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CPR Exam 2 > 10. Endocrinology Integrative Session > Flashcards

10. Endocrinology Integrative Session Flashcards

1
Q

how are the hypothal & post pit connected

A

hypothal (supraoptic nucleus & paracentricular nucleus)

–> send axons (hypothalamic-hypophyseal tract)

to post pit - release ADH

connection = neural

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2
Q

where are most of the ADH cell bodies located

A

supraoptic nucleus (SON)

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3
Q

what triggers ADH secretion

A

decreased BP - (sensed by cardiac & aortic baroreceptors)

decreased arterial stretch due to low BV - (sensed by artial stretch)

increased osmolality - (sensed by hypothalamic osmoreceoptors) *MOST SENSITIVE*

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4
Q

carotid sinus and aortic arch uses which nerves to signal the medulla oblangata

A

vagus N & glossopharyngeal N

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5
Q

what is the response generated by ADH

A

vasoconstrict blood vessels (V1​ receptors)

increase reabs in kidneys (V2 receptors)

==> increase BP & blood vol

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6
Q

what happens during hyperosmolarity (dehydration)

A

decreased h2o & hypernatremia –>

stimulate osmoreceptor in ant. hypothalmus –>

increase thirst & post pit release ADH –>

increase h2o permeability of principal cells in distal tubule & collecting duct –>

increase h2o reabs –>

–> kidneys removed LESS h2o from blood –> increase [urine]

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7
Q

what is the response to hypoosmolarity (hypervolemia)

A

inhibit osmoreceptors in ant hypo –>

decrease thirst & ADH secretion from post pit –>

decrease h2o permeability of principal cells –>

decrease h2o reabs

–>kidneys remove MORE h2o from blood = urine more dilute

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8
Q

what is caused by decreased levels or effects of ADH on renal collecting duct

A

diabetes insipidus (DI)

freq urination & polydyspia

large vol urine & its diluted

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9
Q

how do you get central DI

A

lack of plasma ADH bc..

damage to pituitary or destruction of hypothal

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10
Q

what is desmopressin

A

drug that prevents h2o excretion

use for central DI

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11
Q

how does nephrogenic DI happen

A

kidney is unable to respond to ADH (increased plasma ADH levels) bc..

drugs like lithium or chronic disorders (polycystic KD, sickle cell anemia)

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12
Q

what is the h2o deprivation test for DI

A
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13
Q

how do you differentiate btn central & nephrogenic DI

A

both - increase plasma Osm & decrease urine Osm

central: decreased ADH & respond to desmopressin (increase urine Osm)
nephrogenic: increased ADH & NO response from drug

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14
Q

what is syndrome of inappropriate ADH secretion (SIADH)

A

excess secretion of ADH –> excess h2o retention, HYPOnatremia, plasma Osm decrease & urine Osm increased

bc : (adrenal insufficiency: drugs, trauma, CNS disorders)

ectopic : small cell lung carcinoma

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15
Q

when is aldosterone stimulated

A

decreased Na/increased K in blood

decreased BV & BP

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16
Q

what does angiotensin II stimulate

A
  1. aldosterone –> increase Na reabs - increase ECF vol
  2. increase Na-H exchange –> (result above)
  3. increase thirst
  4. vasoconstriction –> increase TPR

all together increase Pa

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17
Q

what is primary adrenal insufficiency

A

adrenal cortex not working

both cortisol & aldosterone decrease

ACTH & CRH increase

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18
Q

what is the cause of secondary adrenal insufficiency

A

ant pit affected -> decrease cortisol

but normal aldosterone bc RAAS stil fxning

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19
Q

what is ANP & BNP

when is its released

A

atria distend –> release ANP

ventricle release BNP

–> reduce BP (decrease TPR) and increase excretion of NaCl and h2o by kidneys (collecting ducts)

20
Q

what is urodilatin

A

secreted by distal tubule & collecting duct

stimulated by increased BP & increase ECF vol

inhibit NaCl and h2o reabs in medullary collecting duct

(like ANP but only fxn of kidneys)

21
Q

how do the natriuretic peptides control NaCl excretion

A

vasodil afferent & vasocon efferent arterioles ==> increase GFR

inhibit renin, aldosterone, ADH secretion

inhibit NaClo reabs by collecting ducts

22
Q

how does sym N contribute to NaCl and h2o reabs

A

catecholamines stimulate NaCl & h2o reabs by PCT, thick ascending limb, DST and collecting tube

