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Flashcards in Spring Final Exam 2018 Deck (65)
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1

Most common neurotransmitters

Acetylcholine (Excitatory/Inhibitory)

Monoamines

    1. Norepinephrine (E)

    2. Serotonin (I)

    3. Dopamine (E)

    4. Histamine (I)

Amino Acids

    1. GABA (I)

    2. Glycine (I)

    3. Glutamate (E)

Neuropeptides

    1.  Endorphins and Enkephalins (I)

    2. Substance P (E)

Purines-Adenosine

Gases-NO, CO

2

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

3

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

4

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

5

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. 

6

PENUMBRA

  • Minimally perfused cells around central core of dead cells
  • Are in electrical failure but structure intact
  • Can recover if blood flow restored

7

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

8

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

9

Compare and contrast ischemic and hemorrhagic strokes

10

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

11

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

12

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

13

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

 

14

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 

15

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

16

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

17

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

18

NADIR

Neutropenia-Nadir (10-14 days after chemo)

An abnormally low count of a type of white blood cell (neutrophils).

19

Benign Vs. Malignant growths

20

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

21

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

22

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

23

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

24

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

25

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

26

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

27

Criteria for declaring brain death

  • No response to painful stimuli (Sternal rub-take knuckles and rub on sternum)
  • No spontaneous movement
    • Can have seizure activity or m. spasms, but no spontaneous mov’t
  • No spontaneous respirations
    • If pt gets up to 60 mmHg of CO2 in blood &still don’t take a breath, it’s criteria for brain death (remember CO2 is a driving force for respiration)
  • No cranial nerve response
    • EEG (Any brain waves that indicate thought/brain activity), cerebral angiography (see if blood flow to brain is adequate), apnea test (taking pt off ventilator and seeing if they breath on own)
  • Status unchanged for 6 hours
    • Wait 6 hours and do tests again to make sure pt is REALLY brain dead

28

HLA system and the use of PRA in determining who can receive an organ

Panel Reactive Antibody

Test detects preformed HLA antibodies (antibodies in body already made against HLA protein)

  • From pregnancy, blood transfusions, previous transplantation
    • If you’ve never had any of these, you won’t have any antibodies against any other prot. b/c you’ve had no other person’s prot. In your body
  • Can restrict access to transplantation b/c it narrows your pool
    • Not only do you have to match these, you have to excluded other HLA protein
  • Given as a percentage – PRA of 50% means that the patient’s serum reacts with 50% of the donors in the panel

29

Subacute Vs. acute Vs. chronic rejection

  • Hyperacute: Occurs minutes to hours after transplant.  Kidney most susceptible.  Due to pre-formed antibodies to organ’s HLA.  Organ must be removed immediately
    • Happens very infrequently nowadays b/c we have figured this out and have good testing
  • Acute:  Highest risk is in first 3 months, risk declines after 1 year.  Must be treated (medically) promptly.  T-cell mediated.
    • That’s why there’s intensive monitoring in the first year (looking for ANY sign of rejection)
  • Chronic:  Long-term loss of organ function due to fibrosis (thickening/scarring) of vasculature which is due to poorly understood chronic inflammatory and immune response.
    • Over time blood supply to organ gets lower and lower and we have slow decline in function
    • Happens with even with best matching
    • When kid gets transplant, they will probably need another transplant later on

30

Sensorineural Hearing Loss

 

From cochlear nerve damage

  • Sudden or progressive
  • Causes:  trauma to 8th cranial nerve, trauma to cochlea, ototoxicity from medications (gentamycin); progressive from aging, noise, systemic disease (syphilis, diabetes)
  • Usually unilateral, may have tinnitus, dizziness, pain