Week 2 Flashcards
About how much of the population is affected by CAH (congenital adrenal hyperplasia)?
1%
What is the root of the dysfunction in CAH?
A lack of the enzyme 21-hydroxylase.
Explain why CAH leads to masculinization of XX individuals.
The lack of 21-hydroxylase means that the other adrenal hormones (cortisol and aldosterone) can’t be produced, even though the pituitary is telling the adrenal glands to produce them. The enzyme deficiency doesn’t affect the production of androgens by the adrenal cortex… so they continue to be produced. The LACK of negative feedback that cortisol & aldosterone would normally provide to the HT and PT means that CRH and ACTH continue to be produced. The adrenal cortex is enlarged (hypertrophy) because of the excess demand on it. There is tons of the precursor for the adrenal hormones being produced, so it all gets converted to androgens which have the masculinizing effects.
Why do XY individuals with CAH have smaller testicles than normal?
Because there is so much androgen circulating, it provides lots of negative feedback to the pituitary, which reduces its secretion of LH and FSH. The cells in the testes need LH and FSH to grow and produce testosterone, and they’re not getting enough.
Why can’t we simply conclude that the overabundance of testosterone in XX individuals with CAH is what causes them to be more aggressive, less interested in stereotypical feminine gender roles, and have higher rates of homosexuality/bisexuality?
- Lack of cortisol and aldosterone are important effects of the syndrome and we can’t be sure that these aren’t responsible for the behavioral effects.
- Environment seems to always have an effect… (if genitalia is ambiguous… does this lead to different treatment of them which could lead to different behavior on their part?)
What were the key points of Lazarus’s appraisal model of stress?
That stress responses depend on primary and secondary (subjective) appraisal of a stimuli. Appraisal requires us to examine the demand of the situation versus the resources we have.
According to Dickerson & Kemeney, social and physical stresses affect our systems differently. How so?
Social/psychological stress activates our HPA axis, whereas physical stress activates our SNS.
What are we more likely to encounter, anticipatory physical stress, or anticipatory social stress?
Anticipatory SOCIAL stress. Physical stress is usually more reactive.
Why have researchers turned to measuring the enzyme alpha-amylase from saliva during stress research?
Because although AA levels go up during both parasymp and SNS activation, it does show ACTIVATION and the magnitude. To confirm they’re really measuring a SNS response, they check other indicators also (BP, HR). This method is used because actual SNS hormones (adrenaline, noradrenaline) break down extremely quickly and so are hard to measure.
Why does normal, unstressed cortisol secretion vary by bursts every 60-90 mins?
Because it takes time for cortisol to circulate in the blood and provide the varying levels of feedback that result in the increases and decreases.
Name two 3rd-level feedback loops.
HPT, HPA, HPG (three glands)
What happens to the subsequent hormone cascade if the hypothalamus is ablated experimentally?
Trick question: DEATH.
An important symptom of Addison’s disease is lack of energy. What is the physiological problem in Addison’s disease?
Adrenal insufficiency, a major lack of cortisol and aldosterone. Some HPA activation is normal and necessary.
What was important about Selye’s stress-disease model?
He talked about different stages of stress system activation –> Short-term being normal and adaptive, and long-term causing an exhaustion of the system (lower activation than normal).
What was important about the diathesis-stress model of disease?
The interaction of an innate vulnerability with a stressful environmental stimuli leads to disease.
