 consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

organophosphate (insecticide, pesticide) poisoning: S/Sx

A

AMS, slurred speech, coma
Headache
Miosis, blurred vision
Lacrimation
Excessive salivation
Bradycardia
Diffuse wheezing
diaphoresis
N/V/D, cramping
Urination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

organophosphate (insecticide, pesticide) poisoning: management

A

atropine
sodium nitrite

Wash skin thoroughly
If insecticide was ingested, give activated charcoal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

cutaneous anthrax: S/Sx, presentation

A

begins 1-7 days after exposure to infected livestock or livestock products

Painless pruritic papule appears and rapidly develops into an ulcer within 24 hours
Over the next 72 hours, the ulcer becomes dry and dark with surrounding edema (“black eschar”)

May cause bacteremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cutaneous anthrax: Dx

A

BC negative unless bacteremia
Tissue biopsy with gram stain, culture, and immunohistochemical stain to confirm Dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

arsenic poinsoning: S/Sx

A

diarrhea with negative workup
Leukonychia (white lines on nails)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Major causes of anion gap metabolic acidosis

A

MUDPILES
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Iron, Isoniazid
Lactate
Ethanol, Ethylene glycol
Salicylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Normal anion gap

A

8-12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How to calculate anion gap

A

Na - (Cl + HCO3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

necrotizing fasciitis: S/Sx

A

Early: flu-like symptoms

Later:
-rapidly spreading erythema
-pain extending beyond borders of erythema
-palpable crepitus
-Swelling of affected tissues
-Blisters filled with bloody or yellowish fluid
-Tissue death (necrosis)
-hypotension, sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

necrotizing fasciitis: labs/Dx

A

CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

necrotizing fasciitis

A

Infection of the fascia
Systemic toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

testicular torsion: presentation

A

acute onset of unilateral testicular pain after exercising
high riding testes
“bell-clapper deformity”
absent cremasteric reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

testicular torsion: management

A

immediate surgical exploration
intraoperative detorsion with fixation of the testes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

delay in correction of testicular torsion results in…

A

necrosis of testicular tissue d/t ischemia
If surgery is unavailable within two hours, manual detorsion can be attempted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

WHO Ladder of Pain Management: Step 1

A

Non-opioid +/- adjuvant (not traditionally used as 1st line for pain, e.g. nortriptylline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

WHO Ladder of Pain Management: Step 2

A

Choice from Step 1 [non-opioid +/- adjuvant] PLUS

Codeine
Dihydrocodeine
Oxycodone
Hydrocodone
Tramadol (not with ASA/APAP)

+/- adjuvants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

WHO Ladder of Pain Management: Step 3

A

Choice from Step 1 [non-opioid +/- adjuvant] PLUS

Morphine
Hydromorphone
Methadone
Levorphanol
Fentanyl
Oxycodone

+/- Nonopioid analgesics
+/- adjuvants (e.g. surgery for terminal cancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is recommended for breakthrough cancer pain?

A

fentanyl patches for sustained release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Metastatic bone pain: management

A

bisphosphonates – inhibit bone resorption and prevent the development of cancer-induced bone lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Stage 1 Pressure Injury

A

Intact skin with erythema that does not blanch
Does not include purple or maroon discoloration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Stage 2 Pressure Injury

A

Partial-thickness loss of skin with exposed dermis
Wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister
Adipose and deeper tissues are not visible

Should not be used to describe moisture associated skin damage including incontinence associated dermatitis, intertriginous dermatitis, medical adhesive related skin injury, or traumatic wounds (skin tears, burns, abrasions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Stage 3 Pressure Injury

A

Full-thickness skin loss
Adipose is visible and granulation tissue and epibole (rolled wound edges) are often present
Slough and eschar may be visible but do not obscure the extent of tissue loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Stage 4 Pressure Injury

A

Full-thickness skin and tissue loss
Exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone
Slough and/or eschar may be visible but do not obscure the extent of tissue loss
Epibole (rolled wound edges), undermining, and/or tunneling often occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Unstageable Pressure Injury

A

Obscured full-thickness skin and tissue loss
Extent of tissue damage cannot be confirmed because it is obscured by slough or eschar

Stable eschar on the heel or ischemic limb should not be softened or removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Deep Tissue Pressure Injury

A

Intact or non-intact skin with localized areas of persistent non-blanch able deep red, maroon, or purple discoloration or epidermal separation revealing a dark wound bed or blood filled blister

Do not use to describe vascular, traumatic, neuropathic, or dermatologic conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Pressure injury management considerations

A

hypoalbuminemia – reliable factor for pressure ulcer development (normal: 3.5-5)
wound care specialist consult
dressings
- weeping: hydrocolloid dressing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Initial treatment of post-op fever

A

In the absence of any indication of infection, the first response should include hydration and measures to expand lung function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Causes of non-infectious post-op fever

