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CPR1 Exam 2 > 11 - Endocrinology CIS > Flashcards

11 - Endocrinology CIS Flashcards

1
Q

The connections between the hypothalamus and posterior lobe of the pituitary are (HORMONAL/NEURAL).

A

Neural

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2
Q

Posterior Pituitary is a collection of axons whose cell bodies are located in the hypothalamus. What are the nuclei of the Posterior Pituitary located in the hypothalamus?

A 
Supraoptic Nucleus (SON)
Paraventricular Nucleus (PVN)
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3
Q

_______ neurons have cell bodies primarily in the SON of the hypothalamus.

A

ADH

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4
Q

This is the major hormone concerned with regulation of body fluid. Its target tissues are the kidney and arterioles.

A

ADH

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5
Q

What are the triggers for ADH secretion?

A

Decreased BP
Decreased arterial stretch due to low blood volume
Increased Osmolality

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6
Q

Describe the pathway to trigger ADH secretion due to decreased BP.

A

Decreased BP —

Cardiac and Aortic Baroreceptors —

Sensory neuron to Hypothalamus —

Hypothalamic neurons that synthesized ADH —

ADH released from Posterior Pituitary

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7
Q

Describe the pathway to trigger ADH secretion due to decreased arterial stretch from low blood volume.

A

Decreased arterial stretch due to low blood volume —

Atrial stretch receptors —

Sensory neuron to hypothalamus —

Hypothalamic neurons that synthesized ADH —

ADH released from Posterior Pituitary

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8
Q

Describe the pathway to trigger ADH secretion due to increased osmolality.

A

Increased Osmolality —

Hypothalamic osmoreceptors —

Interneuron to hypothalamus —

Hypothalamic neurons that synthesized ADH —

ADH released form Posterior Pituitary

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9
Q

Secretion of ADH is most sensitive to ________ ________ changes. An increase of only 1% will increase ADH secretion.

A

Plasma Osmolality

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10
Q

What are the secretion triggers for ADH?

A 
Increased Plasma Osmolality
Decreased BP
Decreased Blood Volume
Increased Angiotensin II
Sympathetic Stimulation
Dehydration
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11
Q

ADH makes an increase in BP and blood volume by making blood vessels __________ and the kidneys increasing their reabsorption of _________.

A

Vasoconstriction

Water

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12
Q

What is the mechanism of action of ADH in the renal collecting duct?

A

ADH leaves the peritubular capillary and binds to V2 receptor. This is a GPCR and causes a cascade activating cAMP and PKA. PKA phosphorylates and activates Aquaporin-2, allowing the reabsorption of water through them.

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13
Q

What happens when you have too little water in your body, aka hyperosmolarity (dehydration)?

A

Hypothalamus detects too little water —

Pituitary gland releases ADH —

Kidneys remove less water from the blood so less water is lost in urine (urine is more concentrated)

***Thirst increases!

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14
Q

What happens when you have too much water in your body, aka hypoosmolarity/hypervolemia?

A

Hypothalamus detects too much water in blood —

Pituitary gland releases less ADH —

Kidneys remove more water from blood so more water is lost in urine (urine is more dilute)

***Thirst decreases!

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15
Q

This can occur due to lack of an effect of ADH on the renal collecting duct. It causes frequent urination and the large volume of urine is diluted.

A

Diabetes Insipidus (DI)

***No ADH present = collecting duct is not permeable to water and there is large volume of dilute urine

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16
Q

This type of Diabetes Insipidus is due to a lack of ADH (there is decreased plasma ADH). It could result from:

    • Damage to the pituitary
    • Destruction of the hypothalamus

Treatment includes desmopressin (drug that prevents water excretion).

A

Central DI

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17
Q

This type of Diabetes Insipidus is due to the kidneys being unable to respond to ADH (there is increased plasma ADH). It could result from:

    • Drugs like lithium
    • Chronic disorders (i.e., polycystic kidney disease, sickle cell anemia)

Desmopressin treatment DOES NOT work.

A

Nephrogenic DI

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18
Q

What is the water deprivation test for DI?

A

1 – Allow fluids overnight before test and give breakfast with no fluids.

2 – Weigh patient.

3 – Allow no fluid for 8 hrs. Every 1-2 hrs. weight patient (Stop test if weight drops by >5% initial body weight). Patient empties bladder (measure urine volume and osmolality). Measure plasma osmolality (Stop test if osm >300 mOsm).

