Spring Final Exam 2018 Flashcards
Most common neurotransmitters
Acetylcholine (Excitatory/Inhibitory)
Monoamines
- Norepinephrine (E)
- Serotonin (I)
- Dopamine (E)
- Histamine (I)
Amino Acids
- GABA (I)
- Glycine (I)
- Glutamate (E)
Neuropeptides
- Endorphins and Enkephalins (I)
- Substance P (E)
Purines-Adenosine
Gases-NO, CO
Ions involved in neuronal transmission and action potentials
Neuronal Transmission
Afferent Neuron: carrying information toward the CNS (ascending)
Efferent Neuron: carrying information away from the CNS to target organs (descending)
Interneuron: connecting areas within the brain
Membrane Potential
- The Na-K ATPase pump maintains membrane potential
- ~-90mV, “polarized”
- More K+ IC; More Na+ EC
- For each molecule of ATP used, 3 NA ions are pumped out of the cell, and 2 K+ ions are pumped into the cell
Normal intracranial pressure reading
and symptoms of increased intracranial pressure
- Normal ICP 0-15mmHg (lateral ventricles)
- Small changes with respiratory movements, coughing, straining, or sneezing
- ICP above 20mmHg is seen as pathologic and should be treated
SYMPTOMS
- Initial Symptoms: Headache, projectile vomiting, papilledema
- Cushing’s Triad: Bradycardia, hypertension (with widening pulse pressure), and irregular respiratory pattern
Calculate and interpret a patient’s cerebral perfusion pressure (CPP)
CPP=MABP-ICP
MABP-mean arterial blood pressure
MABP and ICP commonly monitored
Normal CPP is 70-100mmHg
Brain ischemia at levels below 50-70mmHg
Cellular consequences of increased ICP or ischemia
- MONROE-KELLIE HYPOTHESIS or DOCTRINE: Volumes of each of 3 compartments (brain, blood, CSF) can vary slightly without causing and marked increase in ICP. Increase in one compartment must be compensated by a decrease in another compartment, otherwise ICP will rise
- Pathologic ICP levels can be caused by volume changes in any of the 3 compartments
- Of the three compartments, brain tissue is least able to compensate.
- Initial ICP changes buffered by CSF shunting to the spinal cord.
- Only small amount of blood, blood flow tightly regulated.
PENUMBRA
- Minimally perfused cells around central core of dead cells
- Are in electrical failure but structure intact
- Can recover if blood flow restored
Conditions associated with Ischemic Stroke
Thrombotic: Due to atherosclerotic plaques -lay off those lipids, hypercoagulation disorders (sickle cell, polycythemia); HTN
Embolic: Usually cardiac source-mural thrombi, valve vegetations, atrial fibrillation; carotid artery plaques; HTN
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Conditions associated with Hemorrhagic Stroke
- Most frequently fatal
- Rupture of blood vessel-hemorrhage into brain tissue, edema, compression, spasm
- Predisposing factors: age, HTN, aneurysm, trauma, tumor, AVM
- Sudden onset, often with activity
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Compare and contrast ischemic and hemorrhagic strokes
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Secondary vs. Primary Seizure
Secondary: Known cause. Any disorder that alters the neuronal environment may cause seizure activity. Fever (especially in children), electrolyte imbalances, hypoglycemia, hypoxia, alkalosis, rapid withdrawal of sedatives, toxemia of pregnancy, water intoxication, CNS infections.
Primary: unknown cause. Frequent seizures of this type lead to diagnosis of seizure disorder
Simple Partial Seizures
Simple partial: one hemisphere, no impairment of consciousness
- Jacksonian March: progressive motor
Complex partial: impairment of consciousness, often from temporal lobe. Automatisms common
Secondarily generalized Partial Seizure: starts as partial but spreads to both hemispheres, thalamus, reticular formation
Complex Seizures
Absence seizures: nonconvulsive disturbances in consciousness
Atonic Seizures: drop attacks
Myoclonic Seizures: Either tonic- rigid, violent contraction of muscles or clonic- repeated contractions and relaxations
Tonic-Clonic Seizures (grand mal): Loss of consciousness, incontinence common, possible cyanosis from constriction of airway and respiratory muscles. Tonic, followed by clonic then post-ictal period
Status Epilepticus
Seizure that will not stop on own, or multiple seizures in a row
- Tonic-clonic status epilepticus can be fatal; leads to respiratory failure
- If cause is known, must address otherwise may not stop seizure
- IV Valium (diazepam) drug of choice
Basic concepts of anti-seizure medications
Old AEDs VS. New AEDs
Old AEDs: We know how and why they work; but have undesirable yet predectable side effects
New AEDs: They tend to have, for now, fewer side effects and are well tolerated; but can be more expensive and some of the side effects are un-predectable
Pathophysiology of Parkinson’s disease
Complex motor disorder accompanied by systemic non-motor and neurologic symptoms. One of the most common causes of neurologic disabilities in individuals over 60 years old
Primary PD: Usually begins after age 40, incidence increases after age 60.
