Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Physiology 1 > Renal (4) > Flashcards

Renal (4) Flashcards

(99 cards)

Start Studying
1
Q

How does Kidney affect RBC

A

Produces Erythropoietin for RBC production in hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Types of Nephrons

A
  • Juxtamedullary Nephron
  • Cortical Nephron (90%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Renal Circulation Arteries

A

Renal A, Segmental A, Interlobar A, Arcuate A, Intralobular A, Afferent a, Glomerular cap, Efferent A, Peritubular cap, Vasa recta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Renal Circulation Veins

A

Venules, Intralobular v, Arcuate v, Interlobar v, Renal V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Renal Blood Flow

A

1200 - 1300 ml/min
(20 - 25% of CO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Renal Plasma Flow

A

600 - 700 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Natriuresis

A

When body excretes excess Na+ in Urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What determines Renal vascular resistance

A

Afferent & Efferent Arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why do we need to regulate BP to kidney

A

To protect Glomerular Capillaries from Overfiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

2 Autoregulatory Mechanisms to regulate RBF and GFR

A
  • Myogenic Mechanism (Bayliss)
  • Tubulo-glomerular Mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Myogenic Autoregulatory mechanism (Bayliss)

A

Tendency of smooth muscle to contract when stretched (AFFERENT ARTERIOLE ONLY)
(90 - 180 mmHg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Tubulo-glomerular Autoregulatory Mechanism

A

Feedback loop where change in GFR leads to alteration in conc. of NaCl in tubular fluid, sensed by macula densa sending signals to affect the Afferent arteriolar resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Adenosine A1 receptor

A
  • Gi
  • Less cAMP
  • Vasoconstriction in Afferent arteriole
    (inh. of granular cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Adenosine A2 receptor

A
  • Gs
  • More cAMP
  • Cardiac/Skeletal m
  • Vasodilator
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Granular cells

A

Synthesize, store, and release Renin into bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Renin Production vs GFR

A
  • High GFR: Inh. Renin production
  • Low GFR: Renin angiotensin cascade leads to Efferent art. vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens when ECFV drops

A

Sympathetic nerves release NE and dopamine and E by adrenal Medulla
- NE/E act on a1-AR (Gq) = VC in Afferent art.
- NE/E act on B1-AR on granular cells (Gs)
- Renin-Ang cascade activated, ANGII, VC in Efferent art.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Angiotensin II

A

Constricts Afferent and Efferent arterioles
(Efferent more sensitive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ANP

A
  • VD in Afferent art.
  • VC in Efferent art.
  • Increased GFR and same RBF (since VC and VD act together)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Glomerular Filtration Rate (GFR)

A

120 ml/min
(180 L/day)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Filtration Fraction (FF)

A

20%
Ratio of plasma filtered to total plasma flowing through glomerulus
FF = GFR / RPF = 120/600

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Glomerular capillary Pressure vs normal capillaries

A

Twice as much Pressure in Glomerular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Filtration Barrier

A

1) Fenestrated Endothelium
2) Basement Membrane
3) Podocytes
(repel negative charges)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

