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139 Cards in this Set

  • Front
  • Back
Parts of the central nervous system
The neuron
Protective structures
The brain
Skull
The spinal cord
Parts of the Neuron
(Dendrite, Body, Axon)
Protective structures of the CNS
(Bones, Meninges)
Parts of the peripheral nervous system
Somatic
Autonomic
The autonomic nervous system
The sympathetic nervous system
The sympathetic nervous system
“Fight-or-flight”
The parasympathetic nervous system
“Feed-or-breed” or “rest-and-repair”
How many pairs of nerves originate from the CNS to form the PNS.
43
12 pairs of cranial nerves originating from the brain
31 pairs of spinal nerves originating from the spinal cord
Pediatric GCS Eye opening
Spontaneous 4
To speech 3
To pain 2
None 1
Pediatric GCS Verbal
Coos, babbles 5
Cries irritably 4
Cries to pain 3
Moans to pain 2
None 1
Pediatric GCS Motor response
Normal movements 6
Withdraws to touch 5
Withdraws to pain 4
Abnormal flexion 3
Abnormal extension 2
None 1
Management of Neurological Emergencies - General Principles
Airway and breathing
Circulatory support
Pharmacological intervention
Psychological support
Transport considerations
Treatable causes of CIMS
Hypoglycemia – Dextrose
Narcotic overdose – Narcan
Suspected poisoning – The solution to pollution is dilution
Increased intercranial pressure - hyperventilation
Causes of altered mental status
AEIOU TIPS
AEIOU TIPS
A—Acidosis or Alcohol
E—Epilepsy
I—Infection
O—Overdose
U—Uremia
T—Trauma
I—Insulin
P—Psychosis
S—Stroke
A in AEIOU TIPS
A—Acidosis or Alcohol
E in AEIOU TIPS
E—Epilepsy
I in AEIOU TIPS
I—Infection
O in AEIOU TIPS
O—Overdose
U in AEIOU TIPS
U—Uremia
T in AEIOU TIPS
T—Trauma
I in AEIOU TIPS
I—Insulin
P in AEIOU TIPS
P—Psychosis
S in AEIOU TIPS
S—Stroke
2 Types of Stroke
Occlusive strokes (85%)
Embolic and thrombotic strokes
Hemorrhagic strokes (15%)
Stroke Signs and symptoms
Signs: Facial drooping, Headache, Aphasia/dysphasia
Hemiparesis, Hemiplegia, Paresthesia, Gait disturbances, Incontinence
Symptoms: Confusion, Agitation, Dizziness, Vision problems
Transient ischemic attacks
Indicative of carotid artery disease
Symptoms of neurological deficit
Symptoms resolve in less than 24 hours.
There are no long-term effects.
Evaluation of TIA
Evaluate through history taking.
History of HTN, prior stroke, or TIA
Symptoms and their progression
Two Types of Partial Seizures
Simple Partial
Complex Partial
Simple partial seizures
Involve one body area and can progress to generalized seizure
Complex partial seizures
Characterized by auras, typically 1–2 minutes in length and there is a loss of contact with surroundings
Management of Seizure
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
Status epilepticus
Two or more generalized seizures
Seizures occur without a return of consciousness.
Management of Status epilepticus
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.
Assessment of Syncope
Assessment
Cardiovascular
Dysrhythmias or mechanical problems.
Noncardiovascular
Metabolic, neurological, or psychiatric condition.
Idiopathic
The cause remains unknown even after careful assessment.
3 types of headaches
Vascular, Tension, Organic
2 types of vascular headaches
Migraines
Cluster headaches
Migraines
Throbbing pain, photosensitivity, nausea, vomiting, and sweats; more frequent in women
May last for extended periods of time
Cluster
One-sided with nasal congestion, drooping eyelid, and irritated or watery eye; more frequent in men.
