Case 2

Clinical History and Physical E*am: This 34 year old woman first noted intermittent horizontal diplopia and droopiness of her eyelids in her early twenties. It was worse when she was tired and it slowly progressed to the point that the diplopia became constant by age 30. The following year, she developed weakness in her legs with frequent falls and difficulty climbing stairs. She noted muscle pain if she walked for a prolonged time. She denied having fatigability in her limb muscles. Cranial nerve testing revealed an almost complete external opthalmoplegia with only a few degrees of movement in all directions. There was also bilateral eyelid ptosis and fatigability. Motor e*amination showed normal tone and bulk. There was mild proximal weakness in the upper and lower extremities with fatigability after repetitive movement. Reflexes were diminished. The rest of the neurological e*am was normal.

Laboratory Findings: A tensilon test showed a positive response with improvement of at least 50% of her eyelid ptosis. Electrodiagnostic studies done to rule out a neuromuscular junction disorder (repetitive nerve conductions and single fiber EMG) were normal. Acetylcholine receptor antibodies were not detected. The serum CK was normal.

Microscopic Analysis: Sections of muscle tissue revealed mild variation in fiber size. Some of the fibers had the features of ragged red fibers with disruption of the intermyofibrillar network and abnormal subsarcolemmal accumulations of granular refractile material which may represent mitochondria. Several fibers had internally placed nuclei. Inflammatory infiltrates were absent.

Diagnosis and medication/treatments?

The ____________ is a cortex area that is perhaps most famous for processing information of our internal state of our body, such as how we are feeling or if we had enough to eat and drink, and is one of the major cortex areas that informs the hypothalamus.

I put the cerebral cortex but my professor said that that is too wide of an answer. She said "which more specific area is very important for the processing of internal states?"

Thank you!

Alexa is a 25 year old graduate student who arranged an urgent appointment with her primary care provider because her ‘vision is blurry’ in her left eye. She states that two days ago her vision changed. She compares her visual field to looking through a fogged up window. Her provider interprets this to mean she has a decrease in contrast and brightness. Eye examination reveals a marked reduction of visual acuity of her left eye. A swinging flashlight test reveals an afferent pupillary defect (Marcus Gunn pupil) of her left eye (i.e., paradoxical papillary dilatation in response to increased light). Visual acuity and pupillary responses in her right eye are normal. Assessment of the retina and retinal vessels in both eyes is normal. Additional findings show patchy but consistent hypoesthesia (decreased feeling) to pin and light touch over her right limbs. On questioning, Alexia states that she experienced a self-limiting episode of numbness and tingling a few months ago. She also states that she has been experiencing fatigue, particularly at the end of the day. She denies depression, and her family history is unrevealing. The remainder of the physical exam in normal. Alexa is referred to an ophthalmologist who diagnoses optic neuritis (inflammation of the optic nerve). She begins corticosteroid treatment, and is referred to a neurologist who schedules a cranial MRI with gadolinium. The MRI reveals the presence of multiple deep white matter lesions scattered throughout the brain, suggesting multiple sclerosis. A subsequent lumbar puncture and analysis of Alexia’s cerebral spinal fluid (CSF) is consistent with possible multiple sclerosis. Further work-up rules out other possible causes. Ultimately, the neurologist diagnoses Alexia with relapsing-remitting multiple sclerosis.

1.One phenomenon that may facilitate the appearance of autoreactive cells in multiple sclerosis is referred to as ‘molecular mimicry.’ What is molecular mimicry and how might an infection lead to such mimicry in multiple sclerosis?

