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139 Cards in this Set
- Front
- Back
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Parts of the central nervous system
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The neuron
Protective structures The brain Skull The spinal cord |
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Parts of the Neuron
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(Dendrite, Body, Axon)
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Protective structures of the CNS
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(Bones, Meninges)
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Parts of the peripheral nervous system
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Somatic
Autonomic |
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The autonomic nervous system
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The sympathetic nervous system
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The sympathetic nervous system
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“Fight-or-flight”
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The parasympathetic nervous system
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“Feed-or-breed” or “rest-and-repair”
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How many pairs of nerves originate from the CNS to form the PNS.
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43
12 pairs of cranial nerves originating from the brain 31 pairs of spinal nerves originating from the spinal cord |
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Pediatric GCS Eye opening
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Spontaneous 4
To speech 3 To pain 2 None 1 |
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Pediatric GCS Verbal
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Coos, babbles 5
Cries irritably 4 Cries to pain 3 Moans to pain 2 None 1 |
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Pediatric GCS Motor response
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Normal movements 6
Withdraws to touch 5 Withdraws to pain 4 Abnormal flexion 3 Abnormal extension 2 None 1 |
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Management of Neurological Emergencies - General Principles
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Airway and breathing
Circulatory support Pharmacological intervention Psychological support Transport considerations |
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Treatable causes of CIMS
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Hypoglycemia – Dextrose
Narcotic overdose – Narcan Suspected poisoning – The solution to pollution is dilution Increased intercranial pressure - hyperventilation |
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Causes of altered mental status
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AEIOU TIPS
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AEIOU TIPS
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A—Acidosis or Alcohol
E—Epilepsy I—Infection O—Overdose U—Uremia T—Trauma I—Insulin P—Psychosis S—Stroke |
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A in AEIOU TIPS
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A—Acidosis or Alcohol
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E in AEIOU TIPS
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E—Epilepsy
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I in AEIOU TIPS
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I—Infection
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O in AEIOU TIPS
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O—Overdose
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U in AEIOU TIPS
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U—Uremia
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T in AEIOU TIPS
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T—Trauma
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I in AEIOU TIPS
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I—Insulin
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P in AEIOU TIPS
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P—Psychosis
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S in AEIOU TIPS
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S—Stroke
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2 Types of Stroke
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Occlusive strokes (85%)
Embolic and thrombotic strokes Hemorrhagic strokes (15%) |
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Stroke Signs and symptoms
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Signs: Facial drooping, Headache, Aphasia/dysphasia
Hemiparesis, Hemiplegia, Paresthesia, Gait disturbances, Incontinence Symptoms: Confusion, Agitation, Dizziness, Vision problems |
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Transient ischemic attacks
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Indicative of carotid artery disease
Symptoms of neurological deficit Symptoms resolve in less than 24 hours. There are no long-term effects. |
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Evaluation of TIA
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Evaluate through history taking.
History of HTN, prior stroke, or TIA Symptoms and their progression |
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Two Types of Partial Seizures
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Simple Partial
Complex Partial |
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Simple partial seizures
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Involve one body area and can progress to generalized seizure
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Complex partial seizures
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Characterized by auras, typically 1–2 minutes in length and there is a loss of contact with surroundings
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Management of Seizure
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Administer high-flow, high-concentration oxygen.
Treat hypoglycemia if present. Do not restrain the patient. Protect the patient from the environment. Maintain body temperature. Treat prolonged seizures with Anticonvulsant medication |
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Status epilepticus
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Two or more generalized seizures
Seizures occur without a return of consciousness. |
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Management of Status epilepticus
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Management
Management of airway and breathing is critical. Establish IV access and cardiac monitoring. Administer 25 g of 50% dextrose if hypoglycemia is present. Administer 5–10 mg diazepam IV. Monitor the airway closely. |
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Assessment of Syncope
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Assessment
Cardiovascular Dysrhythmias or mechanical problems. Noncardiovascular Metabolic, neurological, or psychiatric condition. Idiopathic The cause remains unknown even after careful assessment. |
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3 types of headaches
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Vascular, Tension, Organic
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2 types of vascular headaches
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Migraines
Cluster headaches |
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Migraines
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Throbbing pain, photosensitivity, nausea, vomiting, and sweats; more frequent in women
May last for extended periods of time |
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Cluster
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One-sided with nasal congestion, drooping eyelid, and irritated or watery eye; more frequent in men.
