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Histology > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

movement of particles across membranes is driven by this

A

gradients

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2
Q

Lipid bilayer prevents movement of what two kinds of molecules

A 
charged (Na+, K+, Mg++, Ca++)
Polar molecules (glucose)
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3
Q

Lipid bilayer allows crossing of what two kinds of molecules

A 
Lipid soluble (antidiuretic, aldosterone)
Small polar (H2O
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4
Q

Diffusion

A

movement of particles from high to low passively across the membrane without a transporter

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5
Q

Facilitated diffusion

A

“money maker”
moves particles from low to high across the membrane with a transporter
particles cannot cross without the transporter

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6
Q

two factors affect the rate of diffusion and facilitated diffusion

A

size of the gradient (larger = faster)

permeability of the membrane to the solute (more permeable/more pores = faster)

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7
Q

active transport

A 
movement from low to high concentration, against electrochemical gradient
requires ATP (converted to ADP by hydrolysis)
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8
Q

secondary active transport

A

movement from low to high concentration, against electrochemical gradient
requires potential energy generated by an active transporter

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9
Q

symport

A

cotransport in the same direction

facilitated by symporter

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10
Q

antiport

A

cotransport in opposite directions

facilitated by antiporter

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11
Q

osmosis

A

movement across a selectively permeable membrane

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12
Q

effective osmole

A

molecule will not cross the membrane, creates a concentration gradient

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13
Q

ineffective osmole

A

molecule will cross the membrane and will not create a concentration gradient

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14
Q

osmolarity

A

concentration of osmotically active things in a solution

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15
Q

Tonicity

A

concentration of effective osmoles (things that cause osmosis)

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16
Q

three types of tonicity

A

hypotonic: low effective osmolarity
hypertonic: high effective osmolarity
isotonic: same effective osmolarity

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17
Q

Gross morphology from exterior to interior

A

capsule, cortex, medulla, pyramid (base, apex, papillae), renal pelvis, hilus

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18
Q

contents of the nephron in the cortex

A

Renal corpuscle, proximal convoluted tubule, proximal straight tubule, some distal straight and distal convoluted

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19
Q

contents of the nephron in the medulla

A

loop of Henle, collecting ducts, some distal straight and distal convoluted tubule

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20
Q

what structures make up the renal corpuscle

A

afferent arteriole, macula densa, glomerulus (podocytes and pedicles), Bowman’s capsule, efferent arteriole

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21
Q

features of the efferent arteriole that increases the blood pressure in the glomerulus

A

small diameter, less stretchy

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22
Q

what components of podocytes/pedicles contribute to filtration apparatus in the glomerulus

A

walls of capillary, basement membrane (lamina rara interna, lamina densa, lamina rara externa), slit diaphragm

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23
Q

components of the proximal tubule that differentiate it’s function

A

microvili and apical canaliculi (increases surface area for absortpion)
lots of mitochondria (uses lots of ATP)

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24
Q

loop of Henle absorption

A

descending limb: H2O and Na/Cl

ascending limb: Na/Cl only

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25
Q

hormone that enables distal part of distal tubule to be permeable to water

A

antidiuretic hormone

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26
Q

three parts of juxtaglomerular apparatus and theyre function

A

macula densa: direct contact with the filtrate

extraglomerular: recieve info from macula densa
juxtaglomerular: secrete renin, angiotensin converting enzymes and angiotensin 1&2

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27
Q

principal cells function and location

A

reabsorption, cortical collecting tubule, inner&outer medullary collecting tubule, papillary collecting tubules

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28
Q

intercalated cells function and location

A

secretion (H, HCO3), cortical collecting tubule, outer medullary collecting tubule

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29
Q

glomerular filtration barriers

A

size: pores with different sizes to exclude large molecules
Charge: negatively (anionic) charged proteins in the glycocalyx

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30
Q

starling’s forces out of the capillary

A

capillary hydrostatic pressure (Pc) and Bowman’s space oncotic pressure (πbs)

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31
Q

starling’s forces into the capillary

A

bowmans space hydrostatic pressure (Pbs) and Capillary oncotic pressure (πc)

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32
Q

constricting/relaxing afferent and efferent arterioles affect on GFR

A

constrict: decrease GFR, decrease Pc
relax: increase GFR, increase Pc

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33
Q

heartworm and lyme disease affect on GFR

A

produces antigens that get stuck in the glomerulus

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34
Q

plasma protein changes affect on GFR

A

affects πc
increase protein: decrease GFR
decrease protein: increase GFR

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35
Q

obstructions in urinary system affect on GFR

A

affects Pbs
increase Pbs: decrease GFR
decrease Pbs: increase GFR

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36
Q

autoregulation

A

the range of blood pressures where the kidney is able to maintain filtration rate independent of systemic blood flow

37
Q

myogenic autoregulation

A

preventative autoregulation

vasoconstriction (at high blood pressure) and vasodilation (at low blood pressure) in the afferent arteriole

38
Q

tubuloglomerular feedback

A

regulatory autoregulation by sensing ultrafiltrate ionic constituents, signaling parts of juxtaglomerular aparatus and stimulating autoregulation

39
Q

NKCC2

A

part of macula densa cells, senses Na, K, Cl concentration in ultrafiltrate

40
Q

release of ATP/adenosine in tubuloglomerular feedback, where and what it does

A

released from macula densa, activates extraglomerular mesangial cell receptors

41
Q

extraglomerular mesengial cell function in tubuloglomerular feedback

A

receives ATP/adenosine signal from macula densa
increases Ca to contract afferent arteriole
inhibits release of renin from juxtaglomerular cells

42
Q

angiotensinogen

A

produced in liver, interacts with renin to become angiotensin 1

43
Q

angiotensin 1

A

interacts with angiotensin converting enzyme in the lung, becomes angiotensin 2

44
Q

functions of angiotensin 2 in high blood pressure

A

systemic arteriolar vasoconstriction (increases blood pressure)
stimulates antidiuretic secretion and thirst
increases tubular uptake of NaCl

45
Q

functions of angiotensin 2 in low blood pressure

A

systemic vasoconstriction (especially on efferent arteriole)
increases PGE2 release from macula densa
stops renin release

46
Q

release of PGE2 during low blood pressure juxtaglomerular feedback

A

released by macula densa
stimulates afferent arteriole vasodilation
stimulates juxtaglomerular to release renin - increases angiotensin 2

47
Q

3 important facts about the Na/K ATPase

A

3Na out for 2K in
requires ATP
maintains the electrochemical gradient (with low intracellular Na)

48
Q

things the proximal tubule reabsorbs

A

water, Na, solutes, glucose, amino acids, bicarb

49
Q

things the proximal tubule secretes into tubular fluid

A

H, anions

50
Q

ways Cl is absorbed

A 
Cl/anion antiporter (with electrochemical gradient)
Paracellular diffusion (will bring Na across too)
51
Q

protein reabsorption

A

occurs in proximal tubule

partially degraded on luminal membrane, fully degraded by lysosomes, amino acids absorbed on basolateral membrane

52
Q

Loop of Henle ascending limb reabsorption

A

NaCl (25%)

passive

53
Q

Loop of Henle descending limb reabsorption

A

H2O (15%)

passive

54
Q

NKCC1 symporter

A

brings Na, K, 2Cl into the cell

K is against concentration gradient

55
Q

loop diuretics

A

inhibit the work of the NKCC1 symporter

56
Q

thiazide diuretics

A

inhibit the work of the Na/Cl symporter

57
Q

antidiuretic hormone affect on distal tubule

A

enables water reabsorption, the cells are otherwise impermeable to water

58
Q

Principal cells in collecting ducts reabsorb what

A

NaCl and H2O if antidiuretic hormone is present

59
Q

channels in principal cells are sensitive to what

A

Na channels: amiloride

aquaporins: antidiuretic hormone

60
Q

Principal cell K homeostasis

A

K leaves down gradient into tubular fluid and interstium via passive channels

61
Q

purpose of intercalated cells and active enzyme

A

maintain acid base balance

carbonic anhydrase

62
Q

concurrent multiplication

A

two factors create the idea environment for the reabsorption of Na and H2O in the loop of henle

