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Acute Care I > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Secondary renal Na retention results from?

A

enhanced sympathetic activity, RAAS activation
CHF (from low CO)
Cirrhosis synthetic dysfunction & hypoalbuminemia

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2
Q

Hypervolemia/Na retention clinical presentation

A

Edema
effusions
rales
elevated JVP/CVP
hepatojugular reflux
S3
HTN
Low urine Na (<15mEq/L

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3
Q

Hypervolemia/Na retention symptoms

A

dypnea
abd distention
edema

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4
Q

Management of Hypervolemia/Na retention primary goals?

A

address underlying problem
limit Na intake (20-40mmol/d)

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5
Q

Management of Hypervolemia/Na retention
What medication should be used?

A

Diuretics

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6
Q

Proxmial tubule diuretic to use in management of Hypervolemia/Na retention?

A

Diamox

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7
Q

Loop Diuretic to use in management of Hypervolemia/Na retention?

A

lasix

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8
Q

Distal tubule diuretic to use in management of Hypervolemia/Na retention

A

HCTZ

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9
Q

Collecting duct diuretic to use in management of Hypervolemia/Na retention?

A

Spironolactone

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10
Q

Which is the most potent diuretic to use in management of Hypervolemia/Na retention?

A

lasix

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11
Q

How does spironolactone work?

A

competes with aldosterone

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12
Q

Antidiuretic hormone secretion leads to hyponatremia how?

A

either appropriate secretion in response to low circulating volume or inappropriate d/t neuro d/o, pulmonary disease, malignancy

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13
Q

Hyperosmolar hyponatremia is d/t?

A

hyperglycemia

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14
Q

Hyperosmolar hyponatremia causes increased ECF resulting in?

A

dilution of Na content

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15
Q

Hyperosmolar hyponatremia
For every 100 mg/dL rise in plasma glucose Na falls by?

A

1.6-2.4 mEq/L

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16
Q

Diagnostic approach to hyponatremia
Hypertonic Hyponatremia >295 mOsm/kg

A

Hyperglycemia
Hypertonic fluid admin

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17
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg first step?

Second step?

A

Assessment of volume status
hypovolemic
euvolemic
hypervolemic

Check urine sodium

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18
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypovolemic: urine sodium > 20 mEq/L

A

Renal solute loss

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19
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypovolemic: urine sodium </= 20 mEq/L

A

Extrarenal solute loss

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20
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Euvolemic: urine sodium always >20 mEq/L

A

SIADH
Endocrinopathies (Glucocorticoid deficiency)
Potassium depletion (diuretic use)

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21
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypervolemic: urine sodium > 20 mEq/L

A

Renal failure

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22
Q

Diagnostic approach to hyponatremia
Hypotonic hyponatremia <280 mOsm/kg
Hypervolemic: urine sodium </= 20 mEq/L

A

Edematous d/o’s
Heart failure
Cirrhosis
Nephrotic Syndrome

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23
Q

Hyponatremic Clinical presentation

A

Neurologic abnormalities d/t cerebral edema from shifting of H2O from ECF to ICF

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24
Q

Hyponatremic Clinical Presentation
neurologic abnormalities severity depends on?

A

magnitude & rapidity of fall

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25
Q

Hyponatremic Clinical Presentation
Acute: timeframe?
symptoms?

A

<2 days
nausea
malaise
H/A
lethargy
confusion
obtundation

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26
Q

Hyponatremic Clinical Presentation
Na 115 mEq/L results in?

A

stupor
seizures
coma

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27
Q

Hyponatremic Clinical Presentation
Chronic: timeframe?
symptoms?

A

> 3 days
minimization of increased ICF/symptoms

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28
Q

Management of Hyponatremia is determined by?

A

ECV (extracellular volume): low, normal, high
Presence of neuro symptoms

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29
Q

Symptomatic hyponatremia requires more rapid correction, however no greater increase in plasma Na than what rate?
not to exceed what level?
or how much Na mEq/L/d?
why?

A

0.5mEq/L/hr
130 mEq/L
>12 mEq/L/d
possible occurrence of central pontine myelinolysis (CPM) from neuronal damage from rapid osmotic shifts

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30
Q

Management of Hyponatremia for low ECV?

A

hypertonic saline 3% if symptomatic
NS if asymptomatic

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31
Q

Management of Hyponatremia for normal ECV?

A

lasix
hypertonic saline if symptomatic
NS if asymptomatic

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32
Q

Management of Hyponatremia for high ECV?

A

lasix
hypertonic saline if symptomatic
lasix if asymptomatic
water restriction

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33
Q

SIADH is what?

A

inappropriate levels of ADH are secreted despite absence of osmotic or volume related stimuli

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34
Q

SIADH is a dysregulation of what?

A

cells secreting ADH or in feedback mechanisms responsible for release

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35
Q

SIADH causes CNS disease

A

tumor
trauma
infection
CVA
SAH
GBS
DTs
MS

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36
Q

SIADH causes pulmonary disease

A

tumor
pneumonia
COPD
PPV

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37
Q

SIADH causes malignancies

A

lung
pancreas
ovarian
lymphoma

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38
Q

SIADH causes meds

A

NSAIDs
narcotics
diuretics
antidepressants
haldol
!

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39
Q

SIADH other causes?

A

surgery
idopathic

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40
Q

SIADH labratory
volume status?
Sodium status?
Urine osmolality?
Urine Na?
Serum osmolality?

A

euvolemia
hyponatremia secondary to H2O excess
Elevated urine osmolality (>200 mOsm/kg)
elevated urine Na (> 20mEq/L)
decreased serum osmolality (<280 mOsm/kg)

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41
Q

Hypernatremia H2O deficit comes from?

A

diaphoresis
diarrhea
osmotic diuresis (hyperglycemia)
diabetes insipidus

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42
Q

Hypernatremia Clinical Presentation symptoms

A

altered MS
weakness
neuromuscular irritability
focal deficits
coma
seizures occasionally
thirst
polyuria if DI

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43
Q

Diabetes insipidus r/t ADH
Central DI causes?

