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Renal hormones Flashcards

1
Q

Angiotensin II activation axon

A

Angiotensinogen (liver) + Renin –> Angiotensin I

Angiotensin I + ACE (lungs and kidney)–> angiotensin II

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2
Q

renin is secreted by

A

juxtaglomerular kidney cells

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3
Q

renin secretion is triggered by

A
  1. low Blood pressure (JG cells)
  2. low Na+ delivery (macula densa cells - distal convoluted tubule)
  3. increased sympathetic tone (β1-receptors)
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4
Q

increased sympathetic tumors increase Renin secretion via ….. receptors

A

β1

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5
Q

Angiotensin-converting enzyme - location

A

capillaries of the lungs but can also be found in endothelial and kidney epithelial cells

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6
Q

beside its action in angiotensin-aldosteron axons, ACE also

A

causes Bradykinin breakdown

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7
Q

Angiotensin II action

A
  1. acts at angiotensin II receptor (type 1-AT1) on vascular SMC –> vasoconstriction –> increases BP
  2. constricts EFFERENT arteriole of glomerus –> increases Filtration fraction to preserve GFR in low volumes states (eg. when low RBF)
  3. Aldosterone secretion (adrenal gland) –> a. increases Na channel and Na/K pump in principal cells b. enchance K+ and H+ exretion by way of prinicipal cell K channels and α-intercalated cells H+ ATPase –> creats favorable Na+ gradient for Na and H20 reabsorption
  4. ADH posterior pituitary –> increases aquaporin insertion in principal cells –> H2O reabsorption
  5. increases PCT Na/H+ exchanger activity –> Na+, HCO3- and H2O reabsorption –> permit contraction alkalosis
  6. Stimulates hypothalamus –> thirst
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8
Q

angiotensin action on vessels

A
  1. acts at angiotensin II receptor (type 1-AT1) on vascular SMC –> vasoconstriction –> increases BP
  2. constricts EFFERENT arteriole of glomerus –> increases Filtration fraction to preserve GFR in low volumes states (eg. when low RBF)
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9
Q

angiotensin action on CNS

A
  1. ADH posterior pituitary –> increases aquaporin insertion in principal cells –> H2O reabsorption
  2. Stimulates hypothalamus –> thirst
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10
Q

angiotensin action on PCT

A

Na/H+ exchanger activity –> Na+, HCO3- and H2O reabsorption –> permit contraction alkalosis

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11
Q

angiotensin action on adrenal gland

A

activates aldosterone syntase (zona glomerulosa) –> Aldosterone secretion

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12
Q

in addition to its pressor effect, ATII also

A

affects baroreceptor function –> limits reflex bradycardia which would normally accompany its pressor effects

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13
Q

ADH primary regulates ….. . also respond to …..

A

osmolarity

low blood volume states

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14
Q

ANP and BNP are released from ….. (and when)

A

from atria (ANP) and ventricle (BNP) in response to increased volume –> may act as a check of renin-angiotensin-aldosterone system

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15
Q

ANP and BNP - action

A
  1. relaxes vascular smooth muscle via cGMP –> increase GFR and decrease Renin
  2. Dilates afferent arteriole, constricts efferent arteriole and promote natriuresis
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16
Q

Juxtraglomerular apparatus consist of

A
  1. mesangial cells
  2. JG cells (modified SMCs of afferent arteriole)
  3. Macula densa (part of DCT)
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17
Q

Macula densa - function

A

NaCL sensor in DCT –> if low –> increase renin secretion –> efferent arteriole vasoconstriction –> Increases GFR

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18
Q

JGA maintain GFR via

A

renin-angiotensin-aldosterone system

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19
Q

β-blockers - BP

A

β-blockers can decrease BP by inhibiting β1 receptors of the Juxtraglomerular apparatus–>decrease renin release

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20
Q

hormones produce by kidney (which hormones are from where exactly)

A
  1. renin –> from Juxtraglomerular apparatus
  2. Erythropoietin –> from interstitial cells in peritubular capillary bed
  3. Prostagladins –> paracrine in afferent arterioles
  4. Calcitriol (1,25 OH2 vitamine D3 - active form) –> from PCT celsl
  5. Dopamine –> from PCT PCT cells
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21
Q

