Pathophysiology Study Guide Spring 2008
The last exam (exam 5) will be given during Finals week on Monday, May 5, from 8:00 - 10:00 a.m.
You are strongly encouraged to read the sections of your text book that pertain to this material!
Look for the answers to the questions in blue in your text book.
Nervous System Review:
What makes up the central nervous system? The peripheral nervous system?
How does the somatic nervous system differ from the autonomic nervous system?
How does the sympathetic nervous system differ from the parasympathetic nervous system?
Name the parts of a neuron.
Be able to give a function for the oligodendrocytes, ependymal cells, microglia, astrocytes, and Schwann cells.
How does a nerve cell work? Why is myelination important?
Do all neurotransmitters excite the cell they synapse with?
Be able to identify the cerebrum, corpus callosum, cerebellum, thalamus, hypothalamus, pons, medulla oblongata. What does each of these areas of the brain do?
What are the basal nuclei and where are they found?
Why do lesions in different parts of the cerebrum cause different symptoms?
What is the cauda equina, and what can we do more safely in this region?
Describe the cross section of the spinal cord. What are tracts ? What type of neurons would we find in the dorsal and ventral roots?
What are the three layers of the meninges? Describe them.
What are the falx cerebri, the falx cerebelli, and the tentorium cerebelli?
Locate the four ventricles in the brain.
Describe the formation and circulation of the cerebrospinal fluid.
Where does CSF drain into?
What is the circle of Willis? What arteries form it? Why is it important?
What is the blood-brain barrier? When is it helpful? When can it be a problem?
Pathophysiology of the nervous system:
What is vasogenic edema? Cytotoxic edema? For which of these conditions could you administer a hypertonic solution? In which case would that be a bad idea? Why?
What is a normal intracranial pressure?
What are the three clinical signs of increased intracranial pressure?
What can cause an increase in ICP?
What is the first substance displaced from the cranial cavity in cases of IICP?
What is decreased next?
What are the four stages of intracranial hypertension?
What signs and symptoms would be seen during each?
When is medical intervention needed? When is it too late?
What do we mean when we say that brain contents herniate?
What is the relationship between arterial blood pressure and intracranial pressure when blood stops flowing to the brain?
Who is at high risk for brain trauma?
What are the two major classes of brain trauma?
What is traumatic pneumocephalus, and what might indicate that it had happened? What simple test could you perform to test this?
What is the most common head trauma?
How does concussion present? What consequences would you expect?
What is a cerebral contusion?
What is the difference between coup and contrecoup injuries?
How does the amount and area of force affect head injury?
How could you differentiate an extradural hematoma, a subdural hematoma and an intracerebral hematoma?
What are the clinical manifestations of cerebral contusions?
How are cerebral contusion and hematomas treated?
What could cause cerebrovascular disease?
Why do ischemia, which is decreased blood flow, and hemorrhage cause the same problems within the brain?
What is a stroke? Who is most at risk?
What are the three types of thrombotic strokes?
Why are TIAs important? What could cause them, and how would they manifest clinically? What should we do about them?
What would cause a stroke-in-evolution?
Of Thrombotic, embolic and hemorrhagic CVA, which is the most common? The most lethal?
What causes do they all have in common?
Why do most thrombotic strokes occur during sleep?
How long do we have to wait to assess the permanent damage caused by an occlusive stroke, and why?
What can cause an embolic stroke?
How could you differentiate a thrombotic stroke from an embolic stroke?
What could cause a hemorrhagic CVA? How would it progress?
Describe the course of Alzheimer Disease. Why is restlessness such a problem?
What neurotransmitter is deficient in Alzheimer Disease?
How is it diagnosed? Treated? What could you see on autopsy or biopsy? What do we know about the cause?
What are the three stages of Alzheimer Disease listed in your book? How long does each last? What is going on with the patient in each stage?
What is the sundown syndrome?
Describe a patient with Parkinson Disease. What is bradykinesia?
What can cause secondary Parkinson Disease?
What is the cause of primary Parkinson Disease? What part of the brain is affected, and what neurotransmitter is involved? Who is affected? How is it treated? Why do we wait so long before using drug therapy? What drugs are now available to treat PD? How is it treated surgically?
Describe the typical Multiple Sclerosis patient at the time of the first symptom. What are some common presenting symptoms for this disease? How do you predict the course of the disease?
Why is depression common with this disease?
What is the underlying pathology for this disease? Why does this occur? Can remyelination of the neurons occur?
How is multiple sclerosis diagnosed? Who is at risk? What can be done about this disease? What drug is usually used to treat acute episodes?
How does a person get Reye's Syndrome? Is the incidence increasing or decreasing?
What are the first signs of Reye's Syndrome? What percent of those afflicted go onto Stage II? How does the disease progress?
What is/are the cause(s) of death? Why doesn't every child get Reye's Syndrome?
How is it treated?
What is a seizure? What is a convulsion?
What is epilepsy? Where does it rank as far as incidence of neurological disorders? What causes epilepsy?
Most epileptics will have their first seizure before what age?
What is petit mal? Grand mal? What is a prodrome ?What is an aura?
What are the stages of a grand mal seizure? Why can seizures be damaging?
What is status epilepticus?
How are seizures treated? What can precipitate a seizure?
What are epileptics like between seizures?
What 3 hormones are produced by the thyroid gland?
What are the signs and symptoms of hyperthyroidism? Why do they occur? What is exophthalmos? What is goiter?