- More prevalent in males. Gene-environment.
Secondary Parkinsonism: caused by disorders other than PD
- Head trauma, infection, neoplasm, atherosclerosis, toxins, medications or drugs
Degenerative disorder of the basal ganglia involving the dopaminergic nigrostriatal pathway
80% loss of dopamine before symptoms appear
Leads to imbalance of dopaminergic (I) and cholinergic (E) input in the caudate nucleus of the basal ganglia
Pathophysiology of Multiple scelrosis
T-cells, macrophages, and possibly antibodies react with myelin protein - BAD
- Demyelination occurs, nerve fibers may be damaged
- Demyelinating lesions (plaques) form in white matter and may extend into gray matter. Axonal conduction interrupted
- Early exacerbations: edema and inflammation but return to baseline after exacerbation remits.
- After many exacerbations, damage becomes permanent
Proto-oncogenes Vs. oncogenes
Proto-oncogenes: code for proteins that help regulate cell growth and differentiation
Tumor suppressor genes: inhibit cell proliferation
Proto-oncogenes become ONCOGENES when genetic mutations alter their activity-get excess proliferation: Growth Factor, Growth Factor receptor, Cytoplasmic Signaling Pathways, Transcription Factors
NADIR
Neutropenia-Nadir (10-14 days after chemo)
An abnormally low count of a type of white blood cell (neutrophils).
Benign Vs. Malignant growths
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TNM grading system
Tumor (T)
- Tx-tumor cannot be evaluated
- T0-no evidence of tumor
- T1, T2, T3, T4-size and/or extent of primary tumor
Regional Lymph Node Involvement (N)
- Nx-regional lymph nodes cannot be evaluated
- N0-no cancer in lymph nodes
- N1, N2, N3-involvement of regional lymph nodes (number and/or extent of spread)
Distant Metastasis (M)
- Mx-distant metastasis cannot be evaluated
- M0-no distant metastasis
- M1-distant metastasis
Side Effects of cytotoxic medications
focusing on bone marrow effects
Bone Marrow Suppression
- Epoetin
- Anemia
- Colony stimulating factor (CSF)
- Neutropenia-Nadir (10-14 days after chemo)
- Neumega
- Thrombocytopenia
Ways to overcome barriers in chemotherapy treatment
- Intermittent Chemo: need time for normal cells to recover.
- Combination of cytotoxic medications
- Suppresses drug resistance-less likely to have multiple mutations
- Increased rate of tumor cells kill
- Decrease in injury to normal cells-use drugs with different toxicities
- Specialized routes
- Arterial, Intrathecal, Bladder, Peritoneal cavity
Tumor lysis syndrome
Commonly in rapidly growing cancers after administration of chemotherapy
- Leukemias and lymphomas; rare in solid tumors
- Starts within 1-3 days of chemotherapy
Massive number of cells killed in short period of time; release of intracellular ions, nucleic acids, proteins into circulation
- Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia
Kidneys damaged by uric acid and other intracellular contents
Cardiac arrhythmias
Inheritance patterns for autosomal dominant disorders
- Father is carrying disease that’s autosomal dominant
- 50% chance that the child will get disease
- Each child is individual chance
- If it’s passed on, it might be expressed in child
- Can be a characteristic like brown eyes
- Getting just one ”A”= expressing disease
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Inheritance patterns for autosomal recessive disorders
- Need two copies of gene to express disease process
- Each of these parents are carrying this autosomal recessive disorder
- Neither are expressing it b/c they only have one copy; May not know you’re a carrier for the disease b/c it’s not expressed
- Need “aa” to express disease
- 25% chance the child will express disease process
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Inheritance of HLA proteins
Human Leukocyte Antigen
HLA: Human Leukocyte Antigen
Proteins that are present on the surface of cell that help you differentiate self from non self
Allows immune system to recognize own cells and makes sure it doesn’t attack your own body’s cells