A

post-op atelectasis
increased basal metabolic rate
dehydration

drug reactions
-amphotericin B
-bactrim
-beta-lactam antibiotics
-procainamide
-isoniazid
-alpha-methyldopa
-quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

treatment of infectious post-op fever

A

supportive fluid and acetaminophpen
treat the apparent underlying source
gram stain, C&S all invasive lines or catheters as indicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

hypoalbuminemia

A

Increased risk for drug toxicity and interactions
Indicates protein malnutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Indications for duodenal tube

A

Able to use GI tract safely
Does not need tube feeds for >6 weeks
Risk for aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Indications for NG tube

A

Able to use GI tract safely
Does not need tube feeds for >6 weeks
Not at risk for aspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Indications for PEG

A

Able to use GI tract safely
Needs tube feeds for >6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Indications for PPN

A

Unable to use GI tract safely
Does not need nutritional support for >2 weeks
Can administer via PIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Indications for TPN

A

Unable to use GI tract safely
Needs nutritional support for >2 weeks
Administer via central line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Complications of enteral nutritional support

A

Involve the solution itself

Aspiration
Diarrhea (Is formula too concentrated? Switch bolus to continuous feeds? Slow down the rate?)
Emesis
GI bleeding
Mechanical obstruction of the tube
Hypernatremia
Dehydration
Refeeding syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Refeeeding syndrome: labs

A

Hypophosphatemia
hypokalemia
hypomagnesemia
hypocalcemia
thiamine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Complications of parenteral nutritional support

A

Involve the mode of delivery

Pneumothorax
Hemothorax
Arterial laceration
Air emboli
Catheter thrombosis
Catheter sepsis
Hyperglycemia
HHNK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

First and most important step in managing poisoning/drug toxicities

A

Obtain a detailed history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Poisoning/drug toxicities: GI decontamination

A

Gastric lavage

Activated charcoal – most beneficial within the first hour of ingestion

Cathartics – not routinely indicated with activated charcoal
-exception: Sorbitol often used with first dose of activated charcoal

Whole bowel irrigation – using polyethylene glycol to treat enteric-coated or sustained-release overdoses

Antidotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Acetaminophen intoxication: S/Sx

A

Usually asymptomatic in the early phase

Around 24-48 hours:
-N/V
-RUQ pain
-Signs of hepatotoxicity: jaundice, elevated LFTs, prolonged PT, -AMS, delirium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Acetaminophen intoxication: management

A

1st line: emesis or gastric lavage
Activated charcoal
N-Acetylcysteine (Mucomyst) with a loading dose of 140 mg/kg orally, as needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Acetaminophen intoxication: examples

A

Acetaminophen
Anacin-3
Panadol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Salicylate intoxication: examples

A

aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Salicylate intoxication: S/Sx

A

Delayed

HA, dizziness, tinnitus
apnea, cyanosis
dehydration
N/V
hyperthermia

metabolic acidosis
elevated LFTs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

salicylate intoxication: management

A

activated charcoal
sodium bicarbonate IV to correct severe acidosis (pH <7.1)
treat S/Sx
gastric lavage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

organophosphate (insecticide, pesticide) poisoning: examples

A

malathion
parathion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

antidepressant toxicity: S/Sx

A

Confusion, hallucinations, blurred vision
Seizures
Hypotension, tachycardia, dysrhythmias
Hypothermia
Urinary retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

antidepressant toxicity: management

A

ICU if CNS or cardiac toxicity evident
Activated charcoal

Dysrhythmias, acidosis/maintain pH: Sodium bicarbonate IV
Seizures: Benzodiazepines
Serotonin syndrome: dantrolene (Dantrium)
Rigors: clonazepam (Klonopin)
Temperature: cooling blankets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Opioid toxicity: S/Sx

A

drowsiness
hypothermia
respiratory depression, shallow respirations
miosis
coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

opioid toxicity: management

A

activated charcoal
naloxone (Narcan)

emetics are contraindicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

benzodiazepine toxicity: S/Sx

A

drowsiness, confusion
slurred speech
hyporeflexia
respiratory depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

benzodiazepine toxicity: management

A

respiratory and BP support
Flumazenil (Romazicon) IV
activated charcoal if recent ingestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

beta blocker overdose: S/Sx

A

delirium
hypotension
sinus bradycardia
bronchospasm
coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

beta blocker overdose: management

A

Charcoal if recent ingestion
glucagon
atropine as needed
stabilization of airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

ethylene glycol (antifreeze) overdose: S/Sx

A

First stage (30 min-12 hrs)
- loss of coordination
- headache
- slurred speech
- N/V

Second stage (12-24 hrs)
- irregular heartbeat
- shallow breathing
- Changes in BP

Third stage (24-72 hrs)
- kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

TCA toxicity: treatment

A

sodium bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

ethylene glycol (antifreeze) overdose: management

A

Fomepizole (Antizole)
Ethanol (if fomepizole not available)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Compartment syndrome

A

Increased interstitial pressure within a closed fascial compartment (skin, fascia, muscle, bone)

May result from hemorrhage, edema, sustained external pressure on a limb or constrictive casts, dressings, etc.