Typically last 1–4 hours
Organic Headaches
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
Types of Degenerative Neurological Disorders
Alzheimer disease
Muscular dystrophy
Multiple sclerosis
Dystonias
Parkinson’s disease
Central pain syndrome
Bell’s palsy
Amytrophic lateral sclerosis
Myoclonus
Spina bifida
Poliomyelitis
Alzheimer disease
Most frequent cause of dementia in the elderly
Results in atrophy of the brain due to nerve cell death in the cerebral cortex
Muscular dystrophy
Characterized by progressive muscle weakness
Multiple sclerosis
Unpredictable disease resulting from deterioration of the myelin sheath
Parkinson’s disease
Tremor, rigidity, bradykinesia, and postural instability
Interventions for Degeneration Neurological Disorders
Determine blood glucose level.
Establish IV access.
Monitor cardiac rhythm.
Transport and reassure the patient
Causes of endocrine gland disorders
Disorders result from over- or underproduction of hormone(s).
Endocrine glands
Hypothalymus
Pituitary
Parathyroid
Thyroid
Thalamus
Adrenal Glands
Pancreas
Gonads
Alpha cells
stimulate the release of glucagon and glycogen stores and promote gluconeogenesis
Beta cells
stimulate the release of insulin which lowers the blood glucose level
Delta cells
produce somatostatin which inhibit glucagon and insulin
Adrenal medulla
Inner segment of adrenal gland
Closely tied to autonomic nervous system
Adrenal cortex
Outer layers of endocrine tissue, which secrete steroidal hormones
Pineal Gland
Located in the roof of the thalamus.
Related to the body’s “biological clock”
Implicated in seasonal affective disorder

Secretes Melatonin
Parathyroid glands
Small, pea-shaped glands, located in the neck near the thyroid, typically four individual glands that regulate the level of calcium in the body
Alpha cells
stimulate the release of glucagon and glycogen stores and promote gluconeogenesis
Beta cells
stimulate the release of insulin which lowers the blood glucose level
Delta cells
produce somatostatin which inhibit glucagon and insulin
Adrenal medulla
Inner segment of adrenal gland
Closely tied to autonomic nervous system
Adrenal cortex
Outer layers of endocrine tissue, which secrete steroidal hormones
Pineal Gland
Located in the roof of the thalamus.
Related to the body’s “biological clock”
Implicated in seasonal affective disorder
Diabetic ketoacidosis
Pathophysiology
Diabetic ketoacidosis results from the body’s change to fat metabolism
Continuous buildup of ketones produces significant acidosis.
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
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.
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.
HHNC Signs and symptoms
Gradual onset over days
Increased urination and thirst, orthostatic hypotension, and altered mental status
HHNC Assessment and management
Difficult to distinguish from diabetic ketoacidosis in the prehospital setting.
Treatment is identical to diabetic ketoacidosis.
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.
Hypoglycemia
Signs and symptoms
Altered mental status with rapid onset
Frequently involves combativeness.
Diaphoresis and tachycardia
Hypoglycemic seizure and coma
Hypoglycemia
Assessment and management
History and physical exam
Obtain SAMPLE and OPQRST histories.
Look for medical identification.
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.
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
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
Thyrotoxic crisis (thyroid storm)
Assessment and management
Support airway, breathing, and circulation.
Monitor closely and expedite transport.
Parkinson’s disease
Tremor, rigidity, bradykinesia, and postural instability
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.
Myxedema
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.
Hypothyroidism and Myxedema
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
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.
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
Assessment and management
of Cushing's Syndrome
Support ABCs.
Use caution when establishing IV access.
Report any observations to the receiving facility.
Adrenal insufficiency
(Addison Disease)
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.
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
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.
Delayed Hypersensitivity
Results from cellular immunity and does not involve antibodies
Commonly results in skin rash
Results from exposure to certain drugs or chemicals
Immediate
Hypersensitivity
Exposure quickly results in secondary response.
More severe than delayed hypersensitivity.
Management of Anaphalaxis
Airway
IV Access
Medications
Oxygen, Epinephrine, Antihistamines, Corticosteroids, Vasopressors, Beta-agonists
Management og Allergic reactions
Determines scene safety.
Protect the airway.
Support breathing.
Establish IV access.