Alexa is a 25 year old graduate student who arranged an urgent appointment with her primary care provider because her ‘vision is blurry’ in her left eye. She states that two days ago her vision changed. She compares her visual field to looking through a fogged up window. Her provider interprets this to mean she has a decrease in contrast and brightness. Eye examination reveals a marked reduction of visual acuity of her left eye. A swinging flashlight test reveals an afferent pupillary defect (Marcus Gunn pupil) of her left eye (i.e., paradoxical papillary dilatation in response to increased light). Visual acuity and pupillary responses in her right eye are normal. Assessment of the retina and retinal vessels in both eyes is normal. Additional findings show patchy but consistent hypoesthesia (decreased feeling) to pin and light touch over her right limbs. On questioning, Alexia states that she experienced a self-limiting episode of numbness and tingling a few months ago. She also states that she has been experiencing fatigue, particularly at the end of the day. She denies depression, and her family history is unrevealing. The remainder of the physical exam in normal. Alexa is referred to an ophthalmologist who diagnoses optic neuritis (inflammation of the optic nerve). She begins corticosteroid treatment, and is referred to a neurologist who schedules a cranial MRI with gadolinium. The MRI reveals the presence of multiple deep white matter lesions scattered throughout the brain, suggesting multiple sclerosis. A subsequent lumbar puncture and analysis of Alexia’s cerebral spinal fluid (CSF) is consistent with possible multiple sclerosis. Further work-up rules out other possible causes. Ultimately, the neurologist diagnoses Alexia with relapsing-remitting multiple sclerosis.

1. Multiple sclerosis is an autoimmune disease, in which the immune system reacts to self-antigen (i.e., loss of self-tolerance). What is self-tolerance? Describe the processes (central and peripheral) that allow the immune system to develop self-tolerance, and how self-tolerance might be compromised.

Alexa is a 25 year old graduate student who arranged an urgent appointment with her primary care provider because her ‘vision is blurry’ in her left eye. She states that two days ago her vision changed. She compares her visual field to looking through a fogged up window. Her provider interprets this to mean she has a decrease in contrast and brightness. Eye examination reveals a marked reduction of visual acuity of her left eye. A swinging flashlight test reveals an afferent pupillary defect (Marcus Gunn pupil) of her left eye (i.e., paradoxical papillary dilatation in response to increased light). Visual acuity and pupillary responses in her right eye are normal. Assessment of the retina and retinal vessels in both eyes is normal. Additional findings show patchy but consistent hypoesthesia (decreased feeling) to pin and light touch over her right limbs. On questioning, Alexia states that she experienced a self-limiting episode of numbness and tingling a few months ago. She also states that she has been experiencing fatigue, particularly at the end of the day. She denies depression, and her family history is unrevealing. The remainder of the physical exam in normal. Alexa is referred to an ophthalmologist who diagnoses optic neuritis (inflammation of the optic nerve). She begins corticosteroid treatment, and is referred to a neurologist who schedules a cranial MRI with gadolinium. The MRI reveals the presence of multiple deep white matter lesions scattered throughout the brain, suggesting multiple sclerosis. A subsequent lumbar puncture and analysis of Alexia’s cerebral spinal fluid (CSF) is consistent with possible multiple sclerosis. Further work-up rules out other possible causes. Ultimately, the neurologist diagnoses Alexia with relapsing-remitting multiple sclerosis.

1. What immune mechanisms contribute to the pathophysiology of multiple sclerosis? In your answer, discuss the subsets of lymphocytes involved and their role in the autoimmune process. Discuss the type and role of cytokines in the autoimmune process underlying multiple sclerosis.

Case 1

Presentation: A five year old boy who was referred to a neurologist by his pediatrician because of an abnormal gait. He was adopted from another country about a year ago, and his adopting parents have noticed that he is clumsy when he runs where he falls often. He runs on his tiptoes, which has occurred since they started taking care of him. Otherwise, he has no other problems. He is doing well in kindergarten despite his language difficulty. His teacher notes that he has trouble getting up from a sitting position at school. His parents deny that he has chronic fevers, leg pain, weight loss, seizures, skin rash, urinary or bowel incontinence, or frequent colds.

History: His past medical, developmental, family, and birth histories are unknown. His immunizations are up-to-date and his PPD this year has been negative.

Physical : His vital signs are normal. His height, weight and head circumference are at the 50th percentile. He is alert, active, shy, well-nourished and slim in no distress. His skin shows no neurocutaneous stigmata. His head is normocephalic and atraumatic. His pupils are equal, round, reactive to light. No nystagmus is evident. His fundi are normal with sharp disk margins. His TMs are clear. His throat is normal with a uvula midline. His lungs, heart, and abdomen are normal. His back shows no sacral dimples.