Should be suspected in any unconscious patient with a swollen limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Compartment syndrome: S/Sx

A

severe ischemic pain
parasthesias
tensely swollen
skin perfusion, arterial pulses normal
passive stretch of muscle is painful
progressive loss of sensory/motor function
repeated examinations are required to check for developing compartment syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Compartment syndrome: Diagnostics

A

Often using a Stryker tonometer; Normal compartment pressure: 0-8 mm Hg
>30 mmHg: Indicates compartment syndrome and a need for fasciotomy
- Within 10-30 mmHg of DBP: Indicates inadequate perfusion and relative ischemia of the involved extremity

Delta pressure: perfusion pressure of a compartment
= (diastolic BP) - (intracompartmental pressure)
<30 mmHg: indicates need for fasciotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

compartment syndrome: management

A

release constricting appliances
fasciotomy: effective only if performed within a few hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Dog, cat, human bites: management

A

Timely, copious, high-pressure irrigation with NS to reduce infection rates
Animal bites: ascertain rabies status

Wounds of the hand or lower extremities should be left open
- >6 hours: leave open to heal by secondary intention
Human and animal bites: ppx ABx to cover staphylococci and anaerobes (e.g. Augmentin) x3-7 days

X-rays as needed
Plastic surgery consultation as appropriate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

staphylococcus: class

A

gram positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

streptococci: class

A

gram positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

enterococci: class

A

gram positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

bacilli: class

A

gram positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

corynebacterium: class

A

gram positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

serrate marcescens: class

A

gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

escherichia coli: class

A

gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

klebsiella: class

A

gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

pseudomonas: class

A

gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

proteus mirabilis: class

A

gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Moraxella catarrhalis: class

A

gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

acinetobacter: class

A

gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

enterobacter: class

A

gram negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

acute otitis media: most likely pathogen and empiric therapy

A

S. pneumoniae

Empiric therapy:
-amoxicillin
-augmentin
-cefuroxime
-bactrim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

sinusitis: most likely pathogen and empiric therapy

A

S. pneumoniae

Empiric therapy:
-amoxicillin
-augmentin
-cefuroxime
-bactrim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

acute endocarditis: most likely pathogen and empiric therapy

A

staphylococcus aureus

vancomycin + ceftriaxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

subacute endocarditis: most likely pathogen and empiric therapy

A

viridian streptococci, enterococci

penicillin + gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

peritonitis d/t ruptured viscus: most likely pathogen and empiric therapy

A

coliforms
bacteroides fragilis

empiric therapy: metronidazole +
-cephalosporin 3rd generation (ceftriaxone, ceftazidime)
-pip/tazo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

intra abdominal infection: most likely pathogen and empiric therapy

A

E. coli
Klebsiella
Enterococci

empiric therapy: metronidazole +
-cefuroxime
-ceftriaxone
-ciprofloxacin
-levofloxacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

cellulitis: most likely pathogens and empiric therapy

A

staphylococcus aureus
Group A streptococcus

1st generation cephalosporin (cefazolin)
vancomycin
clindamycin
daptomycin
linezolid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

s. pneumoniae is the #1 pathogen causing…

A

otitis media
sinusitis
bronchitis
meningitis
CAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

colorectal, non-perforated appendectomy: ABx prophylaxis for staphylococci, streptococci, enteric gram-negative rods

A

cefazolin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

colorectal, non-perforated appendectomy: ABx prophylaxis for MRSA+

A

vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

colorectal, non-perforated appendectomy: ABx prophylaxis for enteric gram-negative rods, anaerobes

A

metronidazole plus:
-cefoxitin
-cefotetan
-cefazolin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

sepsis: most likely pathogens and empiric therapy

A

staphylococcus aureus

empiric therapy:
- 1st generation cephalosporins (cefazolin, cephalexin)
- 5th generation cephalosporins (ceftaroline)

vancomycin
linezolid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

osteomyelitis: most likely pathogens and empiric therapy

A

staphylococcus aureus

empiric therapy:
- 1st generation cephalosporins (cefazolin, cephalexin)
- 5th generation cephalosporins (ceftaroline)

vancomycin
linezolid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

CAP: most likely pathogens and empiric therapy

A

streptococcus pneumoniae

amoxicillin + macrolide (azithromycin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

MRSA: empiric therapy

A

1st line treatment: vancomycin

Alternative:
-daptomycin
-linezolid
-doxycycline
-ceftaroline
-clindamycin
-bactrim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

pharyngitis: most likely pathogen and empiric therapy

A

streptococcus pyogenes

Empiric therapy: vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

impetigo: most likely pathogen and empiric therapy

A

streptococcus pyogenes

Empiric therapy: vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

meningitis: most likely pathogen and empiric therapy

A

staphylococcus pneumoniae

empiric therapy: penicillin G

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Cephalosporins: best Gram+ coverage

A

1st generation: cefazolin, cephalexin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Cephalosporins: best Gram- coverage