4 – If results suggest DI, allow patient to drink (no more than twice urine volume of period of fluid deprivation). Administer Desmopressin.

5 – Measure plasma and urine osmolality. Measure urine volume.

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19
Q

This is a disease from excessive secretion of ADH. There is excessive water retention. Hypoosmolality fails to inhibit ADH release.

A

Syndrome of Inappropriate ADH Secretion (SIADH)

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20
Q

Briefly describe the pathway of decreased blood pressure and the use of aldosterone to raise it.

A

Decreased BP –

Kidney secretes Renin –

Liver secretes Angiotensinogen –

Renin converts Angiotensinogen to Angiotensin I –

Angiotensin I is converted to Angiotensin II via ACE –

Angiotensin II stimulates Adrenal Cortex to release Aldosterone –

Aldosterone causes water and Na+ reabsorption and K+ excretion in the kidney –

Increased BP

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21
Q

This type of adrenal insufficiency occurs when both cortisol and aldosterone secretion is low. The Adrenal Cortex itself has a problem.

A

Primary Adrenal Insufficiency

***Addison’s Disease

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22
Q

This type of adrenal insufficiency occurs when cortisol is low, but the renin-angiotensin-aldosterone axis still exists.

A

Secondary (or Tertiary) Adrenal Insufficiency

  • **Secondary is something wrong with the Anterior Pituitary because it can’t make ACTH, resulting in no Cortisol.
  • **Tertiary is something wrong with Hypothalamus because it can’t make CRH, resulting in no ACTH and no Cortisol.
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23
Q

Myocytes of the atria synthesize and store _______. This is released when the atria are distended, which reduces blood pressure and increases excretion of NaCl and water by the kidneys.

A

ANP (Atrial Natriuretic Peptide)

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24
Q

The ventricles of the heart also produce a natriuretic peptide called ________. It was first isolated from the brain and its actions are similar to those of ANP.

A

BNP (Brain Natriuretic Peptide)

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25
Q

Natriuretic peptides decrease NaCL and water reabsorption by the collecting duct. ANP and BNP (INCREASE/DECREASE) blood pressure by decreasing TPR and enhancing urinary excretion of NaCl and water.

A

Decrease

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26
Q

This is encoded by the same gene as ANP. It is secreted by the distal tubule and the collecting duct and it influences only the function of the kidneys.

A

Urodilatin

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27
Q

Secretion of _________ is stimulated by increase in BP and increase in ECF volume. It inhibits NaCl and water reabsorption across the medullary portion of the collecting duct.

A

Urodilatin

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28
Q

Natriuretic peptides will (VASODILATE/VASOCONSTRICT) afferent arterioles and (VASODILATE/VASOCONSTRICT) efferent arterioles of the glomerulus. This leads to increase in GFR and filtered load of sodium.

A

Vasodilate

Vasoconstrict

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29
Q

What other things do natriuretic peptides inhibit?

A
    • Inhibit Renin secretion
    • Inhibit Aldosterone secretion
    • Inhibit NaCl reabsorption by collecting duct
    • Inhibit ADH secretion
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30
Q

___________ released from the sympathetic nerves stimulate reabsorption of NaCl and water by the proximal tubule, thick ascending limb, distal tubule, and collecting tube.

A

Catecholamines

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31
Q

Renal Sympathetic Nerves have increased Activity and decrease NaCl excretion. What other effects does it have?

A

Decreased GFR
Increased Renin secretion
Increased Na+ reabsorption along the nephron

32
Q

Renin-Angiotensin-Aldosterone system increases secretion and decreases NaCl excretion. What other effects does it have?

A

– Increased Angiotensin II stimulates Na+ reabsorption along nephron

– Increased Aldosterone stimulates Na+ reabsorption in the thick ascending limb of Henle’s loop, distal tubule, and collecting duct

– Increased Angiotensin II stimulates AVP (ADH) secretion

33
Q

Natriuretic Peptides: ANP, BNP, and Urodilatin increase secretion and increase NaCl excretion. What other effects does it have?

A

– Increased GFR

– Decreased Renin secretion

– Decreased Aldosterone secretion (indirect through Angiotensin II and direct on Adrenal Gland)

– Decreased NaCl and water reabsorption by the collecting duct

– Decreased AVP (ADH) secretion and inhibition of AVP (ADH) action on the distal tubule and collecting duct

34
Q

AVP (ADH) has increased secretion and decreased water excretion. What other effects does it have?

A

– Increased water reabsorption by the distal tubule and collecting duct

35
Q

If you have increased Na+ intake, what happens?

