Readings AMS quiz

Question 1

Hypoglycemia in diabetics is usually a complication of ——-

Answer 1

treatment with insulin or sulfonylureas

Question 2

Clinical features of hypoglycemia

Answer 2

Sweating
Shakiness
Anxiety
Nausea
Dizziness
Palpitations
Slurred speech
Blurred vision
Headache
Seizure
Focal neurological deficits
Altered mental status from confusion to coma

Question 3

Diagnosis of hypoglycemia

Answer 3

Low blood glucose with typical signs and symptoms that resolve with treatment

Question 4

Emergency department care of hypoglycemia

Answer 4

1) glucose and provide carbohydrate meal when tolerate PO
If altered mental status: 50% dextrose 50 mL IV; continuous infusion of 10% dextrose may be required to keep glucose above 100 mg/dL
2) Administer glucagon 1 mg IM or SC if no IV access
3) Treat refractory due to sulfonylureas with octreotide 50-100 ug SC, continuous infusion may be needed
4) Repeat BG every 30 minutes for rebound

Question 5

Disposition of hypoglycemia

Answer 5

If good response to treatment, good social support, and treatment of cause of hypoglycemia –> discharge with instructions to monitor glucose and continue carbs
If due to sulfonylureas or long acting insulins, admit

Question 6

Inpatient care for type 2 diabetes mellitus is generally appropriate for which clinical situations?

Answer 6

DKA or hyperglycemic hyperosmolar nonketotic state
Severe complications, comorbidities, or inadequate social support
Hyperglycemia (>400 mg/dL) with severe volume depletion or refractory to appropriate interventions
Hypoglycemia with neuroglycopenia that does not resolve with correction of hypoglycemia
Hypoglycemia from long-acting oral hypoglycemic agents
Fever without obvious source in poorly controlled diabetes

Question 7

What generally causes DKA?

Answer 7

Insulin deficiency and counter-regulatory hormone excess —> hyperglycemia and ketonemia

Question 8

Clinical features of DKA

Answer 8

Dehydration
Hypotension
Tachycardia
Acidosis
Myocardial depression
Vasodilation
Kussmaul respiration
Nausea, vomiting, abdominal pain
Acetone –> fruity odor of breath

Question 9

Diagnosis of DKA

Answer 9

Glucose >250 mg/dL
Anion gap >10 mEq/L
Bicarb <15 mEq/L
pH <7.3
Moderate ketonemia/ketonuria
Can have euglycemic ketoacidosis if taken insulin, impaired gluconeogenesis, or takes sodium-glucose cotransporter 2 inhibitor

Question 10

What causes anion gap metabolic acidosis in DKA?

Answer 10

formation of ketone bodies

Question 11

If a nitroprusside test is used to detect serum or urine ketones, what can results be?

Answer 11

Falsely low or negative because of conversion of acetoacetate to B-hydroxybutyrate (test only detects acetoacetate)

Question 12

What happens to electrolytes in DKA?

Answer 12

Osmotic diuresis –> loss of sodium, chloride, calcium, phosphorus, and magnesium
Serum and urine glucose and ketones are elevated
Potassium may be low (vomiting/osmotic diuresis), normal, or high (acidosis)

Question 13

Laboratory evaluation of DKA

Answer 13

serum pH (venous blood)
Glucose
Electrolytes
Cr/BUN
phosphorus
Magnesium
CBC
UA
ECG
CXR

Question 14

ED care of DKA

Answer 14

Correct volume deficit, acid-base imbalance, and electrolyte abnormalities
administer insulin
treat underlying cause
Administer bicarb if pH <6.9
Monitor glucose, anion gap, potassium, and bicarb hourly until recovery: glucose <200 mg/dL, bicarb >18, and pH >7.3

Question 15

What is a complication of DKA treatment? What are its risk factors and when should you treat?

Answer 15

Cerebral edema
Young age and new-onset diabetes
If change in neurological status

Question 16

What should be done if change of neurological status early in therapy for DKA?

Answer 16

Begin treatment with mannitol 1 g/kg before obtaining diagnostic CT scan

Question 17

Any disease process that interrupts normal blood flow to the brain

Answer 17

stroke

Question 18

what is the most common type of stroke?