A

trauma
anoxic encephalopathy
surgery
meningitis
brain death
ethanol
neoplastic
idiopathic

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44
Q

Diabetes insipidus r/t ADH
Nephrogenic DI is d/t?

A

defective end-organ responsiveness to ADH

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45
Q

Diabetes insipidus r/t ADH
Nephrogenic DI causes?

A

ampho
lithium
dye
hypokalemia

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46
Q

Diabetes insipidus hallmark is what?
urine osmolarity in central is?
urine osmolarity in nephrogenic is?

A

dilute urine
<200 mOsm/L
200-500 mOsm/L

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47
Q

Diabetes insipidus causes what Na balance?

A

hypernatremia

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48
Q

Diabetes insipidus serum osmolality is?

A

> 290 mOsm/kg

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49
Q

Diabetes insipidus dx is confirmed by?

A

response to fluid restriction
failure of urine osmolarity to increase by >30 mOsm/L in initial hours is diagnositc

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50
Q

How to distinguish central DI from nephrogenic DI?Q

A

Response to vasopressin/dDAVP (1mcg SQ or IV)

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51
Q

Diagnostic Approach to Hypernatremia
Urine Output is low?

A

Urine Osmolality will be high
Was there hypotonic fluid loss?
insensible losses
GI losses
Prior Renal Losses from Diuretics

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52
Q

Diagnostic Approach to Hypernatremia
Urine Output is High; Urine Osmolality is Low

A

Diabetes Insipidus
Response to DDAVP indicates Central
No Response to DDAVP indicates Neprhogenic

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53
Q

Diagnostic Approach to Hypernatremia
Urine Output is High; Urine Osmolality is High

A

Osmotic Diuresis?

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54
Q

DI H2O deficit should not be corrected more rapid than?

A

10-12 mEq/L/d
less if chronic state

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55
Q

Management of Diabetes Insipidus free H2O admin should be done how?

A

calculate free H2O deficit
Correct H2O deficit over 2-3 days to reduce risk of cerebral edema

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56
Q

Management of Diabetes Insipidus if central?

A

DDAVP 2-5 u SQ q 4-6hrs

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57
Q

Management of Diabetes Insipidus if neprhogenic?

A

low Na diet
thiazide diuretic

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58
Q

A-fib anticoagulation/antiplatelet therapy
Scores to calculate when patient has CHF, HTN, AGE, sex, DM, Prior stroke TIA, Vascular disease?

A

CHADS2 score
CHA2DS2-VASc Score

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59
Q

A-fib anticoagulation/antiplatelet therapy
Scores to calculate when patient has HTN, abnormal renal function, abnormal liver function, stroke, bleeding, labile INR, elderly >65, alcohol or drug use?

A

HAS-BLED

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60
Q

Possible Differential Diagnosis for pts experiencing stroke like symptoms

A

Tumors
SDH
Cerebral abscess
Todd’s paresis or paralysis
Hypoglycemia
Encephalitis
Conversion D/O
Migrainous aura
focal seizure
periveral nerve lesions

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61
Q

Clinical Manifestations for MCA stroke

A

Hemiparesis
Hemiplegia
Hemianesthesia
Hemianopia
Aphasia
Neglect
Gaze deviation
!

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62
Q

Clinical Manifestations for Anterior Cerebral artery stroke

A

Lower extremity hemiplegia
Primitive reflexes
confusion
abulia
behavioral changes
disturbance in memory

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63
Q

Clinical Manifestations for Vertebral and basilar artery stroke

A

Decreased LOC
Vertigo
Dysphagia
Diplopia
Ipsilateral CN findings
Contralateral (or bilateral) sensory and motor deficits

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64
Q

Initial Evaluation
10 min or sooner from arrival

A

Evaluation by physician

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65
Q

Initial Evaluation
</= 15 min

A

Stroke or neurologic expertise contacted

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66
Q

Initial Evaluation
</= 20 min

A

NCCT or MRI

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67
Q

Initial Evaluation
</= 45 min

A

interpretation of neuroimaging

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68
Q

Initial Evaluation
</= 60 min

A

initiation of IV alteplase

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69
Q

Initial Evaluation
What should be assessed?

A

ABCs
Time of Onset
Circumstances surrounding onset of neuro symptoms
Hx
Neuro eval (NIHSS)
Labs and ECG
STAT Head CT
Vascular imaging

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70
Q

Initial Evaluation
Exclude stroke mimics such as

A

Psychogenic
Seizures
Hypoglycemia
Migraine
HTN encephalopathy
Wernicke’s encephalopathy
CNS abscess
CNS tumor
Drug toxicity

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71
Q

Initial Evaluation
All patients need

A

Non-Con CT (NCCT)
MRI
Blood glucose
Cardiac monitoring
EKG
Troponin
BMP, CBC, PT/INR/aPTT
Maintain O2 sats > 94%

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72
Q

Emergent Management of Ischemic Strokes
ABCs

A

avoid hypotension, hypoxia and hypovolemia

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73
Q

Emergent Management of Ischemic Strokes
Supplemental O2 for sats of?

A

> 94%

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74
Q

Emergent Management of Ischemic Strokes
Antipyretic medications for temp of?

A

> 38 C

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75
Q

Emergent Management of Ischemic Strokes
Fluid resuscitation w/?

A

isotonic fluids

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76
Q

Management of Ischemic Strokes includes?

A

Thrombolytic therapy
Mechanical thrombectomy
Antiplatelet therapy
BP management

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77
Q

Contraindications for IV Alteplase
Presentation to GI

A

Presentation outside window (>4.5 hrs)
Mild, nondisabling stroke (NIHSS 0-5)
HCT w/ extensive areas of hypoattenuation or frank hypodensity
ICH
AIS w/n 3 mo
Severe Head Trauma w/n 3 mo
Acute head trauma
Intracranial or intraspinal surgery w/n 3 mo
symptoms suggestive of SAH
GI malignancy or GI bleed w/n 21 days

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78
Q

Contraindications for IV Alteplase
Infective to Concomitant

A

Infective endocarditis
Aortic arch dissection
intra-axial intracranial neoplasm
coagulopathy (plt count < 100,000/mm3, aPTT > 40 sec, INR >1.7 or PT > 15 sec)
LMWH - therapeutic dose in last 24 hrs
Thrombin or Factor Xa inhibitors w/ elevated sensitive lab test (aPTT, INR, plt count, ECT; TT; appropriate factor Xa activity assays)
Concomitant Abciximab
Concomitant IV Aspirin

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79
Q

BP requirements for pts that are candidates for reperfusion therapy
Systolic and diastolic prior to infusion?
IVP medications that can be given to control BP? Dose? Frequency? (2)
IV infusions that can be given to control BP? Initial dose, titration parameters, max dose? (2)
Systolic and diastolic following infusion? for how long?