A
    • Decreased sympathetic activity
    • Increased ANP
    • Decreased Renin-Angiotensin-Aldosterone
    • Decreased πc (pulls fluid into capillaries)

***Leads to Na+ excretion

36
Q

If you decreased Na+ intake, what happens?

A
    • Increased sympathetic activity
    • Decreased ANP
    • Increased Renin-Angiotensin-Aldosterone
    • Increased πc (pulls fluid into capillaries)

***Leads to Na+ reabsorption

37
Q

Causes of K+ shift out of cells can lead to ________. Some of these causes are:

    • Insulin Deficiency
    • ß2-Adrenergic antagonists
    • a-Adrenergic agonists
    • Acidosis
    • Hyperosmolarity
    • Cell lysis
    • Exercise
A

Hyperkalemia

38
Q

Causes of K+ shift into cells lead to _________. Some of these causes are:

    • Insulin
    • ß2-Adrenergic agonists
    • a-Adrenergic antagonists
    • Alkalosis
    • Hypoosmolarity
A

Hypokalemia

39
Q

Insulin stimulates K+ uptake into cells by increasing the activity of _________.

A

Na+/K+ ATPase

40
Q

One effect of this insulin action is to stimulate K+ uptake into cells, which ensures that ingested K+ does not remain in the ECF and produce _________.

A

Hyperkalemia

41
Q

Deficiency of insulin, as in _______ _______ _______, results in decreased uptake of K+ into cells and hyperkalemia. Conversely, high levels of insulin can produce hypokalemia.

A

Type I Diabetes Mellitus

42
Q

The renal effects of _________ show overlap of functions to conserve sodium and to eliminate potassium.

A

Aldosterone

43
Q

Undesired losses of _________ are prevented when sodium retention (via the Angiotensin II stimulus), is required to maintain extracellular volume.

A

Potassium

44
Q

Undesired retention of ________ is prevented when potassium fading alone provides the stimulus to Aldosterone secretion.

A

Sodium

45
Q

The negative feedback that couples _________ with serum potassium is fundamental in potassium regulation.

A

Aldosterone

46
Q

Hyperaldosteronism results in _________ loss, whereas Hypokalemia reduces _________ production.

A

Potassium

Aldosterone

47
Q

Hyperkalemia stimulates _________ release, thereby facilitating urinary potassium secretion.

A

Aldosterone

48
Q

The mineralocorticoid receptor is protected from activation by cortisol by the enzyme _________.

A

11ß-HSD2

49
Q

This congenital adrenal hyperplasia disorder has the following characteristics:

    • Increased Mineralocorticoids
    • Decreased Cortisol
    • Decreased Sex Hormones
    • Increased BP
    • Decreased K+
    • Decreased Androstenedione
    • Males have undescended testes and females lack secondary sexual development
A

17-alpha enzyme deficiency

50
Q

This congenital adrenal hyperplasia disorder is the most common and has the following characteristics:

    • Decreased Mineralocorticoids
    • Decreased Cortisol
    • Increased Sex Hormones
    • Decreased BP
    • Increased K+
    • Increased Renin activity and 17-hydroxy-progesterone
    • Salt wasting (presents in infancy)
    • Precocious puberty and virilization
A

21ß enzyme deficiency

51
Q

This congenital adrenal hyperplasia disorder has the following characteristics:

    • Decreased Aldosterone and Increased DOC (Increased BP)
    • Decreased Cortisol
    • Increased Sex Hormones
    • Increased BP
    • Decreased K+
    • Decreased Renin activity
    • Virilization
A

11ß enzyme deficiency

52
Q

(HYPERKALEMIA/HYPOKALEMIA) causes low ECF or BP, while (HYPERKALEMIA/HYPOKALEMIA) causes high ECF or BP.

A

Hyperkalemia

Hypokalemia

53
Q

This is the term for decreased plasma Calcium concentration. Symptoms include hyperreflexia, spontaneous twitching, muscle cramps, tingling and numbness. Indicators are Chvostek sign and Trousseau sign.

A

Hypocalcemia

54
Q

This sign of Hypocalcemia is the twitching of the facial muscles elicited by tapping on the Facial N.

A

Chvostek Sign

55
Q

This sign of Hypocalcemia is a carpopedal spasm upon inflation of a blood pressure cuff.

A

Trousseau Sign

56
Q

This is the term for increased plasma Calcium concentration. Symptoms include decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, and coma.

