Exam 1 - Nuero

Question 1

What is the specific etiology for MS?

Answer 1

Unknown - experimental and clinical studies have pointed to a possible genetic, immune, and infectious etiology

Question 2

What is the pathogenesis of parkinson’s disease related to neurotransmitter deficiency (what part of brain is this deficient in?)

Answer 2

• Loss of neurons in the Substantia Nigra
  
  • reduction in dopamine content of that region
• Clinically presents as tremors at rest, muscular rigidity, expressionless face and emotional lability.

Question 3

What is Von Economo’s encephalitis and how does this relate to Parkinson’s - history lesson?

Answer 3

• von Economo Encephalitis occured during the influenza epidemic of 1916 to 1920, and resulted in injury to the substantia nigra (with a gross loss of pigmentation).
• Clinical expresions of “postencephalitic parkinsonism” were immediate or delayed

Question 4

Characteristic cells in Parkinson’s are called what?

Answer 4

Lewy Bodies - residual atrophic nerve cells, contain spherical, granular, eosinophilic cytoplasmis inclusions.

Question 5

What are the major clinical features of Parkinson’s

Answer 5

• Slowness of all voluntary movements
• Muscular rigidity through range of movement
• Course tremor of distal extremities (pill-rolling)
• Tremor present at rest and disappears with movement
• Face is expressionless (mask-like)
• Reduced swallowing - drooling

Question 6

What are the conditions/classes of drugs can cause Parkinson’s like conditions?

Answer 6

1. Drugs:
   
   1. Phenothiazines & Haldol
2. CO or Manganese poisoning
3. Bilateral infarcts of basal ganglia
4. Hydrocephalus
5. Tumors near the basal ganglia
6. Cerebral trauma

Question 7

75% - Where is most common site for hypertensive associated hemorrhage out of the three?

Answer 7

• Basal ganglia thalamus - 75%
• Pons - 15%
• Cerebellum - 10%

Question 8

What is the underlying etiology of a Berry aneurysm - Where are they located? If ruptured, where would it go in the brain?

Answer 8

• Arterial defects that originate during embryonic development at a y-shaped bifurcating artery. Circumferential muscular layer of parent vessel may fail to interdigitate into two branches, creating a point of congenital muscular weakness, bridged only by endothelium, the internal elastic lamina, and slender adventitia. (no muscular layer)
• 90% located at branch points in Circle of Willis
• Rupture causes subarachnoid hemorrhage. ⅓ patients rupture can cause intracerebral or intraventricular hemorrhage. Large aneurysms of internal carotid complex.

Question 9

What is the etiology of rupture of small Charcot-Bouchard aneurysms?

Answer 9

• Lipohyalinosis in the walls
• Associated with long-standing HTN

Question 10

What is the etiology for strokes?

Answer 10

• AKA Cerebral Infarction
• Cerebrovascular occlusive disease
• Atherosclerosis predisposes to vascular thrombosis and embolic events

Question 11

What are the different clinical presentations of strokes blockage striated arteries, trifurcation of the middle cerebral?

Answer 11

• Trifurcation of the middle cerebral
  
  • Produces motor and sensory deficits, aphasias when dominant hemisphere is involved
• Striated arteries
  
  • Hemiparesis or Hemiplegia

Question 12

What are the clinical presentation, gross features, and characteristic cells involved in Alzheimer’s.

Answer 12

• Gradual loss of memory, cognitive function, language and changes in behavior
• Senile plaques - hippocampus, amygala
• Neurofibrillary tangles - flame cells
• Amyloid angiopathy - blood vessels (congo red)
• Alzheimers gene located on chromosome 21

Question 13

What chromosome contains the Alzheimer gene?

Answer 13

21

Question 14

MS has periventricular MS plaques, MS plaques.

Answer 14

Yes it does.

The plaque is the hallmark of the disease - usually situated in white matter

Question 15

What is Hydrocephalus ex Vacuo?

Answer 15

The loss of brain parenchyma found within Alzheimer’s disease makes the lateral ventricles appear dilated - which the appearance is called hydrocephalus ex vacuo.

Question 16

What parts of the brain are more likely to reveal changes in MS, vs Parkinson’s vs Alzheimer’s?

Answer 16

• MS
  
  • Optic nerves & chiasm, perventricular white matter, cerebellum, brainstem, spinal cord
• Parkinson’s
  
  • Substantia Nigra
• Alzheimer’s
  
  • Frontal lobe, cortex, hippocampus, amygdala, all over brain parenchyma

Question 17

What 2 tissues and organ normally have insulin receptors allowing glucose to penetrate?

Answer 17

• Liver
• Fat cells
• Muscle

Question 18

What are the 2 types of primary diabetes, which one is worse? And what is the pathophysiology of both?

Answer 18

• Type I Diabetes (worse)
  
  • Lack an absolute deficiency of insulin (lack beta cells)
• Type II Diabetes (most common)
  
  • Target tissues are resistant to insulin

Question 19

What cells produce insulin vs glucagon vs somatostatin?

Answer 19

• Alpha cells - Glucagon
• Beta cells - Insulin
• Delta cells - Somatostatin

Question 20

What are the 2 sugar components that glucose breaks down to that has an osmotic diuresis effect?