Erytrhopoietin is released by ….. in response to

A

interstitial cells in peritubular capillary bed in response to hypoxia

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22
Q

Erytrhopoietin - function

A

stimulates RBCs proliferation in bone marrow

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23
Q

Erytrhopoietin - clinica use as a drug

A

chronic kidney disease

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24
Q

kidney - Calcitriol

A

PCT cells convert 25-OH vitamin D3 to 1,25 (OH)2 vitamin D3 (calcitriol, active form) via PARATHORMONE ACTION (increases 1α-hydroxylase)

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25
Q

Kidney - prostagladins action and secretion

A

paracrine secretion vasodilates the afferent arterioles to increase RBF

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26
Q

effect of NSAID on renal function

A

NSAIDs inhibit prostagladins (that preferentially dilated afferent arteriole and increase RPF and GFR, not the FF)

  • -> constriction of afferent arteriole –> decrease of RPF and GFR, not the FF –> IN LOW RENAL BLOOD SATES
  • -> ACUTE RENAL FAILUE
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27
Q

Kidney - dopamine is secreted by

A

PCT cells

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28
Q

Kidney - dopamine action

A
  • Promotes natriuresis
  • at low doses –> dilates interlbular arteries, afferent arterioles and eferent arterioles –> increased RBF, little or no change in GFR
  • at higher doses –> acts as vasoconstrictor
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29
Q

ANP - net effect

A

Na+ loss and volume loss (increases GFR and Na filtration with no compensatory Na reabsorption)

30
Q

which hormone preserve renal function (GFR) in low-volume-states and how

A

Angiotensin II: 1. constricts efferent arteriole (Increases FF) 2. Na+ reabsorption in proximal and distal nephron)

31
Q

aldosterone - secreted in response to

A
  1. low blood volume (via ATII)

2. high K+ concentration

32
Q

aldosterone - effect on K+, Na+, H+

A

causes Na+ reabsorption, K+ secretion and H+ secretion

33
Q

ADH is secreted in response to

A
  1. High plasma osmolarity
  2. low blood volume
  3. angiotensin II action
34
Q

PTH is secreted in response to

A
  1. low plasma Ca2+
  2. high plasma PO4-
  3. low plasma 1,25-OH2 D3
35
Q

PTH generally causes in KIDNEY (and area)

A
  1. increase Ca2+ reabsorption in DCT
  2. decrease PO4- reabsorption in PCT
  3. Increases 1,25 OH2 D3 production in PCT (increases Ca2+ and PO4- absorption from gut via vitamin D)
36
Q

factors that shift K+ out of cells (causing hyperkalemia)

A
  1. digitalis (blocks Na+/K+ ATPase)
  2. Hyperosmolarity
  3. Cell lysis (crush injury, tumor lysis synsdrome, rhabdomyolysis)
  4. Acidosis
  5. β-blocker
  6. insulin deficiency
  7. exercise
37
Q

β-blocker shift K+ causes hyperkalemia - mechanism

A
  1. Beta blockers suppress catecholamine-stimulated renin release, thereby decreasing aldosterone synthesis.
  2. nonselective beta blockers decrease cellular uptake of potassium
38
Q

acidosis causes hyperkalemia - mechanism

A

exchange of extracellular H+ for intracellular K+

39
Q

hyperosmolarity causes hyperkalemia - mechanism

A

H20 flows out of the cell –> K+ diffuses out with H20

40
Q

Cell lysis causes hyperkalemia - examples (3)

A
  1. crush injury
  2. tumor lysis synsdrome
  3. rhabdomyolysis
41
Q

factors that shift K+ into cells (causing hypokalemia)

A
  1. hyposmolarity
  2. alkalosis
  3. β-adrenergic agonist (increase Na+/K+ ATPase)
  4. insulin (increase Na+/K+ ATPase)
42
Q

alkalosis causs hypokalemia - mechanism

A

exchange of intracellular H+ for extracellular K+

43
Q

insulin shifts K+ into cells - mechanism

A

increase Na+/K+ ATPase

44
Q

β-adrenergic agonist shifts K+ into cells - mechanism

A

increase Na+/K+ ATPase

45
Q

hypo-osmolarity shifts K+ into cell - mechanism

A

H2o flows into the cell, K+ diffuse with H20

46
Q

concentration of sodium, potasium, chloride, biocarbonate, magnesium, calcium, phosphorus