Neurological : A standard cranial nerve e*am reveals no deficits. His strength is +4/5 in his deltoids, knee flexors and extensors; +5/5 in his biceps and triceps. His calves are visibly enlarged with a firm, rubbery feeling. He gets up to a standing position using a Gowers' maneuver. No dysdiadochokinesia. Negative Romberg sign. Sensation to light touch is intact. His reflexes are +2/4 in his biceps, triceps, brachioradialis, patella and ankle. His plantar reflex is down going (negative Babinski sign). No clonus is elicited. Normal anocutaneous and abdominal reflexes are present. His gait is best described as a wide based waddling. When running, he tends to run on his toes. He is unable to jump.

Diagnosis? and what medication or treatment?

CSI: Hot Tub..too hot to handle?

            After waking up in the yard with a severe hangover, a woman finds her husband dead in the hot tub in Palm Springs. It had been a cool day for January, with temperatures hovering around 60 degrees Fahrenheit. The couple had apparently come home the previous night and gone to the hot tub, which was set at 110 degrees Fahrenheit. Both had been drinking a great deal of wine, and the male had been taking Lasix (a high-ceiling loop diuretic) for congestive heart failure.   Your job is to come up with a probable cause of the male’s death.

Clues and Background:

1. The hot tub's upper safe temperature is 104 degrees Fahrenheit.

2. The blood alcohol level (BAL) in each person was 0.2% (legally intoxicated is 0.08% in CA).

3. The man weighed 160 lbs and the woman weighed 120 lbs.

4. LASIX is a diuretic. A is a drug that elevates the rate of urination and thus provides a means of forced diuresis.

5. Alcohol is a depressant (i.e., it decreases the activity of the nervous system).

6. ADH (antidiuretic hormone or vasopressin) is synthesized in the nervous system (hypothalamus) and is released in response to osmotic stress.

7. Normal to high ADH levels result in water reabsorption by the body (act on kidney collecting tubules).

9. Heat tends to cause vasodilation of blood vessels.

Please answer the following questions in a logical way:.

2. How would Lasix affect the feedback loops regulating blood pressure?

3. How would heat affect the feedback loops regulating blood pressure?

4. How would alcohol affect the feedback loops regulating blood pressure?

1. Define the following terms contained in this case:
   1. Bilateral

2. Hypoventilation

3. Hemothorax

4. Arrhythmias

2. What are the normal ranges for the measurements listed in the blood and urine tests? You may use your textbook to look these up.

3. Explain how Mr. Henderson’s rib fractures are related to the suspected hemothorax.

4. Mr. Henderson’s P_CO2 is elevated. Under normal conditions, what would be the PRIMARY mechanism that his body would use to reduce the amount of P_CO2 in the blood? Why is this mechanism not working in this case?

5. Describe how the high P_CO2 and low pH in Mr. Henderson’s blood are related in this case.

6. Describe how the high bicarbonate in Mr. Henderson’s blood is related to the low pH in his urine.

7. What type of intervention might the doctors and nurses initiate in order to address the hemothorax? Explain how this intervention will lead to changes in P_CO2 and blood pH.

15). Your patient asks you which cell type in the skin is the most important cell and why? How would you reply? Explain.

16). Describe the stages of intramembranous ossification and name at least one (1) bone that is formed using this process.

25). Describe the sequence of injuries to specific tissues that might occur if a patient’s knee receives blunt force trauma to the lateral side of the knee.

24). For the six (6) synovial joint classifications, identify which possess uniaxial, biaxial, or multiaxial movement. Also, identify which might be most likely to sustain injury and why that could happen.

What is the overall “strategy” of fatty acid synthesis, and how does it compare with that for fatty acid degradation? Explain.

What metabolic pathways provide molecules from which plants, microbes and mammals make amino acids? List, and name a few of the most important metabolites that provide those carbon parts.

After ovulation, the granulosa cells from the ovulated follicle differentiate into luteal cells. Steroid production by granulosa cells in a developing follicle is different from those forming the corpus luteum because:

choose the correct answer

Trace the isotopic label of --[¹⁴C]-glycine through one round of the citric acid cycle. How many ATPs equivalents would be made if the ETS was working?

The labeled carbon is the alpha carbon. Please show all the structures showing the labeled carbon all the way through.