Typically last 1–4 hours |
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Organic Headaches
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These occur due to tumors, infection, or other diseases of the brain, eye, or other body system.
Headaches associated with fever, confusion, nausea, vomiting, or rash can be indicative of an infectious disease |
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Types of Degenerative Neurological Disorders
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Alzheimer disease
Muscular dystrophy Multiple sclerosis Dystonias Parkinson’s disease Central pain syndrome Bell’s palsy Amytrophic lateral sclerosis Myoclonus Spina bifida Poliomyelitis |
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Alzheimer disease
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Most frequent cause of dementia in the elderly
Results in atrophy of the brain due to nerve cell death in the cerebral cortex |
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Muscular dystrophy
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Characterized by progressive muscle weakness
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Multiple sclerosis
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Unpredictable disease resulting from deterioration of the myelin sheath
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Parkinson’s disease
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Tremor, rigidity, bradykinesia, and postural instability
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Interventions for Degeneration Neurological Disorders
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Determine blood glucose level.
Establish IV access. Monitor cardiac rhythm. Transport and reassure the patient |
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Causes of endocrine gland disorders
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Disorders result from over- or underproduction of hormone(s).
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Endocrine glands
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Hypothalymus
Pituitary Parathyroid Thyroid Thalamus Adrenal Glands Pancreas Gonads |
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Alpha cells
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stimulate the release of glucagon and glycogen stores and promote gluconeogenesis
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Beta cells
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stimulate the release of insulin which lowers the blood glucose level
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Delta cells
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produce somatostatin which inhibit glucagon and insulin
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Adrenal medulla
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Inner segment of adrenal gland
Closely tied to autonomic nervous system |
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Adrenal cortex
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Outer layers of endocrine tissue, which secrete steroidal hormones
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Pineal Gland
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Located in the roof of the thalamus.
Related to the body’s “biological clock” Implicated in seasonal affective disorder Secretes Melatonin |
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Parathyroid glands
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Small, pea-shaped glands, located in the neck near the thyroid, typically four individual glands that regulate the level of calcium in the body
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Alpha cells
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stimulate the release of glucagon and glycogen stores and promote gluconeogenesis
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Beta cells
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stimulate the release of insulin which lowers the blood glucose level
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Delta cells
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produce somatostatin which inhibit glucagon and insulin
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Adrenal medulla
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Inner segment of adrenal gland
Closely tied to autonomic nervous system |
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Adrenal cortex
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Outer layers of endocrine tissue, which secrete steroidal hormones
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Pineal Gland
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Located in the roof of the thalamus.
Related to the body’s “biological clock” Implicated in seasonal affective disorder |
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Diabetic ketoacidosis
Pathophysiology |
Diabetic ketoacidosis results from the body’s change to fat metabolism
Continuous buildup of ketones produces significant acidosis. |
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Diabetic ketoacidosis
Signs and symptoms |
Extended period of onset (12–24 hours)
Sweet, fruity breath odor Potassium-related cardiac dysrhythmias Kussmaul respiration Decline in mental status and coma |
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Diabetic ketoacidosis
Assessment and management |
History and physical exam
Obtain history. Look for medical identification. Management Maintain airway and support breathing as indicated. Determine blood glucose level and obtain blood sample. If blood glucose is unknown, administer 25 g of 50% dextrose. Establish IV and administer normal saline per local protocol. Monitor cardiac rhythm and vital signs. Expedite transport. |
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Hyperglycemic hyperosmolar nonketotic coma (HHNC)
Pathophysiology |
Found in type II diabetics.