A
  1. Na+ –> 136-145 mEg/L
  2. CL- –> 95-105 mEq/L
  3. K+ –> 3.5-5 mEq/L
  4. HCO3- –> 22-28 mEq/L
  5. Mg2+ –> 1.5-2.5 mEq/L
  6. Ca2+ –> 8.4-10.2 mg/dL
  7. Pi –> 3-4.5 mg/dL
47
Q

high Na+ concentration - clinical manifestations

A
  1. irritability
  2. stupor
  3. coma
48
Q

low Na+ concentration - clinical manifestation

A
  1. nausea
  2. malaise
  3. stupor
  4. coma
  5. seizures
49
Q

high K+ concentration - clinical manifestations

A
  1. wide QRS and peaked T waves on ECG
  2. Arrhytmias
  3. muscle weakness
50
Q

low K+ concentration - clinical manifestation

A
  1. U waves and flattened T waves on ECG
  2. Arrhytmias
  3. muscle cramps
  4. spasms
  5. weakness
51
Q

high Ca2+ concentration - clinical manifestations

A
  1. renal stones
  2. Bone pain
  3. abdominal pain and constipation.
  4. urinary frequency
  5. anxiety, altered mental status
    NOT NECESSARILY CALCIURIA
52
Q

low Ca2+ concentration - clinical manifestation

A
  1. Tetatny
  2. seizures
  3. Proloned QT
  4. twitching (Chvostek sign)
  5. Spasm (Trousseau sign)
53
Q

high Mg2+ concentration - clinical manifestations

A
  1. low deep tendon reflexes
  2. lethargy
  3. Bradycardia
  4. Hypotension
  5. Cardiac arrest
  6. Hypocalcemia
54
Q

low Mg2+ concentration - clinical manifestation

A
  1. Tetany
  2. torsades de pointes
  3. hypokalemia
55
Q

high Po4- concentration - clinical manifestations

A
  1. Renal stones
  2. mestatic calcificationss
  3. Hypocalcemia
56
Q

low Po4- concentration - clinical manifestation

A
  1. Bone loss
  2. osteomalacia (adults)
  3. rickets (children)
57
Q

stupor vs coma according to definition

A

stupor: unresponsiveness from which a person can be aroused only by vigorous, physical stimulation
Coma: unresponsiveness from which a person cannot be aroused

58
Q

Electrolyte disturbances - ECG?

A
  1. U waves and flattened T waves in low K+
  2. wide QRS and peaked T waves in high K+
  3. torsades de pointes in low Mg2+
  4. QT prolongation in low Ca2+
  5. Bradycardia/cardiac arrest in high Mg2+
59
Q

Renin-secreting tumor - BP, renin, Aldosterone levels

A

BP: increased

renin: increased
aldosterone: increased

60
Q

Prmary hyperaldosteronism (Conn syndrome) - BP, renin, Aldosterone levels

A

BP: increased

renin: decreased
aldosterone: increased

61
Q

SIADH - BP, renin, Aldosterone - levels

A

BP: increased

renin: decreased
aldosterone: decreased

62
Q

Liddle syndrome - BP, renin, Aldosterone - levels

A

BP: increased

renin: decreased
aldosterone: decreased

63
Q

Bartter syndrome - BP, renin, Aldosterone - levels

A

BP: not affected

renin: increased
aldosterone: increased

64
Q

Gitelman syndrome - BP, renin, Aldosterone - levels

A

BP: not affected

renin: increased
aldosterone: increased

65
Q

Bartter syndrome vs Gitelman syndrome according serum Mg 2+ levels

A

Barrter –> low (but more characteristic in Gitelman)

Gitelman –> decreased

66
Q

Bartter syndrome vs Gitelman syndrome according urine Ca2+ levels

A

Barrter –> high

Gitelman –> low

67
Q

angiotensin Effect on heart rate

A

in addition to its pressor effect, ATII also affects baroreceptor function –> limits reflex bradycardia which would normally accompany its pressor effects

68
Q

Hypercalcemia causes frequent urination - mechanism

A

Excess calcium –> kidneys have to work harder to filter it out –> excessive thirst and frequent urination.

69
Q

Electrolyte disturbances - ECG?

A
  1. waves and flattened T waves in low K+
  2. wide QRS and peaked T waves in high K+
  3. torsades de pointes in high Mg2+
  4. QT prolongation in high Ca2+
70
Q

other electrical disturbances caused by Mg2+ level disturbances

A

low Mg –> hypokalemia

high Mg –> hypocalcemia

71
Q

Causes of hypomagnesemia

A
  1. diarrhea
  2. aminoglycosides
  3. diuretics
  4. alcohol abuse

Renal (15 decks)

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