A

5th generation: ceftaroline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Acute rejection of an organ: presentation

A

Immediate failure of that organ
Flu-like symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Acute rejection of an organ: labs/Dx

A

immediate biopsy of the transplanted organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Acute rejection of an organ: management

A
  1. corticosteroid:
    - methylprednisolone
    - prednisone
  2. antimetabolite:
    - azathioprine (Imuran)
    - mycophenolate mofetil (CellCept)
    - mycophoneolate sodium (Myfortic)
    - cyclophosphamide (Cytoxan)
  3. calcineurin inhibitor or mammalian target of rapamycin inhibitor:
    - calcineurin inhibitors: tacrolimus, cyclosporine
    - mTOR inhibitors: sirolimus, temsirolimus, everolimus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Shingles: S/Sx

A

Pain along a dermatomal distribution, usually on the trunk or chest
Grouped vesicle eruption of erythema and exudate along the dermatomal pathway
Regional lymphadenopathy may be present

110
Q

Shingles: management

A

Treatment:
-acyclovir
-famciclovir
-valacyclovir

If suspected ocular involvement, immediate referral to ophthalmologist

Post-herpetic neuralgia: gabapentin, pregabalin

111
Q

Shingles vaccine

A

Indicated for all adults >50, regardless of previous vaccine
- two dose regimen with 2nd dose given 2-6 months after 1st dose

112
Q

actinic keratoses

A

Premalignant
Asymptomatic, small rough flesh colored/pink/hyperpigmented patches

113
Q

actinic keratoses: treatment

A

liquid nitrogen to freeze off

114
Q

squamous cell carcinoma

A

arise out of actinic keratoses
Firm, irregular papule or nodule

115
Q

squamous cell carcinoma: management

A

biopsy and surgical excision (Mohs)

116
Q

seborrheic keratoses

A

benign, not painful lesions
beige, brown, or black plaques
“stuck on” appearance

117
Q

seborrheic keratoses: treatment

A

none or liquid nitrogen

118
Q

basal cell carcinoma

A

Most common skin cancer
Slow growing lesion
Waxy pearly appearance, may be shiny red
Central depression or rolled edge
May have telangiectatic vessels

119
Q

basal cell carcinoma: treatment

A

shave/punch biopsy and surgical excision

120
Q

malignant melanoma: criteria

A

highest mortality rate of all skin cancers
Median age at diagnosis: 40

Yes to 2+ = 97% sensitive to malignant melanoma:
- Assymetry
- Border irregularity
- Color variation
- Diameter >6 mm
- Elevation, Enlargement

121
Q

malignant melanoma: treatment

A

biopsy and surgical excision

122
Q

brain death criteria

A

coma
absence of brain stem reflexes
apnea

123
Q

most important feature of headaches to assess in order to determine the type of headache

A

chronology

124
Q

Components of headache evaluation

A

Chronology – most important
Location, duration, quality
Associated activity: exertion, sleep, tension, relaxation
Timing of the menstrual cycle
Presence of associated symptoms
Presence of “triggers”

125
Q

most common type of headache

A

tension headache

126
Q

tension headache: S/Sx

A

vise-like or tight in quality
usually generalized
may be most intense around the neck or back of the head
no associated focal neurological symptoms
usually last for several hours

127
Q

migraine headaches: causes

A

Related to dilation and excessive pulsation of branches of the external carotid artery
Onset usually in adolescence or early adult years
Often family history
Females > males
Nitrate containing foods
Changes in weather

128
Q

migraine triggers

A

emotional or physical stress
lack or excess sleep
missed meals
specific foods, esp nitrate containing foods
alcohol
menstruation
OCPs
changes in weather

129
Q

migraines: S/Sx

A

Unilateral, lateralized throbbing headache that occurs episodically
May be dull or throbbing
Build gradually and last typically for 2-72 hours
Focal neurologic disturbances may precede or accompany migraines (may present like TIA)
Follow the trigeminal nerve pathway
Visual disturbances: field deficits, luminous visual hallucinations
Aphasia, numbness, tingling, clumsiness, or weakness
Nausea, vomiting
Photophobia, phonophobia

130
Q

Concerns with new migraines

A

rule out tumor

131
Q

migraines: labs/Dx

A

BMP, CBC
VDRL to rule out tertiary syphillis
ESR
head CT to rule out tumor

132
Q

migraines: prophylaxis

A

Avoidance of trigger foods
Relaxation/stress management
Prophylactic daily therapy if >2-3 acute attacks/month

133
Q

migraines: prophylactic daily therapy

A

Anticonvulsants: topiramate, valproic acid
Beta-blockers: atenolol, metoprolol, propranolol, timolol
Botox: around face and scalp Q3 months; indicated if >15 headaches/month
CCBs: diltiazem, verapamil
TCAs: amitriptyline, nortriptyline
Calcitonin gene-related peptide (CGRP) inhibitors: eptinezumab, erenumab, fremanezumab, galcanezumab
NSAIDs and certain triptans: naproxen; can be helpful in treating women with migraines that are associated with menstrual cycle