A

Hypercalcemia

57
Q

Plasma calcium is the extracellular calcium. If there is low extracellular calcium (hypocalcemia) it reduces the activation threshold for ________ channels, which makes it easier to evoke AP. This results in an increase in membrane excitability (spontaneous APs).

A

Sodium

58
Q

Generation of spontaneous AP is the physical basis for hypocalcemic _________ (spontaneous muscle contractions due to low extracellular calcium). It produces tingling and numbness (on sensory neurons) and spontaneous muscle twitches (motoneurons and muscle).

A

Tetany

59
Q

T/F. High extracellular calcium (hypercalcemia) is the opposite of the hypocalcemia mechanism. It decreases membrane excitability and makes it harder to reach threshold for AP. The nervous system becomes depressed and reflex responses are slowed.

A

True

60
Q

Calcium in the plasma can be altered. Changes in plasma protein concentration will alter total calcium concentration in the (SAME/OPPOSITE) direction. There is no change in calcium ionized.

A

Same

***i.e., Increase in plasma protein concentration will increase total calcium concentration

61
Q

Calcium in the plasma can be altered. Changes in _______ concentration will change the fraction of calcium complexed with anions. (i.e., if there is increased phosphate concentration, there is decreased ionized calcium concentration).

A

Anion

62
Q

Acid-base abnormalities can alter the ionized concentration of calcium by changing the fraction of calcium bound to ________.

A

Albumin

63
Q

This acid-base abnormality occur when free ionized Calcium concentration is increased because less Calcium is bound to Albumin.

A

Acidemia

***More H+ are bound to Albumin

64
Q

This acid-base abnormality occur when free ionized Calcium concentration is decreased because more Calcium is bound to Albumin. This is often accompanied by hypocalcemia.

A

Alkalemia

***More Calcium bound to Albumin, less H+

65
Q

To maintain Calcium balance, the ________ must excrete the same amount of Calcium that is absorbed by the GI tract.

A

Kidneys

66
Q

The extracellular concentration of ________ is inversely related to that of Calcium. It is also regulated by the same hormones that regulate Calcium concentration.

A

Phosphate (Pi)

67
Q

This regulates the concentration of Calcium in plasma. It is stimulated to be secreted when there is decreased plasma Calcium.

A

PTH

68
Q

Decreased plasma Calcium leads to increased PTH secretion. What does this cause?

A
    • Increased bone resorption
    • Decreased Phosphate reabsorption by kidney
    • Increased Calcium reabsorption by kidney
    • Increased urinary cAMP by kidney
    • Increased Calcium absorption in intestines (Vitamin D)

***These all lead to increased plasma Calcium

69
Q

In the kidney, PTH binds to a GPCR. This produces cAMP in the cells of the proximal tubule, which is secreted in urine (urinary cAMP). PTH also inhibits ________, which causes phosphaturia (increased excretion of Pi in urine).

A

NPT2

70
Q

In terms of Calcium homeostasis, _______ stimulates Calcium reabsorption by the TAL and distal tubule. Overall, the net effect is to increase Calcium reabsorption and reduce urinary Calcium excretion.

A

PTH

71
Q

Increased extracellular Calcium concentration inhibits _______ synthesis and secretion.

A

PTH

72
Q

25-OH-cholecalciferol is the main circulating form of Vitamin D, but it has very low activity. It goes to the kidney to be activated by the enzyme _________ (in renal proximal tubule). Here, it becomes the active form of Vitamin D which is 1,25-(OH)2-cholecalciferol. This is a steroid hormone.

A

1a-hydroxylase

73
Q

T/F. Liver 1a-hydroxylase enzyme is tightly regulated at the transcriptional level.

A

False. Kidney 1a-hydroxylase enzyme is tightly regulated at the transcriptional level.

74
Q

This is an autosomal dominant disorder that is caused by mutations that inactivate CaSR in parathyroid glands and parallel Calcium receptors in the ascending limb of the kidney. This results in decreased urinary Calcium excretion (hypocalciuria) and increased serum Calcium (hypercalcemia).

A

Familial Hypocalciuric Hypercalcemia (FHH)

75
Q

Describe the levels of the following in FHH:

    • PTH
    • Serum Calcium
    • Urine Calcium
    • Pi
    • Vitamin D
A 
PTH = Normal or increased
Serum Calcium = Increased
Urine Calcium = Decreased
Phosphate = Normal
Vitamin D = Normal

CPR1 Exam 2 (27 decks)

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