Going through the notes Flashcards
Where is the lesion: PE shows + pronator drift
spinothalamic tract, contralateral side of drift. UMN (b/c without visual input, brain must rely on proprioception for info about where the hand is in space)
What things could cause a fixed split of S2? (4)
ASD
right heart failure
pulm htn
pulm stenosis
What conditions would cause paradoxical splitting of S2? (hear it better with inspiration) (2)
aortic stenosis
COPD
If you wanted to test pancreas functions, you would check a _________level, which increases as pro-insulin is converted to insulin and is therefore an indirect measurement of insulin production
c-peptide
Angiotensin converting enzyme is synthesized where?
lungs
hence it’s elevation in sarcoidosis
where is the enzyme renin synthesized? what triggers its release?
kidneys
released in response to:
1) baroreceptor reflex (low pressure in renal arterioles)
2) macula densa cells detect decreased NaCl concentration in kidneys
3) dopamine, epi, NE, cortisol (sympathetic activation)
Renin-Angiotensin system recap:
Angiotensinogen (liver) and renin (kidneys) are released by cortisol in response to stress. Renin converts angiotensinogen to AT1. ACE (lungs) converts AT1 to AT2. AT2 causes vasoconstriction and triggers aldosterone. Aldosterone (adrenals) causes reabsorption of Na+ and H2O, and K wasting. End game is to increase blood volume, cause vasoconstriction, and is in response to stress/sympathetic activation
Besides the renin-angiotensin sequence, what is another hormone that helps increase fluid volume?
ADH/vasopressin
…which also causes increased water resorption and vasoconstriction
If there is too much fluid volume and the heart becomes stretched, it will attempt to protect itself by releasing ___________, which functions to __________
BNP, do the opposite of AT2: vasodilate waste Na+ inhibit ADH inhibit renin inhibit aldosterone parasympathetic stimulation
What are the 4 major types of adrenergic receptors, and what do they do when stimulated?
1) alpha 1: vasoconstriction
2) alpha 2: “brake” for neurotransmitter release (if alpha 2 is stimulated then there will actually be a decrease in catecholamine release aka epi and NE)
3) beta 1: increased HR, heart contractility
4) beta 2: bronchodilation, dilation of skeletal muscles
(albuterol is so good for exercise induced asthma b/c it opens airways and increases blood supply to muscles)
What is the metabolic effect of catecholamines?
make glucose available for energy right now
What type of cells produce epi and NE?
chromaffin cells….hence the name pheoCHROMOcytoma = increased catecholamines
what triggers the adrenal cortex to produce cortisol?
ACTH
Your patient confides she has been unusually stressed out over the last 6 months after her dear friend left her heartbroken. She has gained 20 pounds and wants to know if it could be stress related. She has changed nothing else in her lifestyle. (She has not, for example, started running or developed crippling tendonitis). What will you tell her and why?
Yes, stress can cause wt gain. During human evolution, stress used to indicate immediate danger, requiring fight or flight which causes sympathetic activation and the initial release of epi/NE/”adrenaline”. However, if the stress continues for any length of time, the adrenal glands stop releasing the adrenaline and start releasing cortisol. The whole goal of cortisol is to make glucose readily available in the blood stream for use to give the host energy to face the stressor. In order to keep glucose in the blood, cortisol breaks down protein (muscle loss and poor wound healing) and increases glucose production in liver (hyperglycemia/insulin resistance) and attempts to protect vital organs by redistributing fat centrally.
What’s the difference between T3 and T4?
T3 = triiodothyronine T4 = thyroxine Thyroid produces: 90% T4 (converted to T3 at target cells), 7 day t(1/2) 9.9% T3, 1 day t(1/2) 0.1% rT3, elevated in starvation