A

SBP </= 185 mmHg or DBP </= 110 mmHg
Labetalol, 10-20mg q1-2 min
Hydralazine, 10-20mg q1-2min
Nicardipine, 5mg/h, titrate up by 2.5mg/h at 5-15min intervals, 15mg/h
Clevidpine 1-2mg/h, titrate by doubling the dose q2-5 min until desired BP reached, 21mg/h
SBP </= 180 mmHg or DBP </= 105 mmHg for 24 hrs

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80
Q

Alteplase Admin
Dose (max dose)
infusion time

A

0.9mg/kg (max dose 90mg)
over 60 min w/ 10% of dose given as bolus over 1 min

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81
Q

Alteplase Admin
What would require the discontinuation of infusion and obtaining an emergency head CT scan?

A

if the patient develops
severe HA
acute hypertension
nausea or vomiting
worsening neuro exam

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82
Q

Alteplase Admin
What would be an indication for increasing frequency of BP measurements?
How to manage this?

A

if SBP > 180 mmHg or DBP > 105 mmHg
administer antihypertensive medications to maintain BP at or below these levels

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83
Q

Alteplase Admin
Before starting anticoagulants or antiplatelet what needs to be done?

A

Obtain a follow up CT or MRI scan at 24 hr after IV alteplase

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84
Q

Tenectaplase Admin
dose and infusion time?

A

Single IV bolus of 0.25mg/kg (max of 25mg) over 10 sec

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85
Q

Tenectaplase Admin
Must be given where?
Not compatible with?
What must be administered before and after?

A

dedicated IV
dextrose containing IVF
NS 0.9% flush

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86
Q

Management of ICH occurring w/n 24 hrs of IV alteplase or tenecteplase
Initial action?
Labs to get?
Imaging?

A

Stop infusion
CBC, PT(INR), aPTT, fibrinogen, type and cross
Emergency non-con head CT

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87
Q

Management of ICH occurring w/n 24 hrs of IV alteplase or tenecteplase
Blood products?
Medications?
Consults?
Anything else?

A

Cryoprecipitate 10 u infused over 10-30 min
Tranexamic acid 1000mg (over 10 min) or Aminocaproic acid 4-5 gm over 1 hr
Hematology and Neurosurgery
Supportive therapy

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88
Q

Mechanical Thrombectomy Criteria
Prestroke mRS score?
Occlusion of?
Age?
NIHSS socre >/=?
Alberta Stroke Program Early Computed Tomography Score (ASPECTS)?
Treatment can be initiated via groin w/n?

A

0-1
ICA or MCA
>/= 18
>/= 6
6 hrs

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89
Q

Mechanical Thrombectomy
Selected pt further criteria
Occlusion?
Mismatch between?
Age?
No what on Head CT or MRI?
No evidence of infarct involving?
Presentation?

A

LVO
severity of clinical deficit and infarct volume
>/= 18
ICH
more than 1/3 of the territory of the MCA
Late

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90
Q

BP management for Ischemic Stroke patient
Excessive BP lowering can have what effect?

A

worsen cerebral ischemia

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91
Q

Post stroke management
admit where?
neuro monitoring for?
antiplatelet agents? consider dual antiplatelet therapy for?
early what?
continue/start what? (check what)

A

stroke unit
hemorrhagic transformation or edema
ASA 24-48 hrs post tPA/TNK; minor noncardioembolic (NIHSS </=3) AIS who did not receive iV Alteplase
Mobilization
statin (check lipid panel)

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92
Q

Post stroke management
Glycemic management? treat BG of?
mental health?
Avoid what?
Skin protection includes?
Assessment of?
Education?
Evaluation of?
Treatment of?

A

normoglycemia (140-180), treat BG <60mg/dL, Check HgbA1c
Depression screening
indwelling catheters
turning, good skin hygeine, specialized mattress, wheelchair cushions
functional assessment
Smoking cessation; stroke education
Cardiac evaluation
Recurrent seizures

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93
Q

Meningitis
Clinical Presentation
Classic Triad?

A

Fever
Nuchal rigidity
AMS

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94
Q

Meningitis
Clinical Presentation
Symptoms outside of the classic triad include?

A

HA
Photophobia
Vomiting
Lethargy
Myalgia
Seizures
Skin manifestations
Symptoms progress hours to days

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95
Q

Meningitis
Clinical Presentation
Clinical findings are often overlooked in?

A

infants
obtunded patients
elderly patients w/ heart failure
elderly patients w/ pneumonia
Immunocompromised individuals

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96
Q

Clinical Signs
Brudzinski’s Sign

A

Spontaneous flexion of the hips during attempted passive flexion of the neck

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97
Q

Clinical Signs
Kerning’s Sign

A

Inability or reluctance to allow full extension of the knee when the hip is flexed 90 degrees

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98
Q

Meningitis
Diagnosis
Hx will include

A

recent illness or sick exposure
change in mental status
focal deficit
cranial nerve palsy

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99
Q

Meningitis
Diagnosis
Physical should include?

A

inspection of skin
otoscopic exam
inspect oral cavity/throat
CSF otorrhea or rhinorrhea

100
Q

Meningitis
Diagnosis
Imaging?