Answer 18

Ischemic > intracerebral hemorrhage >SAH

Question 19

What is a TIA

Answer 19

transient episode of neuro dysfunction caused by ischemia typically 1-2 hours long

Question 20

clinical features of stroke

Answer 20

depends on region of brain compromised and severity

Question 21

clinical features of anterior cerebral artery stroke

Answer 21

contralateral leg weakness
sensory changes

Question 22

clinical features of middle cerebral artery stroke

Answer 22

contralateral hemiparesis arm >leg
facial plegia
sensory loss
aphasia if dominant hemisphere (usually left) affected
inattention, neglect, dysarthria without aphasia if nondominant side effected

Question 23

clinical features of posterior circulation stroke

Answer 23

unilateral limb weakness
dizziness
vertigo
blurry vision
headache
dysarthria
visual field loss
gait ataxia
cranial nerve VII dysfunction
lethargy
sensory deficits

Question 24

clinical features of basilar artery occlusion

Answer 24

posterior circulation stroke symptoms as well as oculomotor signs
Horner’s syndrome
“locked in state”

Question 25

clinical presentation of cerebellar strokes?

Answer 25

similar to posterior stroke deteriorate rapidly

Question 26

how do patients with cervical artery dissection present?

Answer 26

internal carotid dissection: unilateral head pain neck pain face pain vertebral artery dissection neck pain headache, bilateral or unilateral

Question 27

SAH clinical presentation

Answer 27

sudden onset headache at maximal intensity associated with activities known to elevate blood pressure such as sexual intercourse, weight lifting, defecation, coughing loss of consciousness diplopia vomiting photophobia nuchal irritation low grade fever altered mental status presence of absence of focal neurological findings depends on location of aneurysm

Question 28

risk factors for stroke

Answer 28

age atrial fibrillation hypertension diabetes smoking coronary atherosclerosis valvular replacement recent myocardial infarction

Question 29

risk factors for SAH

Answer 29

excessive alcohol consumption polycystic kidney disease family history of SAH marfan's/ehlers-danlos history of drug use, chiropractic manipulation, or blood-pressure elevation

Question 30

if ischemic stroke is primary working diagnosis and thrombolytic therapy considered, obtain ---------

Answer 30

accurate determination of time patient last known baseline and whether may be candidate for thrombolytics

Question 31

assessment of stroke

Answer 31

focused on neuro motor weakness sensory deficits cerebellar dysfunction meningismus carotid bruits signs of embolic disease papilledema preretinal hemorrhage

Question 32

when would a NIHSS score be determined?

Answer 32

If thrombolytic therapy considered

Question 33

what imaging should be performed for stroke?

Answer 33

emergent noncontrast CT scan of brain to determine if hemorrhage (most acute ischemic strokes not visualized on CT early)

Question 34

If SAH suspected and CT negative, what should be performed?

Answer 34

lumbar puncture for red blood cells

Question 35

diagnostic tests to exclude stroke mimics or concurrent conditions

Answer 35

bedside glucose CBC ECG pulse ox electrolyte and coag panels cardiac enzyme levels tox screen blood alcohol level echo carotid duplex scanning\ MRI, MR angiogram, and CT angiogram when suspicion for alternative disease entities high

Question 36

Inclusion criteria by AHA/ASA for IV rtPA

Answer 36

Measureable diagnosis of acute ischemic stroke via use of NIHSS Onset of symptoms <3 h prior to rtPA administration Age >18 yo (there are many exclusion criteria that I'm hoping we won't have to memorize)

Question 37

General ED care for stroke

Answer 37

ABC IV access bedside glucose testing cardiac monitoring and pulse ox supplemental oxygen if hypoxic to keep >94% determine last baseline neuro status if not candidate for thrombolysis, correct BP if >220/>120 by decreasing by 15% in first 24 hrs if candidate for thrombolysis, labetolol or nicardipine to maintain <185/<110 (if can't decrease with these drugs, not good candidate) Informed consent prior to thrombolytics supportive care: aspiration prevention, normalization of glucose, fall precautions admit acute stroke to stroke unit early consult of specialists, emergent neurology consult in stroke

Question 38

time recommendations via ASA and AHA to care for stroke patient

Answer 38

10 mins from ED arrival to physician eval 15 mins til activation of stroke team 25 mins til head CT 45 mins tile completion of CT interpretation thrombolytics within 1 hr admission to stroke unit within 3 hrs

Question 39

How long from time of last baseline can rtPA be given?