Answer 20

• Sorbitol
• Fructose

Question 21

What organ systems are involved with diabetes that do not require insulin receptors?

Answer 21

• blood vessels
• nerves
• lens
• kidney tubules

Question 22

What 1 word characterizes the pathology of diabetes that has to do small blood vessel disease?

Answer 22

Microangiopathy

Question 23

Characteristics of Hashimotos thyroiditis? Is it auto-immune? Is it hypo or hyper? Which one is associated with the development of lyhphomas (Grave’s, hashimoto’s or Addisons)?

Answer 23

• Inflammation of the thyroid that is most often immune-related
• Gradual failure because of an immune destruction
• Hypothyroidism
• Hashimoto’s - increased risk for development of B-cell lymphomas*

Question 24

What is a goiter? Most common cause? Lab values of a goiter? Difference between nontoxic vs toxic goiters?

Answer 24

1. Enlargement of the thyroid
2. Iodine deficiency
3. Low concentrations of T3, T4 in serum, high levels of TSH
4. Nontoxic
   
   1. Enlargement of thryoid without functional, inflammatory or neoplastic alterations (diffuse and multinodular)
5. Toxic
   
   1. Sudden autonomous hyperfunctioning of a previous, long-standing non-toxic goiter.

Question 25

Clinical features of myxedema, organ systems involved? What are the clinical presentations between Grave’s disease vs Myxedema?

Answer 25

1. Myxedema - Seen in face with puffy eyelids, swollen hands and feet, enlarged tongue, cool and pale skin.
2. Organ sysmtems - Hypofunctioning - Skin, Heart, Nervous system, GI, Reproductive tracts,
3. Graves
   
   1. Diffuse goiter, exopthalmos, dermopathy
4. Myxedema
   
   1. Tiredness, lethargy, can’t concentrate, sensitive to cold

Question 26

What’s the underlying pathophysiology of Grave’s disease? What type of antibodies are they? Where do they attach? What is exophthalmos?

Answer 26

1. Increased circulating antibodies (IgG) that bind to the surface of the thyroid cells, exerting a stimulus similar to the effects of TSH itself.
2. IgG
3. Bind to TSH receptors stimulate hypersecretion of T3 and T4, thyroid cells
4. Protrusion of the eyeballs, caused by enlargement of the orbital extraocular muscles

Question 27

Who’s more likely to get any of these 3 autoimmune diseases (Hashimoto’s, Grave’s, Myxedema)?

Answer 27

• Women
• Other autoimmune diseases
  *

Question 28

What is cretinism and how do you get it?

Answer 28

• Congenital hypothyroidism
• Endemic, sporadic or genetic
  *

Question 29

Differentiate Cushing’s disease vs Cushing syndrome?

Answer 29

• Cushing’s Disease
  
  • Hypercortisolism, ACTH hypersecreting pituitary
  • 5 times more common
• Cushing Syndrome
  
  • Result of hypersecretion of glucocorticoids from adrenal cortical tumors of hyperplasias
  • From chronic corticosteroid administration

Question 30

What are the causes of hyperfunctioning of the adrenal gland? What is the most common reason for hyperfunctioning of the adrenal gland?

Answer 30

1. Hyperfunctioning adrenal gland
   
   1. Adrenal cortical ademona, adrenal carcinoma, exogenous corticosteroids
2. Most common reason - exogenous corticosteroids

Question 31

What are the clinical features of Addison’s disease? What is the Dexomethazone test? Is it an auto-immune disease?

Answer 31

• Addison’s Disease
  
  • Autoimmune destruction of the adrenal gland
  • Extreme weakness, fatigue, bed rest, weight loss, anorexia, nausea, personality changes
  • DXM test - suppresses pituitary ACTH secretion. This test distinguishes ACTH-dependent from ACTH-independent forms for Cushing Syndrome

Question 32

? Remember – any autoimmune disease whether is Grave’s, Hashimoto’s or Addison’s it is characterized by what?

Answer 32

infiltrates with lymphocytes, plasma cells, monocytes, lymphoid nodules with germinal centers – that reflects the immune phenomenon.

Question 33

What are the clinical features of Cushing’s Syndrome?

Answer 33

trunkal obesity, ruby red congestion, moon face, buffalo hump.

Question 34

What is Waterhouse fredrickson syndrome and what causes it? What does it do to the adrenal glands?

Answer 34

• Acute meningococcemia
• Overwhelming neisseria meningitidis septicemia with rapidly progressive shock with hypotension, widespread purpura, widespread adrenocortical insufficiency.
• Massive bilateral adrenal hemorrhage, infarction and rupture

Question 35

What is a pheochromocytoma? Primary or secondary hypertension? What is released from the adrenal medulla and what are the signs and symptoms?

Answer 35

1. Rare neoplasm of chromaffin cells of the adrenal medulla that makes catecholamines (epi norepi)
2. Secondary hypertension
3. Epinephrine and norepinephrine released from adrenal medulla
4. Signs & Symptoms:
   
   1. HTN, tachycardia, palpitations, H/A, sweating, tremor, chest pain