A

Head CT
Exclude mass lesion or elevated ICP
Prevent herniation d/t CSF removal

101
Q

Algorithm
With suspicion for bacterial meningitis, ask if the patient is/has

A

Immunocompromised
hx of CNS disease
new onset seizure
papilledema
altered consciousness
focal neruo deficit
delay in performatnce of diagnostic procedures

102
Q

Algorithm
If pt has any of the following what are the next steps?
Immunocompromised
hx of CNS disease
new onset seizure
papilledema
altered consciousness
focal neruo deficit
delay in performatnce of diagnostic procedures

A

Blood cultures STAT
Dexamethasone (b) + empirical antimicrobial therapy(c)
Negative CT scan of the head
Perform LP
CSF findings c/w bacterial meningitis
Perform Gram Stain

103
Q

Algorithm
If pt does not have any of the following, what are the next steps?
Immunocompromised
hx of CNS disease
new onset seizure
papilledema
altered consciousness
focal neruo deficit
delay in performatnce of diagnostic procedures

A

BC and LP STAT
Dexamethasone (b) + empirical antimicrobial therapy
CSF findings c/w bacterial meningitis
Perform CSF gram stain

104
Q

Algorithm
Positive CSF Gram Stain
Yes?
No?

A

Yes - Dexamethasone (b) + targeted antimicrobial therapy
No - Dexamethasone (b) + empirical antimicrobial therapy

105
Q

When to Order a Head CT for suspected meningitis

A

Immunocompromised
CNS disease
New onset seizure
Papilledema
Altered LOC
Focal Neuro deficit

106
Q

LP contraindications

A

Coagulopathy/thrombocytopenia
Clinical signs of impending herniation
Infection at LP site

107
Q

CSF analysis should include?

A

Color/clarity
cell count
protein
glucose
gram stain
culture
PCR and viral studies
CSF to plasma glucose is about 2/3

108
Q

CSF Characteristics in Bacterial vs. Viral Meningitis
Bacterial:
Color
Cell count
Glucose
Protein
Opening pressure

A

cloudy
200-20,000 PMN
<40
>50-100
Markedly high

109
Q

Most common organisms and treatment
Age 2-50
Common bacterial pathogens?

Antimicrobial therapy

A

N. meningitidis, S pneumoniae

Vancomycin plus a third gen cephalosporin

110
Q

Most common organisms and treatment
Age > 50 years
Common bacterial pathogens?

Antimicrobial therapy

A

S. Pneumoniae, N. meningitidis, L. monocyotogenes, aerobic gram-negative bacilli

Vancomycin plus ampicillin plus a third gen cephalosporin

111
Q

Most common organisms and treatment
Head trauma (Basilar Skull Fx)
Common bacterial pathogens?

Antimicrobial therapy

A

S. pneumoniae, H. influenzae, group A Beta-hemolytic streptococci

Vancomycin plus a third gen cephalosporin

112
Q

Most common organisms and treatment
Head Trauma (Penetrating Trauma)
Common bacterial pathogens?

Antimicrobial therapy

A

Staphylococcus aureus, coagulase-negative staphylococci (especially Stahpylococcus epidermidis), aerobic gram-negative bacilli (including Pseudomonas aeruginosa)

Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem

113
Q

Most common organisms and treatment
Postneurosurgery
Common bacterial pathogens?

Antimicrobial therapy

A

Aerobic gram-negative bacilli (including p. aeruginosa), S. aureus, coagulase-negative staphylococci (especially S. epidermidis)

Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem

114
Q

Most common organisms and treatment
CSF shunt
Common bacterial pathogens?

Antimicrobial therapy

A

Coagulase-negative staphylococci (especially S. epidermidis), S. aureus, aerobic gram-negative bacilli (including P. aeruginosa), Propionbacterium acnes

Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem

115
Q

Antibiotics
Third Gen Cephalosporine/dose/frequency?

A

Ceftriaxone 2g q12hr

Cefotaxime 2g q4-6hr

116
Q

Antibiotics
Glycopeptide/dose/frequency?

A

Vancomycin 15-20mg/kg q8-12hrs

117
Q

Antibiotics
PCN/dose/frequency?

A

Ampicillin 2g q4hrs (in adults > 50y/o)

118
Q

Antibiotics
In immunocompromised patients add what?
Instead of ceftriaxone or cefotaxime use what?

A

pseudomonal coverage
cefepime 2g q8hr or meropenem 2g q8hr

119
Q

Antibiotics
Antiviral for HSV meningitis/dose/frequency?

A

Acyclovir 5-10 mg/kg TID

120
Q

Steroids
steroid/dose/frequency/duration

A

dexamethasone 0.15mg/kg IV q6 hr for 2-4 days

121
Q

Steroids
Reduces risk of poor neurological outcome in pt with?
Must be given when?
Believed to minimize?

A

S. pneumoniae
early
inflammatory cascade

122
Q

What are the 6 herniation syndromes?

A

Uncal
Central
Subfalcine
Transcalvarial
Infratentorial
Tonsillar

123
Q

Indications for ICP monitoring include?

A

GCS <9 and w/ an abnormal CT
Comatose pts w/ normal CT scan and two or more of the following
1. Age > 40
2. Posturing
3. SBP < 90 mmHg

124
Q

Elevated ICP treatments include?

A

Resuscitation
Positioning
Sedation
BP control
Fever Control
Hyperventilation
Osmotic Therapy
Surgical Intervention
Hypothermia

125
Q

Positioning should be focused on?

A

HOB Elevated
Head in neutral position
Avoid tight c-collars

126
Q

Acute Hyperventilation causes?

A

Cerebral vasoconstriction
Decreased CBF
Decreased CBV
Decreased ICP
Effects are temporary
Should only be used as a temporizing measure

127
Q

Osmotic Therapy includes what?
What are it’s effects?

A

Mannitol and hypertonic saline
Reverse clinical herniation, even w/ normal ICP
Reduces ICP
Effects are due to osmotically induced fluid shifts

128
Q

Mannitol Therapy
Rapidly deteriorating patients require what dose for bolus?
What are the maintenance doses?
Labs required?

A

1g/kg IV
0.25-1g/kg q6hrs
BMP and serum osmolality q12hrs (baseline required prior to 1st mannitol dose)

129
Q

Hypertonic Saline - 23.4%
Effectiveness compared to Mannitol?
What kind of access can it be administered through?
How much is equiosmolar to 1g of Mannitol?