134
Q

migraines: management of an acute attack

A

Rest in a quiet, dark room
Simple analgesic (ASA) right away
Sumatriptan (Imitrex) 6mg SQ at onset, repeat in 1 hour TID PRN
Sumatriptan (Imitrex) 25mg PO at onset of headache

135
Q

Cluster headaches: incidence

A

mostly affecting middle aged women

136
Q

Cluster headaches: causes

A

Often no family history of headache or migraine
May be precipitated by alcohol

137
Q

Cluster headaches: S/Sx

A

Severe, unilateral, periorbital pain occurring daily for several weeks
Usually occur at night, awakening the person from sleep
Usually lasts less than 2 hours
Pain free months or weeks between attacks
Ipsilateral nasal congestion, rhinorrhea, and eye redness may occur

138
Q

Cluster headaches: management

A

Treatment of individual attacks with oral drugs is usually unsatisfactory

100% O2
Sumatriptan (Imitrex) 6mg SQ
Ergotamine tartrate aerosol inhalation (Ergostat)

139
Q

most common electrolyte abnormality

A

hyponatremia

140
Q

hyponatremia: first step in treating

A

determine the cause

141
Q

hyponatremia: evaluation to determine the cause

A

Urine sodium
Serum osmolality
Clinical status

142
Q

normal urine sodium

A

10-20 mEq/L

143
Q

normal urine osmolality

A

50-1200 mOsm/kg

144
Q

normal serum osmolality

A

275-295

145
Q

isotonic hyponatremia: labs

A

serum osmolality 284-295 mOsm/kg

146
Q

isotonic hyponatremia

A

A laboratory artifact
Occurs with extreme hyperlipidemia or hyperproteinemia
Asymptomatic

147
Q

isotonic hyponatremia: treatment

A

cut down fat
no fluid restriction

148
Q

hypotonic hyponatremia: labs

A

serum osmolality <280 mOsm/kg

149
Q

hypotonic hyponatremia

A

State of body water excess diluting all body fluids

150
Q

hypotonic hyponatremia: first step in management

A

Assess if the patient is hypovolemic or hypervolemic

If hypovolemic, determine if hyponatremia is due to extrarenal salt losses or renal salt wasting by measuring urine sodium

151
Q

urine sodium >20 mEq/L

A

suggests renal salt wasting (a problem with the kidneys)

152
Q

urine sodium <10 mEq/L

A

suggests renal retention of sodium to compensate for extrarenal fluid losses (a problem other than the kidneys)

153
Q

hypovolemic hyponatremia w/urine Na+ <10 mEq/L: causes

A

dehydration
diarrhea
vomiting

154
Q

hypovolemic hyponatremia w/urine Na+ >20 mEq/L: causes

A

diuretics
ACE inhibitors
mineralocorticoid deficiency

155
Q

hypervolvemic, hypotonic hyponatremia: causes

A

edematous states
CHF
liver disease
advanced renal failure

156
Q

hypervolvemic hypotonic hyponatremia: treatment

A

restrict water

157
Q

hypertonic hyponatremia: serum osmolality

A

> 290 mOsm/kg

158
Q

hypertonic hyponatremia: cause

A

hyperglycemia – most common cause

159
Q

rapid correction of hyponatremia can result in…

A

osmotic demyelination syndrome

160
Q

hypovolemic hyponatremia: management

A

mild (Na >120): NS
severe (Na <120): 3%

161
Q

hyponatremia w/urine Na+ >20 mEq/L: management

A

treat the cause (diuretics, ACEIs, mineralocorticoid deficiency)

162
Q

Symptomatic hyponatremia: management

A

NS with loop diuretic

If CNS symptoms are present, consider 3% saline with loop diuretics
- raise Na+ slowly. Too fast can cause cerebral edema

163
Q

Hypernatremia: causes

A

Usually due to excess water loss
Always indicates hyperosmolality

Excessive sodium intake is rare

164
Q

normal sodium

A

135-145 mEq/L

165
Q

hypernatremia: management

A

Depends on cause

Severe hypernatremia with hypovolemia: NS (isotonic to increase BP) followed by 1/2 NS (when normotensive)

Hypernatremia with euvolemia: free water (D5W)

Hypernatremia with hypervolemia: free water and loop diuretics; may need dialysis

166
Q

Normal potassium

A

3.5-5.2 mEq/L

167
Q

hypokalemia: causes

A

Diuretics
GI loss
Excess renal loss
Alkalosis

Trauma patients: elevated serum epinephrine

168
Q

hypokalemia: S/Sx

A

muscle weakness, fatigue, cramps
constipation or ileus d/t smooth muscle involvement