23
Q

what happens if there is increased Na intake

A
24
Q

what happens if there is decreased Na intake

A
25
Q

what can cause hyperkalemia

A

insulin deficiency

beta2- antagonists

alpha agonists

acidosis

hyperosmolarity

cell lysis

exercise

26
Q

what can cause hypokalemia

A

insulin

beta2 agonists

alpha antagonists

alkalosis

hyposmolarity

27
Q

what does insulin do to K+

A

stimulates K+ uptake into cell by increasing Na/K ATPase

(deficiency leads to hyperkalemia)

28
Q

what happens with decreased beta-hydroxysteroid dehydrogenase, apparent mineralocorticoid excess, licorice

A

renin & aldosterone: low

extracell vol or BP: high

-hypokalemia

29
Q

what would a adrenal tumor or hyperplasia lead to

A

renin: low

aldosterone, extracell vol or BP: high

-hypokalemia

30
Q

what would congenital adrenal hyperplasia (17-hydroxylase deficiency)

A

renin: low

aldosterone, extracell vol, blood pressure: high

-hypokalemia

31
Q

what would a renin-secreting tumor lead to

A

high renin, aldosterone, extracell vol &/or BP

hypokalemia

32
Q

what would a 17-alpha enzyme deficiency lead to

A

increased: mineralocorticoids, BP
decreased: cortisol, sex hormones, [K+], androstenedione
male: undescended testes
female: lack secondary sexual development

33
Q

what does 21-beta enxyme deficiency lead to

A

increased: sex hormone, [K+}, renin activity, 17 hydroxy-progesterone
decreased: mineralocorticoids, cortisol, BP
infants: salt wasting

precocious puberty

virulation

34
Q

what would a 11-beta enzyme defiency lead to

A

increased: DOC, BP, sex hormone
decreased: aldosterone, cortisol,[K+}, renin activity

virilization

35
Q

what occurs with hypoaldosteronism (adrenal insufficiency)

A

high: renin
low: aldosterone, extracel vol or BP

=hyperkalemia

36
Q

what is present when renin, aldosterone, extracel vol &/or BP are low

(hyperkalemia)

A

hyporenin-hypoaldosteronism:

beta-blockers, autonomic neuropathy

37
Q

what are symptoms present with hypocalcemia

A

hyperreflexia, spontaneous twitching, M cramps, tingling & numbness

chvostek sign: twitch face when tapping facial N

trousseau sign: carpopedal spasm up inflation of BP cuff

38
Q

what are the symptoms of hypercalcemia

A

decreased QT interval

constipation, polyuria, polydispia

lack of appetite

M weakness, lethargy

hyporeflexia

coma

39
Q

how can you change Ca in the plasma

A

change in plasma protein concentration (proportional)

change in [anion] (increase phosphate -> increase Ca)

acid-base abnormalities (change amount of Ca bound to albumin)

40
Q

what happens to Ca in acidemia

A

increase free [Ca]

bc less bound to albumin

41
Q

what happens to Ca in alkalemia

A

decrease free [Ca]

bc more bound to albumin

-associated with hypocalcemia

42
Q

what happens in the bone, kidneys and intestine w/ decreased plasma Ca

A

increase PTH

  1. bone: increase resorption
  2. kidney: decrease Pi reabsorption, increase Ca reabs & urinary cAMP
  3. intestine: increase Ca abs (indirect via vit D)
43
Q

what is the action of PTH on kidneys

A

inhibit NPT2 receptor –> decrease Pi reabs

cAMP made in cells of proximal tubule is excreted in urine (increase urinary cAMP)

stimulates Ca reabs by TAL and distal tubule

(overall: increase Ca reabd and reduce excretion)

44
Q

what is the regulation of vit D synthesis

A
45
Q

how is kidney 1alpha-hydroxylase enzyme regulated

A

transcriptonal level

Ca and Vit D inhibits the CYP1alpha gene

PTH stimulates CYP1alpha gene –> make more 1alpha-hydroxylase

46
Q

what is familial hypocalciuric hypercalcemia

A

auto dont

cause mutations that inactivate CaSR in parathyroid glands & parallel Ca receptors in ascending limb of the kidney

==> decreased urinary Ca excretion (hypercalcemia)

47
Q

what is prepropressophysin

A

peptide precursor for ADH

cleave into propressophysin & then packages in vesicles to travel down hypothalamic-hypophyseal tract

(en route- they’re cleaved into ADH)

CPR Exam 2 (20 decks)

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