Administer medications
Antihistamines
Epinephrine
Hilum
–recessed central fissure of the kidney
Medula
– innermost part of kidney
Pyramids
–7 parts of Medula, contains nephrons
Papilla
– channel for emptying urine into the Minor Calynx
Renal Pelvis
– funnels Urine into the ureter from the Calynx
Nephrons
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.
Kidney - Glomerulus –
capillary sac
Kidney - Collecting duct
–urine leaves to Renal Papilla
Kidney - Distal tubule
– Ca regulation
Kidney - Loop of henle
– decending-water, ascending-ions
Kidney - Proximal tubule
– area of absorption
Kidney - Bowman capsule
– collecting fluids for processing
Functions of the kidneys
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
Glomerular filtration
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
Substance Permeability:
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.
Thin section of Ascending loop of Henle
- Impermeable to water, but is permeable to ions in particular Na and Cl.
Thick Section of Ascending loop of Henle
- Impermeable to water. Sodium, potassium (K+)and chloride (Cl-) ions are reabsorbed by active transport. K+ is passively transported along its concentration gradient
Assessment of GI and Urologic Complaints
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
Management of Renal and urologic emergencies
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
Prerenal acute renal failure
Dysfunction before the level of kidneys
Most common and most easily reversible
Postrenal acute renal failure
Dysfunction distal to the kidneys
Renal acute renal failure
Dysfunction within the kidneys themselves
Assessment of acute renal failure
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
Management of Acute Renal Failure
Airway, breathing, circulation
IV access
Protect fluid volume.
Positioning and transport
Causes of Priapism
Sickle Cell Disease
Leukemia
Multiple myeloma
Tumors
Spinal cord injury
Spinal anesthesia
Carbon monoxide poisoning
Malaria
Black widow spider bites
Prescription and nonprescription drugs
Assessment and Physical of UTI
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
Management of UTI
Maintain ABCs.
Establish IV access.
Consider analgesics.
Transport to appropriate facility.
Components or Plasma
Water
90–92% by volume
Proteins
6–7% by volume
Other
2–3% by volume
Fats, carbohydrates, electrolytes, gases, and chemical messengers
Red Blood Cells
Most abundant cells in the body
Responsible for tissue oxygenation
Mainly water and hemoglobin
Lifespan of Red Blood Cells
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
Hematocrit (Hct)
Fraction of total volume of blood that is RBCs
Normally about 45%
Normal WBC count
5000-10,000 cells/mm3
Types of WBCs
Monocytes: 5%
Increase with chronic infections
Lymphocytes: 27.5%
Neutrophils: 65%
Eosinophils and basophils together: 2.5%
T cells
develop cellular immunity.
B cells
produce humoral immunity
Cellular immunity
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.
Humoral immunity
is mediated by secreted antibodies produced in the cells of the B lymphocyte lineage (B cell).
Autoimmune diseases
arise from an overactive immune response of the body against substances and tissues normally present in the body. (Crones, Graves, Rheumatoid Artheritis)
The inflammatory Process
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
Megakaryocytes
= a large cell in bone marrow that fragments to produce blood platelets
Thrombocytopenia
= low platelet count
Thrombocytosis
= too many platelets
Signs and symptoms of Transfusion Reaction
Facial flushing, hyperventilation, tachycardia, hives, chest pain, wheezing, fever, chills, and cyanosis
Treatment of Transfusion Reaction
Stop transfusion, change all IV tubing, and initiate IV therapy with normal saline or lactated Ringer.
Consider furosemide, dopamine, and diphenhydramine.
Febrile nonhemolytic reactions (tubing)
Signs and symptoms
Headache, fever, and chills
Consider diphenhydramine and an antipyretic.
Observe closely to ensure reaction is nonhemolytic.
Febrile nonhemolytic reactions (tubing)
Treatment
Stop transfusion, change all IV tubing, and initiate IV therapy with normal saline or lactated Ringer.
Diseases of the red blood cells
– Anemia, Sickle Cell, Polycethemia
Diseases of the white blood cells
– Leukopenia, Neutropenia, Leukemia, Lymphomas
Diseases of the platelets/blood clotting abnormalities –
Thrombocytosis, Thrombocytopenia
Other hematopoietic disorders
– Hemophelia, DIC