Severe (<2.5): flaccid paralysis, tetany, hyporeflexia, rhabdomylosis

169
Q

hypokalemia: EKG changes

A

decreased amplitude
broad T waves
prominent U waves
PVCs, VT, VF

170
Q

hypokalemia: management

A

If K >2.5 mEq and no EKG abnormalities: oral replacement
If K <2.5 mEq or severe signs/symptoms: 40 mEq/L/hr IV
-check Q3h
-continuous telemetry

Mg+ deficiency frequently impairs K+ correction

171
Q

hyperkalemia: causes

A

Excess intake
Renal failure
Drugs (e.g. NSAIDs)
Hypoaldosteronism
Cell death
Acidosis

172
Q

hyperkalemia: S/Sx

A

weak, flaccid paralysis
Abdominal distention
Diarrhea

173
Q

hyperkalemia: EKG changes

A

tall, peaked T waves

174
Q

hyperkalemia: management

A

Exchange resins (e.g. Kayexalate)

If >6.5 or cardiac toxicity or muscle paralysis is present:
- insulin 10 U with one amp D50
- calcium gluconate

175
Q

normal total calcium

A

2.2-2.6 mmol/L
8.5-10.5 mg/dL

176
Q

normal ionized calcium

A

1.1-1.4 mmol/L
4.5-5.5 mg/dL

177
Q

ionized calcium

A

Does not vary with the albumin level
-Useful to measure when serum albumin is not within normal range
Increases with acidemia, decreases with alkalemia

178
Q

What does a normal calcium level in the presence of low albumin suggest?

A

hypercalcemia

179
Q

hypocalcemia: causes

A

hypoparathyroidism
hypomagnesemia
pancreatitis
renal failure
severe trauma
multiple blood transfusions

180
Q

hypocalcemia: S/Sx

A

increased DTRs
muscle/abdominal cramps
convulsions
Chvostek’s sign
Trousseau’s sign (captopedal spasm)
prolonged QT

181
Q

Chvostek’s sign

A

twitching of ipsilateral facial muscles on percussion d/t irritability of facial nerve
sign of hypocalcemia

182
Q

hypocalcemia: management

A

check blood pH for alkalosis

acute: IV calcium gluconate
chronic: oral supplements, vitamin D, aluminum hydroxide

183
Q

hypercalcemia: causes

A

hyperparathyroidism
hyperthryroidism
vitamin D intoxication
prolonged immobilization

rarely, thiazide diuretics

184
Q

hypercalcemia: S/Sx

A

fatiguability
muscle weakness
depression
anorexia
N/V
constipation
severe hypercalcemia can cause coma and death

185
Q

hypercalcemia: management

A

calcitonin if impaired cardiovascular or renal function
NS with loop diuretics
severe: dialysis

186
Q

respiratory acidosis: labs

A

pH <7.35
pCO2 >45

187
Q

respiratory acidosis: cause

A

decreased alveolar ventilation

188
Q

respiratory acidosis: S/Sx

A

somnolence
confusion
coma
myoclonus with asterixis

189
Q

normal pH

A

7.34-7.45

190
Q

normal pCO2

A

35-45

191
Q

normal HCO3-

A

22-26

192
Q

normal PaO2

A

75-100

193
Q

respiratory acidosis: management

A

narcan for all patients with no obvious cause
improve ventilation, intubate if necessary
increase rate on ventilator

194
Q

respiratory alkalosis: cause

A

hyperventilation

195
Q

respiratory alkalosis: labs

A

pH >7.45
pCO2 <35
serum HCO3 low if chronic

196
Q

respiratory alkalosis: S/Sx

A

light-headedness
anxiety
parasthesias
stocking/glove tingling
tetany if very severe

197
Q

respiratory alkalosis: management

A

manage underlying cause
If an acute hyperventilation syndrome is present, have the patient breathe into a paper bag
Decrease rate on ventilator as needed
Sedation if needed
Rapid correction of chronic alkalosis may result in metabolic acidosis

198
Q

metabolic acidosis: labs

A

pH <7.35
HCO3 <22

199
Q

anion gap formula

A

Na - (HCO3 + Cl)

200
Q

normal anion gap

A

5-15

201
Q

metabolic acidosis with increased anion gap: causes

A

DKA
alcaholic ketoacidosis
lactic acidosis

202
Q

metabolic acidosis with normal anion gap: causes

A

diarrhea
ileostomy
renal tubular acidosis
recovery from DKA

203
Q

metabolic acidosis: management

A

treat underlying cause
fluid resuscitation

204
Q

metabolic alkalosis: labs

A

pH >7.45
HCO3- >26
pCO2 >55 compensatory

205
Q

metabolic alkalosis: causes

A

post-hypercapnia alkalosis
NG suction
vomiting
diuretics

206
Q

metabolic alkalosis: management

A

correct volume deficit with NaCl and KCl
-if volume replacement is contraindicated: acetazolamide 250-500mg IV Q4-6 hours
discontinue diuretics
H2 blockers if GI loss