A

Equally as effective
Requires Central Access
0.686 ml of 23.4%

130
Q

Hypertonic Saline - 5%
How to dose it?
What kind of access can it be administered through?

A

3.2mL/kg
Dose not require a central line for bolus dose

131
Q

Hypertonic Saline - 3%
How to dose it?
What kind of access can it be administered through?

A

5.3mL/kg
Dose not require a central line for bolus dose

132
Q

Clinical Manifestations of DVT include

A

May be asymptomatic, nonspecific
Leg Edema
Tenderness
Discoloration/erythema
Difficulty walking

133
Q

Diagnosing DVT
DVT unlikely what test?
Positive?
Negative?

A

D-DImers
Positive complete venous US
Negative = no DVT

134
Q

Diagnosing DVT
DVT likely what test?

A

complete venous US

135
Q

Treatment for Proximal DVT

A

At least 3 mo AC; DOAC in noncancer pts if no contraindications

136
Q

Reassessment of Proximal DVT occurs when?
may extend for how long? and why?

A

3mo
May extend AC to yearly evaluation d/t risk/benefit, compliance, and patients preference

137
Q

Treatment of Isolated Distal DVT with High risk recurrence?

138
Q

Treatment/Surveillance options of Isolated Distal DVT with High risk recurrence?

A

Treatment AC (full or lower dose) or surveillance 4-6 wk venous US surveillance

139
Q

Prox DVT/PE, no cancer can be treated w/ what?
For how long?

A

Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo

140
Q

DVT provoked by surgery can be treated w/ what?
For how long?

A

Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo

141
Q

DVT with no surgery can be treated w/ what?
For how long?

A

Dabigatran
Rivaroxaban
Apixaban
Edoxaban
3mo

142
Q

1st unprovoked DVT can be treated with?
for how long?

A

Rivaroxaban - reduced dose
Apixaban - reduced dose
Extended treatment

143
Q

Active CA & + VTE/PE can be treated with? GI? for how long?

A

Rivaroxaban
Apixaban
Edoxaban
LMWH - may be preferred if luminal GI malignancy
Extended treatment

144
Q

If unprovoked DVT & DCing anticoag use what?

145
Q

Drugs that are Factor Xa inhibitors?

A

Rivaroxaban
Apixaban
Edoxaban

146
Q

Drugs that are Thrombin inhibitors?

A

Dabigatran

147
Q

Drugs that are Factor Xa/Thrombin Inhibitors?

148
Q

Complications of DVT: Post-thrombotic syndrome
Occurs in up to what % of patients with proximal DVT, within how long, despite anticoagulation?
Results from?
Duration?
Symptoms?

A

50%
~ 1-2yrs
valvular incompetence &/or residual obstruction
Chronic & progressive
Pain, edema, sometimes ulcerations

149
Q

Complications of DVT: Venous Ulceration
From what?
Usually appears where?
Prevent by use of?

A

post-thrombotic syndrome
usually appear perimalleolar area
compression stockings

150
Q

What type of PE can be life-threatening in normal persons?
What type of PE can be life-threatening in person with impaired physiologic reserves?

A

Massive emboli
Submassive

151
Q

In those with HD instability, mortality from PE increases by how much?

152
Q

Heart Failure d/t PE results from?

A

Vascular resistance leading to decreased RV output to increased RV pressure leading to ventricular wall stress increase leading to cardiac ischemia.

153
Q

In early phase of Heart Failure d/t PE what compensatory mechanisms maintain flow?
Which leads to?

A

Tachycardia & RV dilation
RV output falls d/t wall stress & ischemia leading to decreased LV preload

154
Q

RV dilation causes interventricular septal shift leading to?

A

decreased LV compliance leading to decreased LV output leading to hypotension

155
Q

Increased pulmonary vascular resistance is d/t?

A

thrombus itself & neural reflexes, humoral factor release from platelets/endothelium, & hypoxia

156
Q

S&S of PE

A

Non-specific/asymptomatic
Dyspnea
Tachypnea
Pleuritic pain
Pre-syncope/sycope
Cough
Orthopnea
Wheezing
Tachycardia/afib
Crackles on lung exam (21%)
Hypoxemia
Hypocapnia

157
Q

PE may lead to acute cor pulmonale which is shown by?

A

distended neck veins, prominent component of 2nd heard sound

158
Q

PE may cause EKG changes such as?

A

signs of R heart strain (New R axis deviation or new RBBB) or ST

159
Q

PE may cause CXR changes such as?

A

elevated R diaphragm
Pleural based opacities,
Westermark’s sign (dilation of pulm. vessels & sharp cutoff)

160
Q

EKG suspicious for PE will Show S1Q3T3 meaning?

A

S-waves in lead I
Q-waves in lead III
Inverted T-waves in lead III

161
Q

Differential Dx of PE can include?

A

MI
Pericarditis
Heart Failure
Pneumonia
Asthma
COPD
PTX
Rib Fx
Musculoskeletal pain
Intrathoracic CA
Sepsis

162
Q

Diagnosing PE
Need what?
May Utilize objective clinical assessments such as?

A

Clinical suspicion
Wells, Geneva, revised Geneva

163
Q

Diagnosing PE
Why use CXR?
may have nonspecific findings of?

A

utilized in general evaluation of pts w/ possible PE to exclude other causes of clinical presentation
Elevated diaphragm, pleural based infiltrates, focal oligemia (Westermark’s sign), hypovascularity

164
Q

Echocardiography (TTE) may show?

A

greater RV diameter & evidence of RV strain & failure
McConnell’s sign: regional RV dysfunction w/ akinesia of mid free wall but normal motion
May actually identify PE
Echo does not r/o presence of PE

165
Q

Suspected PE in patient w/o hemodynamic instability
Assess clinical probability of PE
Low or intermediate clinical probaility or PE unlikely what test(s)?

A

D-dimer: if negative no treatment
D-dimer: If positive CTPA
CTPA: no PE no treatment
CTPA: PE confirmed treatment

166
Q

Suspected PE in patient w/o hemodynamic instability
Assess clinical probability of PE
High clinical probability or PE likely what test(s)?