Other than T3 and T4, what hormone do we look for to determine thyroid function? Why do we look at this hormone?
What can cause hyperthyroidism? What is the most common cause and how does it cause the disease? Which gender is most likely to develop this disease? How is it treated?
What are the signs and symptoms of hypothyroidism? Who is most likely to get this disease? What are the causes? What is the treatment?
Is the pancreas an exocrine or endocrine organ? What's the difference?
What cells are part of the exocrine function of the pancreas, and what do they produce?
What cells in the pancreas produce glucagon? What does glucagon do?
What cells in the pancreas produce insulin? What does insulin do? Why does insulin affect only certain tissues? What does it affect within the cell?
Specifically, how does insulin decrease blood glucose levels? What can't insulin be taken by mouth (orally)?
What factors cause insulin to be secreted? What factors suppress insulin secretion?
About what percentage of diabetics are undiagnosed? In which ethnic groups is it prevalent?
How do glucose transporters (GLUT -1, GLUT-2 and GLUT-4) differ?
What are the 3 "P's" associated with diabetes?
Be able to differentiate Type1 and Type 2 diabetes mellitus by age of onset, cause, and need for insulin.
What is type 1 DM? What happens to the pancreas to cause it? How is glucagon involved? What is the typical age of onset for this form of diabetes mellitus?
What would lead you to believe there could be a genetic basis for diabetes mellitus? What environmental factors can trigger it?
How does the ratio of insulin to glucagon come into play?
Why is glucose found in the urine of these patients? What can this cause?
Why do these patients lose weight? What is ketoacidosis and why does it occur? What are the signs of this? Why is this not a good thing?
How is type 1 DM controlled? What must the patient do? What should the patient be eating?
How can exercise influence blood glucose levels?
Which is more common, type 1 DM or type 2 DM? Which has the stronger genetic component?
What is the typical age of onset for type 2 DM? How is this changing, and why?
What is the greatest risk factor for type 2 DM?
What is the problem in type 2 DM on a cellular level? Why does this occur?
What symptoms might these patients have?
How is type 2 DM treated? Why can oral medications be used, and what do they do?
What commonly used drugs can cause hyperglycemia?
Why is gestational diabetes important?
What would you expect to see in a diabetic who has become hypoglycemic? How would you treat this person?
What would you expect to see in a diabetic who was in a state of ketoacidosis? How should they be treated?
What is the Somogyi effect?
What are the chronic complications of diabetes?
How is the nervous system affected by diabetes mellitus? The microvascular system? The macrovascular system? Why can gangrene, which is caused by anaerobic organisms, be a problem in diabetics? Why is wound healing a problem?
How are the kidneys affected? The eyes?
Creutzfeldt-Jacob Disease ( and other Transmissible Spongiform Encephalopathies (TSEs):
What is a prion? Note: these infectious agents are not destroyed by high doses of ultraviolet or ionizing radiation and are resistant to autoclaving, detergents, and disinfectants such as formalin, phenol, alcohol, and chlorine bleach. They are partially destroyed by some agents that hydrolyze or modify proteins.
Why is the Prion Hypothesis controversial?
PrPc is a normal glycoprotein found on the outer membranes of neurons and some other cells. It is denatured, as are most proteins, by heat, detergents, and chemicals. PrPsc or prion protein scapie (after the disease in sheep) is the active component of prions and is an abnormal version of the PrPc protein and is found inside the cells rather than on the surface. The difference in the two proteins is in their 3 dimensional structure - PrPc has more alpha helices, whereas PrPsc has a predominance of beta sheets. The PrPsc causes the normal form to be converted into the abnormal form, starting a chain reaction within the cell. It may also be caused by a random misfolding of a protein, or by a mutation or defect in the gene that produces the protein. To enter a host from the outside prion must be injested (eaten) or injected. Normal contact will not cause infection. How has it been spread by the medical community?
How is the disease Kuru (or Kuru Kuru) spread?
TSEs are normal transmitted inefficiently between species, and when they do cross the species barrier, their incubation times are very long. New Variant Creutzfeld-Jacob disease (nvCJD or vCJD), the human version of "mad cow" disease seems to be an exception to this. By 1996 ten people had died in Great Braitain of nvCJD with compelling evidence that it had come from eating infected beef. Since that time the death toll from nvCJD has risen to over 120.
Creutzfeldt-Jacob Disease was first identified in the 1920's and is the most common TSE in humans. How common is it? It mostly strikes people between the ages of 55- 75. What signs and symptoms do these individuals display? Transmission from person to person occurs iatrogenically, through other medical treatments, such as the administration of growth hormone from the pituitary glands of infected individuals, and contaminated surgical instruments. Incubation times in these cases have ranged from 3 to 20 years. (Now growth hormone is produced by recombinant DNA technology.) How is CJD diagnosed?
Because of the difficulty in disinfecting medical instruments, those instruments used on suspected CJD patients should be destroyed by incineration or at least quarantined until a final diagnosis has been made.
How does the fact we now have a blood test for vCJD impact humans and animals? Animals (and humans) with TSEs do not form anitbodies or Tc cells against the PrPsc protein.
Treatment at present just relieves symptoms. What can be done? There have been over 60 drugs tested, but these show results only when given before infection or during the early stages of the disease. Antiviral drugs such as acyclovir, and some antimalarial and anti-psychotic drugs have been tested in a few individuals with disappointing results. The ideal treatment would be vaccination, but this is still in the research stage. What is the one drug that has effected a single cure for CJD?