207
Q

1st degree burn

A

dry, red, no blisters
involves epidermis only

208
Q

2nd degree burn

A

partial thickness
moist, blisters
extends beyond epidermis

209
Q

3rd degree burn

A

full thickness
dry, leathery, black, pearly, waxy
extends from epidermis to dermis to underlying tissues, fat, muscle and/or bone

210
Q

Adult Rule of Nines

A

Each arm = 9%
Each leg = 18%
Thorax: front = 18%, back = 18%
Head = 9%
Perineum/genitals = 1%

211
Q

Parkland formula

A

4 ml/kg x TBSA % burned = fluid in 24 hours

212
Q

Fluid resuscitation in burns

A

1/2 of all fluid requirements during the first 24 hours administered within 8 hours of injury
Remaining 1/2 of fluid to be given over the next 16 hours

213
Q

burns: monitoring

A

metabolic acidosis expected in the early resuscitation phase
hyperkalemia during the first 24-48 hours; hypokalemia following fluid resuscitation/diuresis around 2 days post burn

214
Q

burns: indications for prophylactic intubation

A

burns to the face
singed nares or eyebrows
dark soot/mucous from nares and/or mouth

215
Q

tar burn injury: management

A

use a petroleum-based product to remove the burning tar

216
Q

diabetic retinopathy: S/Sx

A

microaneurysms are the earliest detectable sign
-ruptured microaneurysms results in retinal hemorrhages either superficially (flamed-shaped hemorrhages) or in deeper layers of the retina (blot and dot hemorrhages)

cotton-wool spots

217
Q

AV nicking

A

sign of chronic hypertension

218
Q

Arcus sinilis

A

a cloudy appearance of the cornea with a gray/white arc or circle around the limbus d/t deposition of lipid material
no effect on vision

cause: hyperlipidemia

219
Q

chemical conjunctivitis: management

A

self-limiting
flush with normal saline

220
Q

bacterial conjunctivitis: management

A

self-limiting
antibiotic drops (e.g. levofloxacin, ofloxacin, ciprofloxacin, tobramycin, gentamycin ophthalmic solution)

221
Q

gonococcal conjunctivitis: management

A

opthalmic emergency
ceftriaxone 250mg IM + azithromycin

222
Q

chlamydial conjunctivitis: management

A

ceftriaxone 250mg IM + azithromycin

223
Q

allergic conjunctivitis: management

A

oral antihistamines
-refer to allergist/ophthalmologist if no response

steroids are not ordered in primary care because of possible increased intraocular pressure and activation of HSV

224
Q

viral conjunctivitis: management

A

symptomatic care
-mild: saline drops, artificial tears
-moderate: decongestants, antihistamines, mast cell stabilizers, NSAIDs

Sulfacetamide 10% ophthalmic solution for bacterial (secondary) prophylaxis

225
Q

herpetic conjunctivitis: management

A

refer to ophthalmologist

226
Q

What type of conjunctivitis has purulent discharge?

A

bacterial

copious: gonococcal

227
Q

What type of conjunctivitis has stringy discharge and increased tearing?

A

allergic

228
Q

What type of conjunctivitis has watery discharge?

A

viral

229
Q

What type of conjunctivitis makes the conjunctiva bright red and irritated?

A

herpetic

230
Q

glaucoma: pathology

A

increased intraocular pressure
closed angle: acute
open angle: chronic

231
Q

closed angle glaucoma: S/Sx

A

closed angle: acute
-extreme pain
-blurred vision
-halos around lights
-pupil dilated or fixed

232
Q

open angle glaucoma: S/Sx

A

Open angle: chronic
-asymptomatic
-elevated IOP
-cupping of the disc (earliest sign)
-constriction of visual fields

233
Q

glaucoma: screening

A

tonometry: screening recommended by age 40

234
Q

open angle glaucoma: management

A

Open angle: chronic
-prostaglandin analogs (latanoprost, bimatoprost, tafluprost, travoprost, latanoprostene bunod)
-alpha 2-adrenergic agonists (brimonide, alphagan)
-beta-adrenergic blockers (timolol)
-miotic agents (pilocarpine)

234
Q

closed angle glaucoma: management

A

closed angle: acute
-carbonic anhydrase inhibitors (acetazolamide)
-osmotic diuretics (mannitol)
-surgery

235
Q

cataract: pathology

A

clouding and opacification of the normally clear lens of the eye
highest cause of treatable blindness

236
Q

cataract: causes

A

Aging – biggest risk factor
heredity
trauma
toxins, drugs, tobacco, alcohol
congenital
diabetes
UV sunlight exposure

237
Q

cataracts: S/Sx

A

painless
clouded, blurred, or dim vision
difficulty with vision at night
sensitivity to light and glare
fading/yellowing of colors
diplopia in a single eye
halos around lights
the need for brighter light for reading
no red reflex
opacity of the lens

238
Q

cataracts: management

A

refer to opthalmologist for surgery

239
Q

sodium phosphate enemas: adverse effects

A

Significant electrolyte abnormalities in patients with renal insufficiency, heart failure, cirrhosis, or elderly frail individuals