A

CTPA: no PE no treatment or investigate further
CTPA: PE confirmed Treatment

167
Q

Suspected PE in a patient w/ hemodynamic instability
Perform what test?
If signs of PE are present, what test(s)?

A

Bedside TTE looking for RV dysfunction
CTPA if immediately available. If not initiate treatment of high-risk PE
CTPA if positive initiate treatment of high-risk PE
CTPA if negative investigate other causes of shock or instability

168
Q

Risk Stratification
PE Lab indicators

A

troponin
BNP
Lactate
hyponatremia

169
Q

Risk Stratification
PE Clinical findings?

A

RV failure (TTE, CT)
tachycardia
hypotension
respiratory insufficiency
syncope

170
Q

Tx of RV failure
Volume optimization
Dose?
Properties and use?
Caveats?

A

Cautious volume loading use NS or LR </= 500 ml over 15-30 min

Consider in patients with low CVP

Volume loading can over-distend the RV worsening ventricular interdependence and reduce CO

171
Q

Tx of RV failure
Vasopressors and inotropes
Norepi
Dose?
Properties and use?
Caveats

A

0.2-1.0 nanogram/kg/min

Increases RV inotropy and systemic BP, promotes positive ventricular interactions, and restores coronary perfusion gradient

Excessive vasoconstriction may worsen tissue perfusion

172
Q

Tx of RV failure
Mechanical circulatory support
Strategy?
Properties and use?
Caveats?

A

Veno-arterial ECMO/extracorporeal life support

Rapid short-term support combined w/ oxygenator

Complications w/ use over longer periods (>5-10 days), including bleeding and infections; no clinical benefit unless combined with surgical embolectomy; requires an experienced team

173
Q

Anticoagulation for high or intermediate probability includes?

A

LMWH, fondaparinux, UFH, NOACs

174
Q

If anticoagulation is initiated parenterally, what is recommended for most patients?

A

LMWH or fondaparinux over UFH

175
Q

Rescue thrombolytic therapy is recommended for patients with what?

A

hemodynamic deterioration or anticoagulation treatment

176
Q

Anticoagulation dosing
Enoxaparin

A

1mg/kg q12 hr
1.5mg/kg once daily

177
Q

Thrombolytic dosing
rtPA

A

100 mg over 2 hr
0.6 mg/kg over 15 min (max dose of 50 mg)

178
Q

Medication tips
LMWH dosing in obesity
VKA monitoring after adjustment
VKA monitoring stable dose
No anti Xa levels in which patients
No monitoring of DOACs when?

A

use actual body weight
</= 4 wks
6-12 wks
obesity or CrCl < 30 ml/min
during bleeding

179
Q

Medication tips
INR w/ VKA 4.5-10 & no bleeding
Elevated INR + life-threatening bleeding
Bleeding on Xa inhibitor
Bleeding on dabigatran
Bleeding on LMWH or UFH
Resume anticoagulation w/n how long of bleed?

A

no intervention
PCC + vit K
+/- PCC or Xa (recombinant), inactivated-zhzo
idarucizumab
protamine
90 days

180
Q

VS findings in Asthma

A

RR often 25-40 breaths/min
tachycardia
pulsus paradoxus
SpO2 near 90% on RA

181
Q

What is Pulsus Paradoxus?
What value suggests moderate severity of exacerbation?

A

Exaggerated inspiratory decrease in systolic BP
15mmHg

182
Q

What inspection finding may suggest respiratory muscle fatigue in patients w/ COPD?

A

paradoxical abdominal wall motion w/ inspiration

183
Q

Thoracic Exam findings in COPD
Auscultation

A

Rhonchi w/ inspiration
Wheezes ww/ forced exhalation
decreased breath sounds in those w/ emphysema
asymmetry raises possibility of pneumothorax

184
Q

Diagnostic requirements for asthma

A

Positive post-bronchodilator response defined as 12% and at least 200 ml increase in FEV1

185
Q

ABG findings in patients w/ asthma

A

PAO2 at sea level is 55-70 mmHg usually
PaCO2 usually between 25-35 mmHg

186
Q

What is concerning when a patient w/ a hx of several days of moderate to severe airflow obstruction has a normal PaCO2?

A

It may indicate the mechanical load on the respiratory system is greater than can be sustained by the ventilatory muscles and that respiratory failure is imminent.

187
Q

Diagnostic criteria for COPD

A

Post-Bronchodilator ratio of FEV1/FVC < 0.7

188
Q

Patients w/ suspected COPD exacerbation may show evidence of what on CXR?

A

infiltrate suggestive of pneumonia

189
Q

What type of imaging is more sensitive in demonstrating parenchymal loss c/w emphysema, bullae, and pulmonary vascular changes suggestive of pulmonary HTN?

190
Q

ABG findings c/w COPD

A

Chronic hypercarbia typically accompanied by a respiratory acidosis w/ a compensatory elevation in the serum pH d/t elevated serum bicarbonate level that incompletely corrects the acidemia

191
Q

Asthma Pharmacologic Management (non-exacerbation)
Track 1 Symptoms per step
Step 1
Step 2
Step 3
Step 4
Step 5

A
  1. infrequent asthma symptoms (1-2 d/wk w/ normal or mildly reduced lung function)
  2. asthma symptoms < 3-5 d/wk w/ normal or mildly reduced lung function
  3. asthma symptoms most days (4-5 d/wk or more); waking d/t asthma once a week or more, or low lung funciton
  4. Daily asthma symptoms, waking at night w/ asthma once a wk or more w/ low lung volumes
  5. Initial asthma presentation is during an acute exacerbation
192
Q

Pharmacologic Management (non-exacerbation)
Track 1 Medications per step
Step 1
Step 2
Step 3
Step 4
Step 5

A

1-2: As needed-only low dose ICS-formoterol (budesonide-formoterol)
3. Low dose maintenance ICS-formoterol w/ reliever ICS-formoterol
4. Medium dose maintenance ICS-formoterol
5. Add on LAMA (like glycopyrolate) Refer for assessment of phenotype. consider high dose maintenance ICS-formoterol. +/- anti-IgE, anti-IL5/5R, anti-IL4Ra, anti-TSLR