Results in blood glucose levels up to 1,000 mg/dL. Insulin activity prevents buildup of ketones. Sustained hyperglycemia results in marked dehydration. Often related to dialysis, infection, and medications. Very high mortality rate. |
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HHNC Signs and symptoms
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Gradual onset over days
Increased urination and thirst, orthostatic hypotension, and altered mental status |
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HHNC Assessment and management
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Difficult to distinguish from diabetic ketoacidosis in the prehospital setting.
Treatment is identical to diabetic ketoacidosis. |
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Hypoglycemia
Pathophysiology |
True medical emergency resulting from low blood glucose levels; rarely seen outside of diabetics
By the time signs and symptoms develop, most of the body’s stores have been used. Diabetics with kidney failure are predisposed to hypoglycemia. |
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Hypoglycemia
Signs and symptoms |
Altered mental status with rapid onset
Frequently involves combativeness. Diaphoresis and tachycardia Hypoglycemic seizure and coma |
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Hypoglycemia
Assessment and management |
History and physical exam
Obtain SAMPLE and OPQRST histories. Look for medical identification. |
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Graves disease
Pathophysiology/ Signs and symptoms |
Pathophysiology
Probably hereditary in nature. Autoantibodies are generated that stimulate thyroid tissue to produce excessive hormones. Signs and symptoms Agitation, emotional changeability, insomnia, poor heat tolerance, weight loss, weakness, and dyspnea. Tachycardia and new-onset atrial fibrillation. Protrusion of the eyeballs or goiters. |
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Thyrotoxic crisis (thyroid storm)
Pathophysiology |
Life-threatening emergency, usually associated with severe physiologic stress or overdose of thyroid hormone
Results when thyroid hormone moves from bound state to free state within the blood |
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Thyrotoxic crisis (thyroid storm)
Signs and symptoms |
High fever (106º F or higher)
Reflected in increased activity of sympathetic nervous system Irritability, delirium, or coma Tachycardia and hypotension Vomiting and diarrhea |
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Thyrotoxic crisis (thyroid storm)
Assessment and management |
Support airway, breathing, and circulation.
Monitor closely and expedite transport. |
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Parkinson’s disease
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Tremor, rigidity, bradykinesia, and postural instability
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Management
of Hypoglycemia |
Maintain airway and support breathing as indicated.
Determine blood glucose level and obtain blood sample. Establish IV access. If blood glucose <60 mg/dL or is unknown, administer 25–50 g of 50% dextrose IV. If IV cannot be established, administer 0.5–1.0 mg glucagon intramuscularly. Monitor cardiac rhythm and vital signs. Expedite transport. |
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Myxedema
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Caused by Chronic untreated hypothyroidism.
creates Thickening of connective tissue in skin and other tissues. Infection, trauma, CNS depressants, or a cold environment can trigger progression to a coma Can be inherited or acquired. |
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Hypothyroidism and Myxedema
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Signs and symptoms
Fatigue, slowed mental function Cold intolerance, constipation, and lethargy Absence of emotion, thinning hair, and enlarged tongue Cool, pale and dough-like skin Coma, hypothermia, and bradycardia |
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Hyperadrenalism (Cushing syndrome)
Pathophysiology |
Often due to abnormalities in the anterior pituitary or adrenal cortex
May also be due to steroid therapy for nonendocrine conditions such as COPD or asthma Long-term cortisol elevation causes many changes. |
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Cushing's Syndrome
SIgns and symptoms |
Signs and symptoms
Weight gain “Moon-faced” appearance Fat accumulation on the upper back Skin changes and delayed healing of wounds Mood swings Impaired memory or concentration |
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Assessment and management
of Cushing's Syndrome |
Support ABCs.
Use caution when establishing IV access. Report any observations to the receiving facility. |
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Adrenal insufficiency
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(Addison Disease)
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Adrenal insufficiency (Addison Disease)
Pathophysiology |
Due to destruction of the adrenal cortex.