240
Q

cutaneous anthrax: management

A

post-exposure prophylaxis and treatment: 60 days of ciprofloxacin and doxycycline regardless of vaccination status

Penicillin is no longer recommended due to increased resistance

241
Q

inhalation anthrax: treatment

A

raxibacumab
rifampin

242
Q

Opioid withdrawal: S/Sx

A

Depressed mood
Insomnia
Mydriasis, lacrimation
Runny nose
Yawning
N/V/D
myalgias
diaphoresis
fever

243
Q

Haemophilus influenzae: class

A

Gram negative

244
Q

HAP: most likely pathogens and empiric therapy

A

S. aureus
S. pneumoniae
H. influenzae

empiric therapy:
-pip/tazo
-cefepime
-levofloxacin
-imipenem or meropenem

If MRSA suspected: + vancomycin or linezolid

If high risk of mortality or IV ABx within previous 90 days:
-two of above ABx + vancomycin or linezolid

245
Q

VAP: most likely pathogens and empiric therapy

A

MRSA
- vancomycin or linezolid

pseudomonas aeruginosa
-pip/tazo
-cefepime or ceftazidime
-imipenem or meropenem
-aztreonam
-levofloxacin or ciprocloxacin
-amikacin or gentamicin or tobramycin
-colistin or polymyxin B

246
Q

necrotizing fasciitis: pathogen and treatment

A

Group A streptococcus

Treatment: ampicillin, penicillin, and clindamycin
Surgery

247
Q

beta lactam antibiotics: examples

A

penicillins
cephalosporins
carbapenems
monobactams (aztreonam)
beta lactamase inhibitors (clavulanic acid, sulbactam, and tazobactam)

248
Q

placenta previa

A

Condition in which the placenta is implanted in the lower uterus, adjacent to or over the os
-Risk factors: multiple pregnancies, multiple surgeries

249
Q

placenta previa: S/Sx

A

soft, nontender uterus
painless right red vaginal bleeding in the third trimester

250
Q

abruptio placenta

A

premature separation of the placenta from the uterine wall
-risk factors: diabetes, renal disease, HTN, eclampsia, abdominal trauma
-DIC can occur

251
Q

abruptio placenta: S/Sx

A

painful dark red bleeding
abdominal pain

252
Q

methanol toxicity: S/Sx, labs

A

optic disc changes including hyperemia of the optic disc (engorged vessels)

anemia
leukocytosis
high osmolar gap

253
Q

methanol toxicity: management

A

ethanol
hemodialysis

254
Q

paronychia

A

infection of the lateral and proximal nail fold

Risk factors:
-nail biting
-diabetes
-sucking
-frequent immersion of hands in water

255
Q

SJS/TEN involves __% of BSA

A

10-30%

256
Q

Stevens-Johnson Syndrome: presentation

A

Erythematous, purpuric rash with scattered bullae that are often painful
Mucosal involvement: eyes, mouth, genitals
Involves <10% of BSA

257
Q

Stevens-Johnson syndrome is most often associated with which drug

A

bactrim

258
Q

treatment for delirium

A

1st line: antipsychotics
precedex

Avoid opioids, benzos

259
Q

Kehr’s sign

A

Pain in the tip of the shoulder caused by irritation of the diaphragm due to the presence of blood in the peritoneal cavity
-characteristically occurs in the left shoulder in patients with a severe splenic injury

Obtain CT A/P

260
Q

Who is at risk for infections caused by cryptococcal meningoencephalitis?

A

opportunistic infection seen in patients with untreated AIDS

261
Q

Who is at risk for listeria monocytogenes?

A

neonates
immunosuppressed
pregnant
elderly

262
Q

CAP d/t Legionella spp.: treatment

A

macrolides (azithromycin)

263
Q

Main sign that a patient will likely need amputation of a limb

A

necrosis of the digits

264
Q

cytomegalovirus: S/Sx

A

profound diarrhea with little to no other abdominal or infectious symptoms

265
Q

cytomegalovirus: treatment

A

ganciclovir (Cytovene)

266
Q

abdominal compartment syndrome

A

Third spacing of fluids into the abdominal cavity –> distended, tense abdomen, which causes:
-increased pressure on the inferior vena cava, impeding blood return to the heart and causing a prerenal state of shock
-increased thoracic pressure

267
Q

Massive transfusions and large amounts of IV fluid administration are risks for…

A

abdominal compartment syndrome

268
Q

erythema multiforme

A

rash most commonly caused by HSV infection
Target lesions demonstrating 3 zones of color change

269
Q

Can a patient’s decision to be an organ donor be overridden by family or HCP?

A

No
Call the local organ procurement agency

270
Q

acute graft vs host disease: presentation

A

Within the first 100 days after bone marrow transplant
Involves skin, liver, GI system
Often febrile

Early stages can present with morbilliform rash
Sunburn-like rash with blistering is concerning for severe disease

271
Q

Recommended carbohydrate intake

A

55-60% of diet
Increases with illness and trauma

Board Exam (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions