Renal hormones Flashcards
(71 cards)
1
Q
Angiotensin II activation axon
A
Angiotensinogen (liver) + Renin –> Angiotensin I
Angiotensin I + ACE (lungs and kidney)–> angiotensin II
2
Q
renin is secreted by
A
juxtaglomerular kidney cells
3
Q
renin secretion is triggered by
A
- low Blood pressure (JG cells)
- low Na+ delivery (macula densa cells - distal convoluted tubule)
- increased sympathetic tone (β1-receptors)
4
Q
increased sympathetic tumors increase Renin secretion via ….. receptors
A
β1
5
Q
Angiotensin-converting enzyme - location
A
capillaries of the lungs but can also be found in endothelial and kidney epithelial cells
6
Q
beside its action in angiotensin-aldosteron axons, ACE also
A
causes Bradykinin breakdown
7
Q
Angiotensin II action
A
- acts at angiotensin II receptor (type 1-AT1) on vascular SMC –> vasoconstriction –> increases BP
- constricts EFFERENT arteriole of glomerus –> increases Filtration fraction to preserve GFR in low volumes states (eg. when low RBF)
- 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
- ADH posterior pituitary –> increases aquaporin insertion in principal cells –> H2O reabsorption
- increases PCT Na/H+ exchanger activity –> Na+, HCO3- and H2O reabsorption –> permit contraction alkalosis
- Stimulates hypothalamus –> thirst
8
Q
angiotensin action on vessels
A
- acts at angiotensin II receptor (type 1-AT1) on vascular SMC –> vasoconstriction –> increases BP
- constricts EFFERENT arteriole of glomerus –> increases Filtration fraction to preserve GFR in low volumes states (eg. when low RBF)
9
Q
angiotensin action on CNS
A
- ADH posterior pituitary –> increases aquaporin insertion in principal cells –> H2O reabsorption
- Stimulates hypothalamus –> thirst
10
Q
angiotensin action on PCT
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Na/H+ exchanger activity –> Na+, HCO3- and H2O reabsorption –> permit contraction alkalosis
11
Q
angiotensin action on adrenal gland
A
activates aldosterone syntase (zona glomerulosa) –> Aldosterone secretion
12
Q
in addition to its pressor effect, ATII also
A
affects baroreceptor function –> limits reflex bradycardia which would normally accompany its pressor effects
13
Q
ADH primary regulates ….. . also respond to …..
A
osmolarity
low blood volume states
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
15
Q
ANP and BNP - action
A
- relaxes vascular smooth muscle via cGMP –> increase GFR and decrease Renin
- Dilates afferent arteriole, constricts efferent arteriole and promote natriuresis
16
Q
Juxtraglomerular apparatus consist of
A
- mesangial cells
- JG cells (modified SMCs of afferent arteriole)
- Macula densa (part of DCT)
17
Q
Macula densa - function
A
NaCL sensor in DCT –> if low –> increase renin secretion –> efferent arteriole vasoconstriction –> Increases GFR
18
Q
JGA maintain GFR via
A
renin-angiotensin-aldosterone system
19
Q
β-blockers - BP
A
β-blockers can decrease BP by inhibiting β1 receptors of the Juxtraglomerular apparatus–>decrease renin release
20
Q
hormones produce by kidney (which hormones are from where exactly)
A
- renin –> from Juxtraglomerular apparatus
- Erythropoietin –> from interstitial cells in peritubular capillary bed
- Prostagladins –> paracrine in afferent arterioles
- Calcitriol (1,25 OH2 vitamine D3 - active form) –> from PCT celsl
- Dopamine –> from PCT PCT cells
21
Q
Erytrhopoietin is released by ….. in response to
A
interstitial cells in peritubular capillary bed in response to hypoxia
22
Q
Erytrhopoietin - function
A
stimulates RBCs proliferation in bone marrow
23
Q
Erytrhopoietin - clinica use as a drug
A
chronic kidney disease
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)
25
Kidney - prostagladins action and secretion
paracrine secretion vasodilates the afferent arterioles to increase RBF
26
effect of NSAID on renal function
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
27
Kidney - dopamine is secreted by
PCT cells
28
Kidney - dopamine action
- 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
29
ANP - net effect
Na+ loss and volume loss (increases GFR and Na filtration with no compensatory Na reabsorption)
30
which hormone preserve renal function (GFR) in low-volume-states and how
Angiotensin II: 1. constricts efferent arteriole (Increases FF) 2. Na+ reabsorption in proximal and distal nephron)
31
aldosterone - secreted in response to
1. low blood volume (via ATII)
| 2. high K+ concentration
32
aldosterone - effect on K+, Na+, H+
causes Na+ reabsorption, K+ secretion and H+ secretion
33
ADH is secreted in response to
1. High plasma osmolarity
2. low blood volume
3. angiotensin II action
34
PTH is secreted in response to
1. low plasma Ca2+
2. high plasma PO4-
3. low plasma 1,25-OH2 D3
35
PTH generally causes in KIDNEY (and area)
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
factors that shift K+ out of cells (causing hyperkalemia)
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
β-blocker shift K+ causes hyperkalemia - mechanism
1. Beta blockers suppress catecholamine-stimulated renin release, thereby decreasing aldosterone synthesis.
2. nonselective beta blockers decrease cellular uptake of potassium
38
acidosis causes hyperkalemia - mechanism
exchange of extracellular H+ for intracellular K+
39
hyperosmolarity causes hyperkalemia - mechanism
H20 flows out of the cell --> K+ diffuses out with H20
40
Cell lysis causes hyperkalemia - examples (3)
1. crush injury
2. tumor lysis synsdrome
3. rhabdomyolysis
41
factors that shift K+ into cells (causing hypokalemia)
1. hyposmolarity
2. alkalosis
3. β-adrenergic agonist (increase Na+/K+ ATPase)
4. insulin (increase Na+/K+ ATPase)
42
alkalosis causs hypokalemia - mechanism
exchange of intracellular H+ for extracellular K+
43
insulin shifts K+ into cells - mechanism
increase Na+/K+ ATPase
44
β-adrenergic agonist shifts K+ into cells - mechanism
increase Na+/K+ ATPase
45
hypo-osmolarity shifts K+ into cell - mechanism
H2o flows into the cell, K+ diffuse with H20
46
concentration of sodium, potasium, chloride, biocarbonate, magnesium, calcium, phosphorus
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
high Na+ concentration - clinical manifestations
1. irritability
2. stupor
3. coma
48
low Na+ concentration - clinical manifestation
1. nausea
2. malaise
3. stupor
4. coma
5. seizures
49
high K+ concentration - clinical manifestations
1. wide QRS and peaked T waves on ECG
2. Arrhytmias
3. muscle weakness
50
low K+ concentration - clinical manifestation
1. U waves and flattened T waves on ECG
2. Arrhytmias
3. muscle cramps
4. spasms
5. weakness
51
high Ca2+ concentration - clinical manifestations
1. renal stones
2. Bone pain
3. abdominal pain and constipation.
4. urinary frequency
5. anxiety, altered mental status
NOT NECESSARILY CALCIURIA
52
low Ca2+ concentration - clinical manifestation
1. Tetatny
2. seizures
3. Proloned QT
4. twitching (Chvostek sign)
5. Spasm (Trousseau sign)
53
high Mg2+ concentration - clinical manifestations
1. low deep tendon reflexes
2. lethargy
3. Bradycardia
4. Hypotension
5. Cardiac arrest
6. Hypocalcemia
54
low Mg2+ concentration - clinical manifestation
1. Tetany
2. torsades de pointes
3. hypokalemia
55
high Po4- concentration - clinical manifestations
1. Renal stones
2. mestatic calcificationss
3. Hypocalcemia
56
low Po4- concentration - clinical manifestation
1. Bone loss
2. osteomalacia (adults)
3. rickets (children)
57
stupor vs coma according to definition
stupor: unresponsiveness from which a person can be aroused only by vigorous, physical stimulation
Coma: unresponsiveness from which a person cannot be aroused
58
Electrolyte disturbances - ECG?
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
Renin-secreting tumor - BP, renin, Aldosterone levels
BP: increased
renin: increased
aldosterone: increased
60
Prmary hyperaldosteronism (Conn syndrome) - BP, renin, Aldosterone levels
BP: increased
renin: decreased
aldosterone: increased
61
SIADH - BP, renin, Aldosterone - levels
BP: increased
renin: decreased
aldosterone: decreased
62
Liddle syndrome - BP, renin, Aldosterone - levels
BP: increased
renin: decreased
aldosterone: decreased
63
Bartter syndrome - BP, renin, Aldosterone - levels
BP: not affected
renin: increased
aldosterone: increased
64
Gitelman syndrome - BP, renin, Aldosterone - levels
BP: not affected
renin: increased
aldosterone: increased
65
Bartter syndrome vs Gitelman syndrome according serum Mg 2+ levels
Barrter --> low (but more characteristic in Gitelman)
| Gitelman --> decreased
66
Bartter syndrome vs Gitelman syndrome according urine Ca2+ levels
Barrter --> high
| Gitelman --> low
67
angiotensin Effect on heart rate
in addition to its pressor effect, ATII also affects baroreceptor function --> limits reflex bradycardia which would normally accompany its pressor effects
68
Hypercalcemia causes frequent urination - mechanism
Excess calcium --> kidneys have to work harder to filter it out --> excessive thirst and frequent urination.
69
Electrolyte disturbances - ECG?
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
other electrical disturbances caused by Mg2+ level disturbances
low Mg --> hypokalemia
| high Mg --> hypocalcemia
71
Causes of hypomagnesemia
1. diarrhea
2. aminoglycosides
3. diuretics
4. alcohol abuse