Answer 39

<3 hrs approved by FDA with inclusion and exclusion criteria review AHA and ASA say up to 4.5 hrs but is off label and use additional European Cooperative Acute Stroke Study III exclusion criteria

Question 40

Total dose of rtPA

Answer 40

.9 mg/kg IV with max dose of 90 mg; 10% as bolus and remaining infused over 60 mins

Question 41

Monitoring/precautions with rtPA

Answer 41

No aspirin or heparin within 24 hrs CLosely monitor BP Intracerebral bleeding may be cause of neuro worsening and emergent CT performed

Question 42

Treatment for TIA

Answer 42

aspirin 75-325 mg PO daily clopidogrel 75 mg PO daily combination of aspirin + extended-release dipyridamole 25 mg PO and 200 mg PO twice daily admission for further eval and obs or workup in ED and starting antiplatelet, educating, and explicit return precautions

Question 43

Treatment for acute ischemic stroke

Answer 43

aspirin 325 mg PO within 24 to 48 hours unless receiving tPA do not recommend heparin or warfarin even in presence of afib

Question 44

Treatment of SAH

Answer 44

BP control at prehemorrhage blood pressure or MAP <140 mmHg if baseline unknown Labetolol or nicardipine can be used Admit to ICU with neurosurgeon consult nimodipine every 4 hrs to decrease vasospasm seizure prophylaxis if specialist wants reverse coagulopathy with vitamin K, FFP, and/or prothrombin

Question 45

treatment for hemorrhagic stroke

Answer 45

admit to CCU treat with antiepileptic meds if seizures occur manage hyperglyceia BP management reverse coagulopathy with vitamin K, FFP, prothrombin concentrates If increased ICP, head elevation to 30 degrees, analgesia, sedation If more agressive ICP reduction indicated with osmotic diuretics or intubation with neuromuscular blockade with mild hyperventilation, invasive monitoring of ICP by neurosurgery

Question 46

what scoring system has been recommended for use to predict stroke risk in TIA patients?

Answer 46

ABCD

Question 47

Diagnosis included in altered mental status

Answer 47

delirium dementia coma

Question 48

clinical features of delirium

Answer 48

impaired attention, perception, thinking, memory, and cognition typically develops over several days disrupted sleep-wake cycles increased somnolence during day and agitation characteristic of sundowning at night decreased alertness and activity fluctuations tremor asterixis tachycardia sweating hypertension emotional outbursts hallucinations

Question 49

categories of medical causes of delirium

Answer 49

infectious (pneumonia, UTI, meningitis/encephalitis, sepsis) metabolic/toxic (hypoglycemia, alcohol ingestion, electrolyte abnormalities, hepatic encephalopathy, thyroid disorders, alcohol or drug withdrawal) neurologic (stroke or TIA, seizure, SAH, intracranial hemorrhage, CNS mass lesion, subdural hematoma) cardiopulmonary (CHF, MI, PE, hypoxia or carbon dioxide narcosis) drug related (anticholinergic drugs, alcohol or drug withdrawal, sedatives-hypnotics, narcotic analgesics, SSRI or SNRI)

Question 49

diagnosis of delirium

Answer 49

directed at identifying underlying process such as infection BMP hepatic studies ammonia level UA CBC cxr cranial CT if mass suspected lumbar puncture if meningitis or SAH suspected

Question 50

ED care of delirium

Answer 50

treat underlying medical illness environmental manipulation ie lighting and emotional support treat acute episodes with haloperidol with reduced dosage in elderly or lorazepam consider inpatient admission unless readily reversible cause treated with improvement

Question 51

clinical features of dementia

Answer 51

loss of mental capacity over time psychosocial level and cognitive abilities deteriorate behavioral problems develop insidious onset gradual and progressive impairment of memory, especially recent hallucinations delusions repetitive behavior naming problems, forgetting items, loss of reading and direction disorientation inability to perform self-care tasks personality changes anxiety, depression speech difficulty vascular dementia: exaggerated or asymmetric dtrs, gait abnormalities, extremity weakness

Question 52

largest categories of dementia

Answer 52

alzheimer's disease vascular dementia

Question 53

diagnosis of dementia

Answer 53

PE for cause focal neuro signs = vascular dementia or mass lesion increased motor tone and extrapyramidal signs = parkinson's urinary incontinence and gait disturbance, large ventricles on CT = normal pressure hydrocephalus CBC BMP UA Thyroid panel B12 syphilis testing ESR folate HIV testing CXR Head CT or MRI, lumbar puncture if diagnosis not apparent

Question 54

care for dementia

Answer 54

workup for medical causes antipsychotic drugs to manage persistent psychosis or severely disruptive or dangerous behavior treatment of vascular dementia addressing risk factors ie hypertension inpatient admission for further eval and treatment discharge if longstanding and stable, consistent caregivers, reliable follow-up

Question 55

what is coma

Answer 55

state of reduced alertness and responsiveness from which patient cannot be aroused

Question 56

how is severity of coma quantified

Answer 56

glasgow coma scale and FOUR pupillary findings, cranial nerve testing, hemiparesis, response to stimulation

Question 58

what is diffuse CNS dysfunction such as toxic-metabolic coma or focal CNS dysfunction characteristic of?

Answer 58

structural coma

Question 58

what are characteristics of toxic-metabolic coma?

Answer 58

lack of focal PE findings pupils small and reactive but may be large in severe sedative poisoning from barbiturates

Question 59

what can cause coma without lateralizing signs

Answer 59

decreased cerebral perfusion from increased intracranial pressure reflex changes in BP and HR observed, such as Cushing reflex (hypertension and bradycardia)

Question 59

presentation of supratentoral lesions or masses

Answer 59

progressive hemiparesis or asymmetric muscle tone and reflexes

Question 60

How can coma from posterior fossa or infratentorial lesions present?

Answer 60

Abrupt in onset abnormal extensor posturing and loss of pupillary reflexes and extraocular movements

Question 61

how does brainstem compression present?

Answer 61

loss of brainstem reflexes that can develop rapidly

Question 62

how can pontine hemorrhage (a type of infratentorial cause of coma) present?

Answer 62

pinpoint pupils

Question 63

findings in pseudocoma or psychogenic coma

Answer 63

pupillary responses, extraocular movements, muscle tone, and reflexes intact Response to manual eye opening with resistance avoidance of gaze with patient looking away from examiner nystagmus with caloric vestibular testing

Question 64

what does abrupt onset of coma suggest?

Answer 64

catastrophic stroke or status epilepticus

Question 65

what does gradual onset of coma suggest?

Answer 65

metabolic process or progressive lesion such as tumor or slow intracranial bleed

Question 66

if a patient has asymmetric findings on pupillary exam, assessment of corneal reflexes, and testing of oculovestibular reflexes what does that suggest?

Answer 66

focal CNS lesions

Question 67

basilar artery thrombosis diagnosis

Answer 67

nondiagnostic CT and absence of alternative diagnsois MRI or cerebral angiography

Question 68

What shoudl be done if patient has seizures and remains unresponsive

Answer 68

may be having electrical seizures without motor activity EEG performed

Question 69

what should be considered in comatose children

Answer 69

toxic ingestions infections nonaccidental trauma

Question 70

ED care of coma

Answer 70

ABC identify and treat reversible causes ie hypoglycemia and opioid toxicity (naloxone) administer thiamine before glucose in hypoglycemic patients with history of alcohol abuse or malnutrition consider nonconvulsive status epilepticus in patients who have ahd a seizure and not returned to baseline if increased ICP, elevate head of bed to 30 deg, give mannitol and dexamethasone if tumor, hyperventilation but not below 35 discharge those with readily reversible causes if home care and f/u adequate and clear cause found admit all other patients