Same

Front 1

What is the etiology of encephalitis?

Back 1

Systemic viral infection crossing BBB causing inflammation of the brain

May be carried by mosquitoes

Herpes simplex can carry it

Systemic childhood viral infections like poliomyelitis, rabies, mononucleosis, rubella, rubeola

Vaccine reaction to live attenuated virus like measles, mumps, rubella

Front 2

What happens to encephalitis patients?

Back 2

Necrosis: neurons and hemorrhage of the cerebral capillaries can occur

Edema: causes an increased intracranial pressure

The neural manifestations are the same as meningitis

Front 3

Schizophrenia

Back 3

Tends to run in families

CNS development problems: viral infection during 2nd trimester of pregnancy increases the chances

The ventricular system of the brain containing the cerebrospinal fluid is enlarged

The basal ganglia, thalamus, and amygdala and hippocampus of the temporal lobe are smaller

Altered production and interaction of certain neurotransmitters and receptors

Levels of GABA are decreased in the prefrontal lobe

Dopamine is elevated int eh temporal lobe linked with initiation of psychotic episode

Positive effects-hallucinations

Difficulty completing goal-oriented tasks

Alogia: an absence of spontaneous speech

Anhedonia: no emotional expression

Avolition: deficit in goal related tasks

Front 4

Mood Disorders

Back 4

Depression=unipolar disorder
Manic-depression=bipolar disorder

Genetic component

Stress or environmental stimuli can precipitate

Hypercortisolism occurs; diagnosis by dexamethasone suppression test; synthetic glucocorticoids like dexamethasone, should negatively feedback on CRH an decrease cortisol to normal

Monoamine deficits occur leading to depressed levels of serotonin and norepinephrine

Antidepressant drugs elevate monoamines by poorly understood mechanisms

Tricyclic antidepressants (TCA's) decrease monoamine reuptake

Front 5

What are the hormones of the anterior pituitary and what is their function?

Back 5

~Prolactin-milk production
~ACTH-secretion glucocorticoids
~TSH-Stimulates thyroid hormone
~LH-induces ovulation; spermatogenesis
~FSH-ovarian follicle maturationn, estrogen production; spermatogenesis

Front 6

What are the hormones of the posterior pituitary and what is their function?

Back 6

~ADH-secreted in response to dehydration, target=distal kidney tubule, increases permeability of the distal kidney tubule causing increased H2O reabsorption, body H20 is conserved and urine if concentrated

~Oxytocin-secreted during final stages of labor, stimulates mammory smooth muscle when infant is suckling as well as uterine smooth muscle contraction

Front 7

What are the 2 major effects of T3 and T4 secreted by the thyroid?

Back 7

1. to regulate basal metabolic rate

2. Induces normal central nervous system and musculoskeletal development in children

Front 8

What is the major glucocorticoid and where is it secreted from?

Back 8

Cortisol secreted from the adrenal cortex.

Front 9

What does cortisol do?

Back 9

It alters metabolism to raise blood glucose and suppresses the immune and inflammatory response

Front 10

What population does Type I Diabetes Mellitus represent? (Ages and %)

Back 10

10% of diabetics

Juvenile onset, manifests in children between 9 months and 12 years

Front 11

Is Type I Diabetes Mellitus insulin dependent or not?

Back 11

Yes it's insulin dependent due to undersecretion of insulin by the beta cells

Ther eis probably an autoimmune response to the beta cells as in most cases there are autoantibodies against insulin, beta cells, and the enzyme glutamic acid decarboxylase

May be related to environmental exposure to certain drugs, viruses, and genetic predisposition

Front 12

What are the signs/symptoms/manifestations of Type I Diabetes mellitus?

Back 12

Hyperglycemia: Fasting blood glucose greater than 126 mg%

Low blood insulin: insulin needed to trigger opening of glucose channels

Polyuria: H2O from blood drawn into kidneys

Glycosuria: excess blood glucose overrides teh kidney's ability to reabsorb sugar resulting sugar in urine

Polydipsia: excessive thirst

Weight loss: due to protein in skeletal muscle and fat catabolism for energy

Ketosis: excess fat and rotein catabolism leads to the formation of ketones, drops blood pH and lead to metabolic acidosis

Polyphagia: body is in starvation state stimulating hunger centers due to protein and fat catabolism and lack of glucose uptake by cells

Fatigue: metabolic changes and nocturia leads to lethargy, fatigue, and loss of sleep

Front 13

What population does Type II Diabetes mellitus represent? (Ages and %)

Back 13

90% of diabetics

Adult onset because it usually manifests in obese people over 40

Front 14

What is the etiology of Type II Diabetes mellitus?

Back 14

Receptor insensitivity to insulin

Initially insulin levels may be normal or higher than normal

Environmental, genetic, overweight factors

Front 15

What are the signs/symptoms/manifestations of Type II Diabetes Mellitus?

Back 15

Hyperglycemia

Polyuria

Polydipsia

Polyphagia

Fatigue

Recurrent infection

Genital puritis: hyperglycemiaand glycosuria provide a good medium for fungal growth near the urinary tract, resulting in itching (puritis)

Visual Changes: hyperglycemia osmotically draws H2O into capillaries of retina causing blurred vision

neuropathy: due to osmotic pressure changes found in capillaries or adverse metabolic alterations

Paresthesias: Abnormal burning or prickling sensation primarily in extremities probably due to neuropathy

Front 16

What is hypoglycemia and what is it's major cause?

Back 16

Blood glucose below 60 mg%

It's major cause is insulin overdose in Type I Diabetics, to much insulin results in to much glucose uptake by the cells.

Front 17

How do low levels of blood glucose affect the brain?

Back 17

The adversely affect the brain since nervous tissue only uses glucose as an energy substrate

Front 18

What is hypoglycemia caused by insulin referred to as?

Back 18

Insulin reaction or shock which can result in death if severe.