63
Q

descending limb concurrent multiplication

A

permeable to H2O, moves passively out because Na osmolarity is higher in interstitium as the loop descends

64
Q

hairpin loop concurrent multiplication

A

tubular fluid osmolarity = interstitium osmolarity BUT Na is more concentrated in tubular fluid

65
Q

Ascending loop concurrent multiplication

A

Na passively moves out by the concentration gradient until the distal tubule

66
Q

distal tubule role in concurrent multiplication

A

active transport of Na into interstitium, creates osmolarity for H2O to leave the tubular fluid

67
Q

antidiuretic hormone function

A

regulate water conservation
no/low is water expelled in the kidney
high is conserved water (reabsorbed into the blood)

68
Q

antidiuretic hormone stimulus and location

A

Released from anterior pituitary
release stimulated by high extracellular osmolarity (osmoreceptors in hypothalamus)
release stimulated by low extracellular volume (baroreceptors in coronary sinus and aorta)

69
Q

antidiuretic hormone function on urea

A

high concentration stimulates medullary collecting duct permeability, allowing urea into interstitial fluid

70
Q

urea function on reabsorbtion

A

effective osmole in tubular fluid in loop of Henle (helps absorb H2O in the descending limb)
ineffective osmole in collecting duct

71
Q

Vasa recta

A

hairpin loop of capillaries throughout the kidney

72
Q

Vasa recta goal

A

removes water from interstitium back into circulation
keeps Na in interstitium
works because there are no permeability differences in the capillary

73
Q

determinant of extracellular osmolarity

A

concentration of Na in extracellular fluid

74
Q

determinant of extracellular volume

A

amount of sodium in extracellular fluid

75
Q

hypernatremia and signs

A

high osmolarity of Na in extracellular fluid
water moves out of cells
cerebral vessel hemorrhage, muscle weakness, neurological signs, coma

76
Q

hyponatremia and signs

A

low osmolarity of extracellular fluid
water moves into cells
cerebral and pulmonary edema, muscle weakness, incoordination, seizures

77
Q

osmoreceptors

A

senses ECF osmolarity
High ECF osmolarity increases ADH, increases thirst
decreases Na in blood

78
Q

hypervolemia and signs

A

increased extracellular volume, ascites and pulmonary edema

79
Q

hypovolemia and signs

A

decreased volume, organ damage (from O2 depletion) low blood pressure, tachycardia

80
Q

baroreceptors

A

senses ECF volume
High releases natriuretic peptide, stops ADH, decreases blood volume
Low stimulates ADH and sympathetic nervous system, increases blood volume

81
Q

Juxtaglomerular appartus role in ECF volume

A

senses low ECF and stimulates renin-angeotensin system

82
Q

sympathetic flow

A

increases Na and H2O reabsorption, increasing ECF volume
releases norepinephrine
stimulates transporters in proximal tubule
stimulates renin release

83
Q

norepinephrine

A

vasoconstrictor, increases glomerular filtration rate

increases Starling’s forces on Na reabsorption at peritubular capillaries

84
Q

Starling’s forces changes because of decreased ECF

A

higher tubular hydrostatic force (because higher golmerular filtration rate) pushes fluid out of tubules
Capillary hydrostatic pressure decreases, capillary oncotic pressure increases - both cause Na and H2O to be reabsorbed into the capillary

85
Q

Angiotensin II effect on low ECF

A 
Increases Na/H2O uptake into capillary
Constricts efferent arterioles
stimulates Na/H antiporter in proximal and distal tubules
Stimulates ADH release
Stimulates aldosteron
86
Q

Aldosterone

A

increases Na uptake
increases Na/K ATPase
increases NKCC1
increases permeability of Na channels in collecting duct

87
Q

Natriuretic peptides goal

A

responds to hypervolemia

promotes Na excretion, reduces H2O reabsorption, decreases ECF

88
Q

Natriuretic peptide function

A

constricts efferent arteriole, dilates afferent arteriole
inhibits renin-angiotensin system (renin, ADH, Aldosterone)
inhibits Na channels - NaCl reabsorption in collecting ducts

Histology (2 decks)

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