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CPR > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

ADH release signal

A

Cell bodies in the supraoptic nuclei of the hypothalamus send axons to the posterior pituitary and release ADH (hypothalamic neurons synthesize ADH)

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2
Q

Signals that trigger ADH release

A

Low BP - carotid (CNIX) and aortic (CNX) baroreceptors
Decreased arterial stretch due to low blood volume
Increased osmolality - hypothalamic osmoreceptors
Sympathetic stimulation
Angiotensin II secretion
Low blood volume

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3
Q

Secretion of ADH is most sensitive to what trigger

A

Plasma osmolality changes

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4
Q

ADH method of action in kidney

A

ADH binds V2 receptors in distal tubule and collecting duct activating GPCR-cAMP-PKA sequence
This causes more aquaporin channels to be inserted in the membrane for more water uptake

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5
Q

Diabetes insipidus and ADH

A

ADH lacks its normal effect on the collecting duct
Causes frequent urination
Large volume of urine is diluted

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6
Q

Central vs nephrogenic diabetes insipidus (DI)

A

Central- lack of ADH- could be from damage to pituitary or hypothalamus. Treat with desmopressin (antidiuretic)
-will have decreased plasma ADH in labs
Nephrogenic- Kidneys unable to respond to ADH
-Can be caused by drugs like lithium, or kidney disease
-Desmopressin will not work

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7
Q

Water deprivation test for DI

A

Drink fluids over night, give breakfast w/o fluids
Weigh patient
No fluid during day, weigh patient every 1-2 hrs
Empty bladder, measure volume and osmolality of urine as well as plasma osmolality
If results suggest DI, patient drinks and desmopressin is administered
Remeasure plasma osmolality and urine osmolality/volume

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8
Q

Syndrome of inappropriate ADH secretion SIADH

A

Excessive ADH secretion
Excessive water retention
Hypoosmolality fails to inhibit ADH release
-Hyponatremia, decreased plasma osmolality, increased urinary osmolality

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9
Q

Factors causing aldosterone production and sequence of events

A

Decreased Na, Increased K+ in blood
Decreased blood volume or blood pressure
Kidney signaled to release renin
Liver releases angiotensinogen which is converted to angiotensin I by renin
AT1–>AT2 –> adrenal cortex –> Aldosterone–> water/Na+ reabsorption

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10
Q

Aldosterone effect on kidney

A

Aldosterone combines with cytosolic receptor in distal tubule
Hormone/receptor complex travels to nucleus and new protein channels/pumps are synthesized
Increased Na reabsorption and K+ secretion in ascending limb, distal tubule, collecting duct

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11
Q

Other effects of angiotensin II besides Aldosterone secretion

A

Increased sodium/hydrogen exchange causing increased sodium reabsorption along nephron
Increased thirst
Vasoconstriction
Increased ADH secretion

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12
Q

Primary adrenal insufficiency

A

Both cortisol and aldosterone secretion decreased

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13
Q

Secondary or tertiary adrenal insufficiency

A

Cortisol decreased but renin-angiontensin-aldosterone axis still exists

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14
Q

ANP

A

When atria are distended, ANP is released
Increases excretion of NaCl/water by kidneys
-vasodilation of afferent and vasoconstriction of efferent arterioles- increasing GFR and filtration load
-Inhibit renin/aldosterone secretion and ADH action on distal tubule/collecting duct
-inhibit NaCl reabsoprtion
Ventricles produce BNP (brain natriuretic peptide) that has a similar function
-both decrease total peripheral resistance

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15
Q

Urodilatin

A

Encoded by the same gene as ANP
Secreted by the distal tubule and collecting duct
Influences only the function of the kidneys
Stimulated by increased BP and ECF volume
Inhibits NaCl and water reabsorption by medullary portion of collecting duct

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16
Q

Sympathetic nerve activity and regulation of NaCl/water reabsorption

A

Catecholamines released from sympathetic nerves stimulate reabsorption of Na and water by proximal tubule, thick ascending limb, distal tubule and collecting duct
Increase renin secretion
Decrease GFR (vasoconstrict afferents)

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17
Q

Addisons disease

A

Atrophy of adrenal gland
Decreased cortisol and aldosterone secretion
Causes increased CRH release from hypothalamus
Causing increased ACTH release from pituitary
Hyperpigmentation

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18
Q

Response to increased sodium intake

A

Decreased sympathetic activity
Increased ANP
Decreased peritubular capillary osmotic pressure
Decreased renin/angiotensin/aldosterone system

19
Q

Causes of K+ shifts out of cells–>hyperkalemia

A 
Insulin deficiency
B2 adrenergic antagonist
a-adrenergic agonists
Acidosis
Hyperosmolarity
Cell lysis
Exercise
20
Q

Causes of K+ shift into cells–>hypokalemia

A 
Insulin
B2 adrenergic agonists
a-adrenergic antagonists
Alkalosis
Hypoosmolarity
21
Q