193
Q

Group A requirements and med management for COPD

A

mMRC 0-1, CAT < 10 0-1 moderate exacerbations (not leading to hospital admission)
Should be prescribed a bronchodilator (albuterol - SABA) (salmeterol - LABA)

194
Q

Group B requirements and med management for COPD

A

mMRC >/= 2, CAT >/= 10, 0-1 moderate exacerbations (not leading to hospital admission) / year
LABA + LAMA (Vilanterol/Umeclidinium)

195
Q

Group E requirements and med management for COPD

A

> /= 2 exacerbations or >/= 1 leading to hospitalization
should be prescribed LABA + LAMA (Olodaterol/tiotropium)

196
Q

What to prescribe Group E if eos >/= 300

A

LABA + LAMA + ICS (Fluticasone/umeclidinium/vilanterol)

197
Q

Mild or Moderate Exacerbation presentation for Asthma

A

Talks in phrases
Prefers sitting to lying
not agitated
RR increased
No accessory muscle use
HR 100-120
SpO2 on RA 90-95%
PEF > 50% predicted or best

198
Q

Severe Exacerbation presentation for Asthma

A

Talks in words
sits hunched forward
agitated
RR > 30/min
Accessory muscle use
HR > 120bpm
SpO2 on RA < 90%
PEF </= 50% predicted or best

199
Q

Exacerbation presentation requirements for COPD

A

Worsening dyspnea, and/or cough and sputum in < 14 days
Often associated w/ increased local and systemic inflammation caused by airway infection, pollution, or other insults to lungs

200
Q

Exacerbation presentation w/ no respiratory failure

A

RR </= 24 breaths/min
HR < 95 bpm
no accessory muscle use
no changes to mental status
hypoxemia improved w/ supplemental O2 given via Venti mask 24-35%
no increase in PaCO2

201
Q

Exacerbation presentation w/ non-life-threatening acute respiratory failure

A

RR >24 breaths/min
Using Accessory muscles
no change in mental status
hypoxemia improved w/ supplemental O2 via venti mask > 35% FiO2
Hypercarbia PaCO2 increased compared w/ baseline or elevated between 50-60 mmHg

202
Q

Exacerbation presentation w/ life-threatening acute respiratory failure

A

RR > 24 breaths/min
using accessory muscles
acute mental status changes
hypoxemia not improved w/ supplemental O2 via venti mask or requiring > 40% FiO2
Hypercarbia PaCO2 increased compared w/ baseline or elevated > 60 mmHg or the presence of acidosis

203
Q

Exacerbation diagnosis for asthma

A

decrease in airflow quantified by PEF or FEV1 compared w/ previous lung function values

204
Q

Mild COPD Exacerbation diagnosis requirements

A

Dyspnea Visual Analog Scale < 5
RR< 24 breaths/min
HR < 95bpm
Resting Spo2 >/= 92% on RA
CRP < 10 mg/L

205
Q

Moderate COPD Exacerbation diagnosis requirements

A

Dyspnea Visual Analog Scale >/= 5
RR >/= 24 breaths/min
HR >/= 95 bpm
Resting SpO2 < 92% on RA and/or change >3% of previous
CRP >/= 10mg/L
ABG may show hypoxemia (PaO2 </= 60 mmHg), hypercapnia (PaCO2 > 45 mmHg) but no acidosis

206
Q

Severe COPD Exacerbation diagnosis requirements

A

Dyspnea Visual Analog Scale >/= 5
RR >/= 24 breaths/min
HR >/= 95 bpm
Resting SpO2 < 92% on RA and/or change >3% of previous
CRP >/= 10mg/L
ABG shows new onset/worsening hypercapnia and acidosis (PaCO2 > 45 mmHg and pH < 7.35)

207
Q

Exacerbation management for Asthma

A

Assess exacerbation severity from the degree of dyspnea, RR, HR, SpO2 and lung function while starting SABA and O2 therapy
Infection control procedures should be followed

208
Q

When and where to transfer a patient w/ asthma exacerbation?

A

Immediate transfer to acute care facility or ICU for signs of severe exacerbation or the patient is drowsy, confused or has silent chest.

209
Q

What to prescribe asthma exacerbatio patients during transfer?

A

SABA (albuterol) and Ipratropium bromide
controlled O2
systemic corticosteroids (prednisone 50mg PO 5-7 day course)

210
Q

What to do after 1 hr from interventions to treat asthma severe asthma exacerbations?

A

Reassess response of symptoms O2 saturation and lung function

211
Q

Only give ipratropium bromide for what?
What to consider for patients w/ severe exacerbation not responding to initial treatment?

A

Severe exacerbations
IV Mag Sulfate

212
Q

Exacerbation management for Severe but not life-threatening COPD Exacerbation?

A

Assess severity of symptoms, blood gases, chest radiograph
Increase doses and/or frequency of SABA
Combine SABA and anticholinergics (Salbutamol/ipratropium)
Consider use of LABA (Salmeterol) when patient becomes stable
Use spacers or air-driven nebulizers when appropriate
Consider systemic corticosteroids (PO prednisone 40 mg for 5 days
Consider ABx when signs of infection are present

213
Q

Classes of abx to use during COPD exacerbation w/ signs of infection?

A

aminopenicillin w/ clauvanic acid (augmentin, Unasyn)
macrolide (azithromycin, Clarithromycin, erythromycin, fidoxomicin, telithromycin)
tetracycline
quinolone (Ciprofloxacin, norfloxacin, ofloxacin, levofloxacin, moxifloxacin)

214
Q

Considerations during management of COPD Exacerbations at all times?

A

monitor IVF balance
consider SQH or LMWH for DVT prophylaxis
ID and treat associated conditions (e.g. heart failure, arrhythmias, PE etc.)

215
Q

Indications for transfer to Respiratory or Medical ICU for COPD exacerbation

A

Severe dyspnea that responds inadequately to initial emergency therapy.
Changes in mental status
Persistent or worsening hypoxemia (PaO2 < 40mmHg) and/or severe/worsening respiratory acidosis (pH < 7.25) despite supplemental O2 and NIV
Need for invasive mechanical ventilation
Hemodynamic instability - need for vasopressors

216
Q

Indications for NIV include at least one of the following

A

1.Respiratory Acidosis (PaCO2 >/= 45 mmHg and arterial pH </= 7.35)
2. Severe dyspnea w/ clinical signs suggestive of respiratory muscle fatigue increased WOB, or both, use of accessory muscles, paradoxical motion of the abdomen, or retraction of the intercostal spaces
3. Persistent hypoxemia despite supplemental O2 therapy

217
Q

Indications for Invasive MV

A

Unable to tolerate NIV or NIV failure
S/p respiratory or cardiac arrest
Diminished consciousness, psychomotor agitation inadequately controlled by sedation
Massive aspiration or persistent vomiting
Persistent inability to remove respiratory secretions
Severe hemodynamic instability w/o response to fluids and vasoactive drugs.
Severe ventricular or supraventricular arrhythmias
Life-threatening hypoxemia in patients unable to tolerate NIV

218
Q

Evaluation of Acute Hyperkalemia includes?

A

ECG
re-send unclotted blood sample for electrolytes, glucose, BUN, Cr, CBC
assess urine for heme to exclude rhabdo/hemolysis
review med list and diet

219
Q

Management of acute hyperkalemia
most exhibit ECG changes with what K level?

A

> 6.7 mEq/L

220
Q

Management of acute hyperkalemia
tx should be immediate for what K level?

A

> 6.5 mEq/L

221
Q

Management of acute hyperkalemia
tx should be immediate regardless of levels when?

A

ECG changes

222
Q

Management of acute hyperkalemia
Membrane stabilization includes?

A

CaGluconate (1g IV over 10 min) onset is immediate

223
Q

Management of acute hyperkalemia
Redistribution of K into cells includes?

A

insulin (10u IVP + 1 amp D50 IV)
albuterol (20mg/4mL)
Bicarb 150 mEq/L

224
Q

Management of acute hyperkalemia
insulin admin lowers K by how much?
Onset is how long?
when to not give D50?

A

approx. 1 mEq/L
20 min
if patient is already hyperglycemic

225
Q

Management of acute hyperkalemia
albuterol lowers K by how much?
drawback of albuterol?

A

approx 1 mEq/L
some may be resistant to albuterol; use as adjunct

226
Q

Management of acute hyperkalemia
Elimination of K includes?

A

diuretics (lasix 40-80 mg IV)
kayexalate - 15-30 g/ 15-30ml or lokelma
hemodialysis

227
Q

Management of acute hyperkalemia
onset for…
diuretics
sodium bicarb
sodium polystyrene sulfonate (kayexalate)

A

15 min
1 hr
> 2 hr

228
Q

Management of acute hyperkalemia
How does sodium polystyrene sulfonate work?
what are the effects?
what adverse reaction is potential?

A

exchanges Na for K in colon
variable
intestinal necrosis

229
Q

ARDS Patho
Overall occurrence is?

A

Diffuse alveolar damage & lung capillary endothelial injury

230
Q

ARDS Patho
(early phase) is? includes:
Increased?
Influx of?

A

Exudative
permeability of alveolar-capillary barrier
protein-rich fluid into alveoli

231
Q

ARDS Patho
Exudative (early phase) includes
injury to?

A

alveolar epithelial cells promoting pulmonary edema formation, decreased clearance from alveoli, & may decrease surfactant production causing decreased compliance and alveolar collapse

232
Q

ARDS Patho
Exudative (early phase) includes
what sells are sequestered/activated?
Leads to an imbalance between?

A

neutrophils, cytokines & platelets
pro-inflammatory & anti-inflammatory cytokines after inciting event

233
Q

ARDS Patho
Later phase is?

A

fibroproliferative

234
Q

Diagnosis of ARDS is?

A

Clinical diagnosis
Acute onset (w/n 7 days of defined event)
BL opacities on CXR or CT
No need to exclude HF

235
Q

ARDS severity
Mild P/F ratio is? Mortality?
Moderate P/F ratio is? Mortality?
Severe P/F ratio is? Mortality?

A

200-300; 27%
100-200; 32%
<100; 45%

236
Q

ARDS Management
Primary goal?

A

treat underlying cause

237
Q

ARDS Management
Lung Protective Strategies include?

A

low TV (4-8ml/kg PBW)
Peep (>5 cm H2O) for O2 say 85-90%
Lower FiO2 to minimize O2 toxicity (DAD, hyaline membrane formation, fibrosis)

238
Q

ARDS Management
Lung Protective Strategies allow for?

A

permissive hypercapnia
Caution for increased end-inspiratory volume (volutrauma), decreased preload, increased RV afterload

239
Q

ARDS Management
Proning
provides what?
is done for how long/day?
Is used in what classification of ARDS

A

mortality benefit
> 12 hrs/day
mod - severe ARDS

240
Q

ARDS Management
ECMO is considered for?

A

P/F ratio < 80 mmHg
High plateau pressures despite other strategies

241
Q

ARDS Management
IVF?
how do we feed them?
DVT propylaxis? yes no?

A

conservative fluids
enteral nutrition
yes

242
Q

Early Management of ARDS
Confirmed ARDS

A

VT about 6ml/kg of PBW
Plateau pressue < 30 cmH2O
PEEP > 5 cmH2O
Check for hypercapnia

243
Q

Early Management of ARDS
P/F ratio < 200

A

High level of PEEP if improves oxygenation

244
Q

Early Management of ARDS
P/F ratio < 150

A

NMB
Proning

245
Q

Early Management of ARDS
P/F ratio < 80

A

discuss VV-ECMO

246
Q

ARDS Prognosis
Mortality rate is about? & increases w/?
Failure of pulmonary function to improve in 1st week is?
Hospital course is?
Development of what?
The patient will lose?
Muscle weakness/functional impairment lasts for how long?
Disease severity & duration of MV are predictors of?
HRQOL significantly < normal @?

A

~30-40%; age
poor prognostic factor
prolonged
HAIs
Weight
months
persistent abnormalities in pulm. function; may have significant impairment for years
6mo

Acute Care I (30 decks)

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