General Filtration Rule

A

The larger and more negative a molecule is, the less likely it will pass the filtration barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Renal Clearance
Volume of plasma / time From which all given substances pass through the filtrate and are excreted in the urine (ml/min)
26
How to determine Amount excreted in Urine?
Filtered - Reabsorbed + Secreted
27
Albumin fate
Not filtered
28
Fate of different substances in Kidney
- Not filtered (albumin) - Filtered & Completely reabsorbed (glucose) - Filtrated and Completely secreted (PAH) - Filtrated and not Reabsorbed, Secreted, or metabolized by Kidney. (creatine)
29
What can give us an Idea of GFR
Blood creatine levels since it is filtrated and not reabsorbed or secreted, all goes into urine. So higher creatine means lower GFR
30
Proximal Tubule structure
- Brush border - Highly invaginated BL membrane with mitochondria for active T
31
Cells in Collecting Duct
- Principal cells - Intercalated cells
32
Principal Cells (collecting duct)
- Moderately invaginated BL membrane with few mitochondria - Important for reabsorption of NaCl and K+
33
Intercalated Cells (collecting duct)
- High mitochondria density - Important for Acid-Base balance - Some secrete H+ (a) and some HCO3- (B)
34
Formation of Urine 3 Processes
1) Ultrafiltration 2) Reabsorption 3) Secretion
35
What drives Ultrafiltration
Starling forces (Hydrostatic & Oncotic pressures of Capillaries and Interstitial fluid)
36
Hydrostatic vs Oncotic Pressures
- Hydrostatic drives fluid/substance OUT - Oncotic pressure KEEPS fluid
37
Hydrostatic Pressure in Capillaries
- Afferent: + 53 mmHg - Efferent: + 51 mmHg
38
Oncotic Pressure in Capillaries
- Afferent: - 26 mmHg - Efferent: - 33 mmHg
39
Hydrostatic Pressure in Bowman's
- Afferent: - 12 mmHg - Efferent: - 12 mmHg
40
Oncotic Pressure in Bowman's
- Afferent: 0 mmHg - Efferent: 0 mmHg
41
NET ultrafiltration Pressure
- Afferent: 15 mmHg - Efferent: 6 mmHg
42
Proximal Tubule functions
- 60-70% of Na reabsorption - Any protein/albumin filtered reabsorbed - Any osmotically active substances reabsorbed are followed by water to prevent a gradient
43
First half of Proximal Tubule
- Na is primarily reabsorbed with HCO3 (a.a, gluc, Pi) - Only 20% of Na reabsorbed
44
Second half of Proximal Tubule
- High Cl- conc due to first half taking other substances - other 40% of Na absorbed here
45
Ways to reduce Na and Water reabsorption in Proximal Tubule
- Acetazolamide: Inhibits carbonic anhydrase (no Na/HCO3) - Hg-containing compounds: Aquaporin inh. - Non-reabsorbing osmolarities: excessive gluc, ketone, cause water drawn back to tubules
46
Loop of Henle
- 20-25% NaCl absorption - Only passive transport in thin ascending/descending limbs - TAL has active transport
47
Thin Descending limb (LOH)
- Passive transport of Water via Aquaporin 1, poorly to NaCl - Water reabsorption without solutes leaves tube hyperosmotic - At the end of the TDL osm. goes from 300mosm to 1200 mosm.
48
Thin Ascending Limb (LOH)
- Passive Transport - Impermeable to water (no aq1) - Permeable to NaCl and Urea leaving tube hyposmotic
49
Thick Ascending Limb TAL (LOH)
- Active transport and reabsorption of osmolytes NKCC - No water reabsorption (no aq1)
50
What inhibits the NKCC transporter in TAL
Furosemide
51
Distal Convoluted tubule
- 5-7% of NaCl reabsorption - Na/Cl Cotransporter - No water reabsorption
52
What inhibits Na/Cl transporter in Distal convoluted tubule
Thiazide
53
Collecting ducts
- eNaCs drive Na into cells - Negative luminal potential created - Drives Cl absorption paracellularly - Luminal K+ channels to balance charge
54
What affects eNaCs
- Aldosterone: Increases expression/activity to raise BP - ANP: Inhibits eNaC causing Natriuresis (lower BP) - Amiloride: inhibits eNaC, no effect on K+
55
Water reabsorption overview
- Water absorbed from PT to end of TDL - Water IMPERMEABLE from thin descending limb to distal convoluted tubule - Water reabsorption from collecting duct to medullary collecting duct in presence of ADH
56
Vasopressin (ADH) action
1) Binds basolateral Gs coupled V2-R 2) cAMP to PKA 3) Vesicle release of AQ2 on luminal side 4) More water reabsorption
57
Where is Urea reabsorbed?
Inner medullary collecting ducts
58
Overall K+ transport
- PT: Paracellular K+ reabsorption - TAL: K+ reabsorption via NKCC - CD: K+ Secretion and Na reabsorption Na/K atpase and ROMK
59
Overall Ca2+ transport
- PT: Paracellular reab. with Na+ - TAL: Paracellular reab. with Na+ - DCT: Active transcellular reabsorp. (PTH stim.)
60
What helps recover/reabsorb filtered proteins
Megalin & Cubulin (endocytosis)
61
Countercurrent Multiplication