Insulin effect on K+ balance

A

Stimulates K+ uptake into cells by increasing Na/K pump activity
Ensures ingested K does not remain in ECF
Deficiency of insulin like in type I diabetes causes decreased K+ uptake and hyperkalemia

22
Q

Three pathways triggering aldosterone release

A

Hypothalamus CRH–>pituitary ACTH–> adrenal cortex aldosterone
High plasma K+–> adrenal cortex secrete aldosterone
Renin-angiotensin system

23
Q

Increased ENaC: Liddle syndrome lab results (renin, aldosterone, EC volume or BP)

A

Low renin
Low aldosterone
High EC volume/BP

24
Q

Decreased B-hydroxysteroid dehydrogenase: apparent mineralocorticoid excess, licorice lab results (renin, aldosterone, EC volume or BP)

A

Low renin
Low aldosterone
High EC volume or BP

25
Q

Adrenal tumor or hyperplasia lab results (renin, aldosterone, EC volume or BP)

A

Low renin
High aldosterone
High EC volume or BP

26
Q

Congenital adrenal hyperplasia 17-hydroxylase deficiency lab results (renin, aldosterone, EC volume or BP)

A

Low renin
High aldosterone
High EC volume or BP

27
Q

Renin-secreting tumor lab results (renin, aldosterone, EC volume or BP)

A

High renin
High aldosterone
High EC volume or BP

28
Q

11B-HSD2 enzyme effect in aldosterone/cortisol pathways

A

Cortisol has the ability to bind mineralocorticoid receptors and carry out aldosterones function
This is prevented by enzyme 11B-HSD2, which converts cortisol to cortisone so it must be converted back to cortisol in a glucocorticoid specific target cell

29
Q

17a Enzyme deficiency (mineralcorticoid, cortisol, sex hormones, BP, K+, labs)

A 
MC- increased
Cortisol- decreased
Sex hormones- decreased
BP- increased
K+- decreased
Labs: decreased androstenedione
30
Q

21B enzyme deficiency (mineralcorticoid, cortisol, sex hormones, BP, K+, labs)

A 
MC- decreased
Cortisol- decreased
Sex hormones- increased
BP- decreased
K+- increased
Labs: increased renin activity, increased 17-hydroxy progesterone
31
Q

11B enzyme deficiency (mineralcorticoid, cortisol, sex hormones, BP, K+, labs)

A 
MC- decreased aldosterone, increased DOC (^^BP)
Cortisol- decreased
Sex hormones- increased
BP- increased
K+- decreased
Labs: decreased renin activity
32
Q

B-blockers, autonomic neuropathy effect on renin system

A

Hyporenin-hypoaldosteronism can result

33
Q

Hypocalcemia symptoms/indicators

A

Hyperreflexia, spontaneous twitching, muscle cramp, numbness/tingling
Chvostek sign- twitching of facial muscles when tap on facial nerve
Trousseau sign- carpopedal spasm upon inflation of BP cuff

34
Q

Hypercalcemia symptoms

A

Decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness/hyporeflexia, lethargy, coma

35
Q

Changes in phosphate concentration effect on calcium

A

Increased phosphate will decrease ionized calcium

Same hormones that regulate calcium also regulate phosphate

36
Q

Acidemia/alkalemia effect on calcium-albumin binding

A

Acidemia will increase ionized calcium by decreasing Ca-albumin binding
Alkalemia has opposite effect

37
Q

Calcitonin

A

Decreases bone resorption- opposite effect of PTH

38
Q

PTH effects on bone/kidney/intestine

A

Increased bone resorption
Decreased phosphate reabsorption, increase calcium reabsorption and increase urinary cAMP in kidney
Increase calcium absorption in intestine (via vitamin D)

39
Q

PTH in kidneys

A

PTH activates GPCR in proximal tubule, increasing cAMP, causing inhibition of Na/phosphate pump which decreases sodium/phosphate reabsorption
Stimulates calcium reabsorption in thick ascending limb and distal tubule

40
Q

Vitamin D and PTH gene expression

A

Vitamin D inhibits PTH gene expression and activates Calcium receptor on parathyroid cell which senses calcium and activates another pathway to further inhibit PTH gene activation

41
Q

Cholecalciferol processing

A

25-hydroxylase in liver converts it to 25-OH-cholecalciferol
1a-hydroxylase (CYP1-a) in kidney converts 25-OH-C to 1,25-OH2-cholecalciferol active form
24-hydroxylase in kidney converts to 24,25-OH2-cholecalciferol inactive form

42
Q

CYP1-a gene regulation

A

Transcription activated by PTH
Inhibited by Calcium and active vitamin D or the 25-OH form
Vitamin D activates CYP24 gene for 24 hydroxylase

43
Q

Familial hypocalciuric hypercalcemia FHH

A

Caused by mutation that inactivates CaSR in parathyroid glands and parallel calcium receptors in ascending limb of kidney
Results in decreased urinary calcium excretion and increased serum calcium
Normal/high PTH, high serum Ca, low urine Ca, normal phosphate and normal vitamin D

CPR (24 decks)

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