Often related to heredity. Stress may trigger ... crisis. May be related to steroid therapy. Sudden withdrawal can trigger an ... crisis. |
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Adrenal insufficiency (Addison Disease)
Signs and symptoms |
Progressive weakness, fatigue, decreased appetite, and weight loss
Hyperpigmentation of skin and mucous membranes Vomiting or diarrhea Hypokalemia and other electrolyte disturbances Unexplained cardiovascular collapse |
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Assessment and management
Addison's Disease |
Maintain ABCs.
Closely monitor cardiac and pulmonary status. Obtain blood glucose level and treat for hypoglycemia if present. Establish IV and provide aggressive fluid resuscitation. Expedite transport. |
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Delayed Hypersensitivity
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Results from cellular immunity and does not involve antibodies
Commonly results in skin rash Results from exposure to certain drugs or chemicals |
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Immediate
Hypersensitivity |
Exposure quickly results in secondary response.
More severe than delayed hypersensitivity. |
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Management of Anaphalaxis
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Airway
IV Access Medications Oxygen, Epinephrine, Antihistamines, Corticosteroids, Vasopressors, Beta-agonists |
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Management og Allergic reactions
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Determines scene safety.
Protect the airway. Support breathing. Establish IV access. Administer medications Antihistamines Epinephrine |
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Hilum
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–recessed central fissure of the kidney
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Medula
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– innermost part of kidney
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Pyramids
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–7 parts of Medula, contains nephrons
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Papilla
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– channel for emptying urine into the Minor Calynx
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Renal Pelvis
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– funnels Urine into the ureter from the Calynx
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Nephrons
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Eliminates wastes from the body
Regulates blood volume and pressure Controls levels of electrolytes and metabolites Regulates blood pH Its functions are vital and are regulated by the endocrine system, with hormones such as antidiuretic hormone, aldosterone, and parathyroid hormone. |
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Kidney - Glomerulus –
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capillary sac
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Kidney - Collecting duct
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–urine leaves to Renal Papilla
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Kidney - Distal tubule
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– Ca regulation
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Kidney - Loop of henle
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– decending-water, ascending-ions
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Kidney - Proximal tubule
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– area of absorption
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Kidney - Bowman capsule
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– collecting fluids for processing
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Functions of the kidneys
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Forming and eliminating urine
Maintaining blood volume with proper balance of water, electrolytes, and ph Retaining key compounds such as glucose, while excreting wastes such as urea Controlling arterial blood pressure Regulating erythrocyte development |
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Glomerular filtration
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GFR-Over the course of a day,125 ml/min. filtered translates into 180 liters. With about 5 liters of blood in the body, the blood gets cleaned about 56 times in one day.
Control of Arterial Blood Pressure Control of erythrocyte production |
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Substance Permeability:
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ions - Low permeability. Sodium and chloride ions do not easily pass through. Urea - Moderate permeability. Water - Highly permeable. Water is readily reabsorbed from the descending limb by osmosis.
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Thin section of Ascending loop of Henle
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- Impermeable to water, but is permeable to ions in particular Na and Cl.
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Thick Section of Ascending loop of Henle
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- Impermeable to water. Sodium, potassium (K+)and chloride (Cl-) ions are reabsorbed by active transport. K+ is passively transported along its concentration gradient
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Assessment of GI and Urologic Complaints
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History of nausea, vomiting, and weight loss
Change in bowel habits and stool Last oral intake Presence of chest pain Uncomfortable appearance Lying with knees drawn up Relief with walking Level of consciousness changes. Are they acute or chronic? Apparent state of health Skin color Examination of the abdomen Inspection for distention, ecchymosis, or scarring Pain associated with percussion of abdomen Palpation Normal or ectopic pregnancy Masses Vital signs |
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Management of Renal and urologic emergencies
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Airway, breathing, circulation
Pharmacologic interventions IV access and analgesics Nonpharmacological interventions Nothing by mouth (NPO). Maintain position of comfort. Reassess mental status and vital signs frequently. Transport considerations |
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Prerenal acute renal failure
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Dysfunction before the level of kidneys
Most common and most easily reversible |
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Postrenal acute renal failure
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Dysfunction distal to the kidneys
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Renal acute renal failure
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Dysfunction within the kidneys themselves
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Assessment of acute renal failure
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Change in urine output
Swelling in face, hands, feet, or torso Presence of heart palpitations or irregularity Changes in mental function Altered mental status Hypertension Tachycardia ECG indicative of hyperkalemia Pale, cool, moist skin Edema of face, hands, or feet Abdominal findings dependent on the cause of ARF |
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Management of Acute Renal Failure
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Airway, breathing, circulation
IV access Protect fluid volume. Positioning and transport |
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Causes of Priapism
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Sickle Cell Disease
Leukemia Multiple myeloma Tumors Spinal cord injury Spinal anesthesia Carbon monoxide poisoning Malaria Black widow spider bites Prescription and nonprescription drugs |
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Assessment and Physical of UTI
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Abdominal pain
Frequent, painful urination A “burning sensation” associated with urination Difficulty beginning and continuing to void Strong or foul-smelling urine Similar past episodes Physical exam Restless, uncomfortable appearance. Presence of a fever. Vital signs vary with degree of pain |
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Management of UTI
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Maintain ABCs.
Establish IV access. Consider analgesics. Transport to appropriate facility. |
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Components or Plasma
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Water
90–92% by volume Proteins 6–7% by volume Other 2–3% by volume Fats, carbohydrates, electrolytes, gases, and chemical messengers |
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Red Blood Cells
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Most abundant cells in the body
Responsible for tissue oxygenation Mainly water and hemoglobin |
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Lifespan of Red Blood Cells
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about 120 days
As cells age: Internal chemical machinery weakens Lose elasticity Become trapped in small blood vessels in bone marrow, liver, and spleen Destroyed by specialized white blood cells Macrophages |
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Hematocrit (Hct)
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Fraction of total volume of blood that is RBCs
Normally about 45% |
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Normal WBC count
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5000-10,000 cells/mm3
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Types of WBCs
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Monocytes: 5%
Increase with chronic infections Lymphocytes: 27.5% Neutrophils: 65% Eosinophils and basophils together: 2.5% |
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T cells
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develop cellular immunity.
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B cells
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produce humoral immunity
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Cellular immunity
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does not involve antibodies or complement (cascade attack) but rather involves the activation of macrophages, natural killer cells, T-lymphocytes, and the release of various cytokines in response to an antigen.
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Humoral immunity
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is mediated by secreted antibodies produced in the cells of the B lymphocyte lineage (B cell).
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Autoimmune diseases
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arise from an overactive immune response of the body against substances and tissues normally present in the body. (Crones, Graves, Rheumatoid Artheritis)
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The inflammatory Process
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Injured cells release histamine and other substances:
Cause blood vessels in injured tissue to dilate Increased blood flow carries neutrophils and monocytes (phagocytic cells) to site of injury |
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Megakaryocytes
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= a large cell in bone marrow that fragments to produce blood platelets
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Thrombocytopenia
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= low platelet count
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Thrombocytosis
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= too many platelets
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Signs and symptoms of Transfusion Reaction
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Facial flushing, hyperventilation, tachycardia, hives, chest pain, wheezing, fever, chills, and cyanosis
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Treatment of Transfusion Reaction
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Stop transfusion, change all IV tubing, and initiate IV therapy with normal saline or lactated Ringer.
Consider furosemide, dopamine, and diphenhydramine. |
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Febrile nonhemolytic reactions (tubing)
Signs and symptoms |
Headache, fever, and chills
Consider diphenhydramine and an antipyretic. Observe closely to ensure reaction is nonhemolytic. |
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Febrile nonhemolytic reactions (tubing)
Treatment |
Stop transfusion, change all IV tubing, and initiate IV therapy with normal saline or lactated Ringer.
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Diseases of the red blood cells
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– Anemia, Sickle Cell, Polycethemia
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Diseases of the white blood cells
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– Leukopenia, Neutropenia, Leukemia, Lymphomas
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Diseases of the platelets/blood clotting abnormalities –
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Thrombocytosis, Thrombocytopenia
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Other hematopoietic disorders
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– Hemophelia, DIC
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