Active Process to generate an osmotic gradient to enable water reabsorption from filtrate & to concentrate urine
62
Countercurrent Exchange
- Happens between Vasa recta and interstitium - Passive process - Maintains a gradient, doesnt create it
63
Urea recycling
- When water absorption is increased by ADH/Vasopressin - More water & Urea reabsorbed - Water in Outer medullary duct - Urea in Inner medullary duct only to form gradient for countercurrent multiplication
64
Effective Arterial Blood Volume (EABV)
Portion of the ECF contained in the arteries and perfusing the tissues that is sensed by the Kidneys and is regulated by changes in Na+ excretion
65
4 Mechanisms that affect Na+ excretion due to EABV
- Sympathetic inn. - ANP - Peritubular capillary starling forces - Renin-ANG-Aldosterone system
66
K+ overall movement
- Proximal tubule reabsorption (2/3) - TAL by NKCC (20%) - DCT principal secrete under high K+ - DCT a-intercallated cells reabsorb K using K/H atpase
67
Aldosterone effect on K+
Increase K+ secretion in DT and CD - Increased eNaC expression - Increased Na/K atpase quantity - Increase of luminal ROMK
68
How do diuretics mostly affect K+
Increase K+ to drive secretion
69
How to ensure Aldosterone specificity in Kidney
11B-OHSDH to convert gluco and mineralocorticoids to inactive form to allow Aldosterone to only bind MC-R
70
What happens when Hyperosmotic activity is detected
Thirst is triggered by Osmoreceptor cells in Hypothalamus and Baroreceptors
71
How do we prevent Overhydration after thirst?
Peripheral osmoreceptors in GI and stomach and mouth stop thirst
72
Osmoreceptor responce in high Plasma effective osmolarity
- Signal to Supraoptic & Paraventricular nuclei - Vasopressin secretion
73
Amount of Non-volatile acid produced per day
- 30 mmol/day Dietary - 40 mmol/day Metabolism = 70 mmol/day total which can not be exhaled
74
How does the Kidney combat non-volatile acids
- Produces 70mmol of HCO3- to buffer - 30 mmol buffered to H2CO3 then CO2 and exhaled - 40 mmol is trapped by NH3 to NH4+ and excreted in Urine
75
pH
7.35 - 7.45
76
paCO2
38 - 40 mmHg
77
Standard HCO3-
23 - 25 mmol/L (= to actual in normal acid-base balance)
78
Base Buffer (BB) and its use
44 - 49 mEq/L - Indicates buffering capacity: How many proton molecules can be buffered in the blood
79
Base Excess (BE) and its use
+/- 2.5 mEq/L - Shows difference/deviation from the normal value
80
Volatile acids
Acids that can be converted into gaseous form and thus be eliminated by the Lungs (mainly CO2)
81
Nonvolatile (fixed) acids
Acid produced from sources other than CO2 and not excreted by the Lungs
82
How are nonvolatile acids formed?
- Amino acids with Sulfur (sulfuric acid) - Phospholipids (phosphoric acid)
83
Buffers
A solution which resists change in pH when a small amount of acid/base is added (weak a/b with its conjugate a/b)
84
Open system
System where buffers can quickly be altered (CO2 buffer - HCO3/H2CO3)
85
Role of Proteins as Buffers
They can be Protonated/Deprotonated - Usually bound to Ca2+ but in acidic conditions H+ can bind instead
86
What is most important buffer in body
CO2/HCO3
87
Why does CSF only use 1 type of buffer
No proteins in CSF so only HCO3 buffer can be used
88
Respiratory Acidosis
- High pCO2 - No change in BB / BE - Unchanged Standard HCO3- - Increased Actual HCO3-
89
Respiratory Alkalosis
- Low pCO2 - No change in BB / BE - Unchanged Standard HCO3- - Lower HCO3-
90
Metabolic Acidosis
- No change in pCO2 - Lower BB / BE - Lower Standard HCO3- - Lower Actual HCO3-
91
Metabolic Alkalosis
- No change in pCO2 - Higher BB / BE - Higher Standard HCO3- - Higher Actual HCO3-
92
Mixed Type Acidosis
- High pCO2 - Low BB / BE - Lower Standard HCO3- - complex Actual HCO3-
93
Anion gap
- The difference between measured Cations and measured Anions in the plasma - Used to diagnose metabolic acidosis = 8 - 16 mEq/L (normal) Na - (Cl + HCO3)
94
High anion gap
- Lower HCO3 - Means there is unmeasured anions / new acid appearance
95
Calcium Levels in High/Low pH
- Low: More free Ca - High: Less free Ca (Albumin loses H+ and binds more Ca)
96
Potassium Levels in High/Low pH
- Low: High (ROMK inh. so less excreted) - High: Low
97
How to calculate NAE
Titratable acidity (H bound to urinary buffers like phosphate) + NH4 excretion - HCO3 excreted
98
Renal Buffers capacities
- Phosphate buffer: 18 mmol - Criatinine buffer: 5.5 mmol = Total 23.5 mmol out of 70 mmol
99
How does Kidney make NEW HCO3-
- From Glutamine via Glutaminase - yields NH4+ and HCO3- - NH4+ broken to NH3 + H+ - NH3 diffuses into tubule - H+ taken out by Na/H exchanger

Physiology 1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions