Kidney Flashcards

1
Q

Hyponatremia

A

plasma sodium is low due to:

  1. dehydration - loss of NaCl (diarrhea, vomiting, diuretics
  2. overhydration - over retention of water - high ADH
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2
Q

Hypernatremia

A

plasma sodium is high due to:

  1. dehydration - H2O loss (excessive sweating, low ADH) production/sensitivity
  2. overhydration - excess NaCl (high aldosterone secretion)
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3
Q

edema

A
  1. intracellular - due to hyponatremia, metabolic depression, lack of adequate nutrition
  2. extracellular - due to fluid leakage, lymphatic failure (Lymphedema)
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4
Q

2 capillary beds (separated by efferent arterioles)

A

Glomerular capillaries

Peritubular capillaries

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5
Q

Blood flow in the capillaries

A

glomerular - high hydrostatic pressure(60 mmHg) causes rapid fluid filtration
peritubular - lower hydrostatic pressure (13mmHg) allows for rapid fluid reabsorption

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6
Q

path of fluid filtration from glomerular capillaries

A

Bowmans capsule -> proximal tubule -> loop of Henle -> distal tubule -> connecting tubule -> collecting duct -> renal pelvis

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7
Q

2 structural types of nephron

A

cortical - short LOH, 70-80% of the nephrons

juxtamedullary - long LOH 20-30% of nephs surrounded by peritubular capillaries called vasa recta

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8
Q

urinary bladder innervation

A
  1. pudendal nerves - somatic - innervate the external bladder sphincter
  2. sympathetic - thru hypogastric nerves (L2) - stimulate blood supply to the bladder
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9
Q

Urine flow

A

Nephron -> collecting ducts -> renal calyces -> ureters -> bladder

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10
Q

contraction of ureters

A
  1. parasympathetic - increase

2. sympathetic - decrease

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11
Q

micturition reflex

A

sensory stretch receptors are initiated as the bladder fills with urine

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12
Q

as micturition reflex increases

A

reflex passes thru the pudendal nerves to the external sphincter, relaxation happens, then urination occurs

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13
Q

voluntary urination

A

contraction of abdominal muscles
increase pressure in the bladder
increase urine that enters the bladder neck
empties mos of the urine from the bladder

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14
Q

nephrotic syndrome

A

caused by different disorders that damage the kidneys

all result in release of excess protein in the urine

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15
Q

symptoms of nephrotic syndrome

A
  1. protein in urine - mostly albumin - foamy urine

2. edema - facial, arms, legs, abdominal swelling

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16
Q

Cystitis

A

UTI - inflammation of the bladder caused by bacterial infection

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17
Q

Symptoms of cystitis

A
  1. persistent urge to urinate
  2. burning sensation when urinating
  3. pelvic discomfort
  4. lower abdominal pressure
  5. cloudy or bloody urine can have strong odor
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18
Q

pyelonephritis

A

acute infection of the renal pelvis or parenchyma usually due to an ascending infection (UTI)

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19
Q

symptoms of pyelonephritis

A

chills, fever, nausea, vomiting, unilateral or bilateral loin pain that can radiate to suprapubic region, children and elderly may be asymptomatic other than mental confusion

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20
Q

nephrolithiasis

A

kidney stones caused by:

  1. imbalance of water
  2. predisposition due to genetics
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21
Q

symptoms of nephrolithiasis

A

flank pain, blood in urine

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22
Q

polycystic kidney disease (PKD)

A

genetic disorder that causes the formation and enlargement of cysts in the kidneys

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23
Q

symptoms of PKD

A

blood in urine, abdominal pain, kidney stones, high blood pressure, frequent UTI, liver and pancreatic systs

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24
Q

how are glomerular capillary different from others in the body

A

3 layers instead of 2;

  1. endothelium - thousands of small holes (fenestrae), negatively charged - prevents passage of plasma proteins
  2. basement membrane - meshwork of proteoglycan fibrillae and collagen, negative charge
  3. epithelial cell layer (podocytes) - not a continous layer
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25
Q

what are the gaps in the podocytes (foot like projections) called

A

slit pores

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26
Q

what happens when the basement membrane loses its electrical charge

A

albumin is filtered ad will appear in the urine - proteinuria/albuminuria

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27
Q

how does filtration work

A

pressure differentials bet. the fluid in the glomeruls and the fluid in the bowmans capsule

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28
Q

GFR = RBF x FF

A

formula for finding:

  1. Glomerular Filtration Rate (GFR)
  2. Filtration Fraction (FF)
  3. Renal Blood Flow (RBF)
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29
Q

How can the body increase GFR

A
  1. by altering RBF - increase overall cardiac output, dilate afferent arterioles in the kidney
  2. by altering FF - contract efferent arteriole, increasing glomerular pressure
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30
Q

Kf = capillary filtration coefficient

A

typical Kf - 12.5 ml/min/mmHg (GFR = Kf x net filtration pressure)

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31
Q

Forces that favor filtration

A

glomerular hydrostatic pressure (60mmHg)

bowmans capsule colloid osmotic pressure (0mmHg)

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32
Q

forces that inhibit filtration

A

bowmans capsule hydrostatic pressure (18mmHg)

glomerular cap. colloid osmotic pressure (32mmHg)

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33
Q

what is the typical net filtration pressure

A

10 mmHg

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34
Q

Angiotensin II (autacoid)

A
  1. powerful renal vasoconstrictor
  2. released due to decreased arterial pressure or volume depletion
  3. all blood vessels of the kidney have receptors - afferent arterioles are not reactive in most instances (stay dilated due to release of vasodilators). efferent arterioles are highly sensitive
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35
Q

tubuloglomerular feedback

A

feedback mechanism linking sodium concentration with renal artery resistance
ensures a constant delivery of sodium chloride to the distal tubules

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36
Q

when renal cells sense a decrease in sodium concentration

A

initiates a signal which does 2 things:

  1. decreases resistance to blood flow in the afferent arterioles
  2. renin is released
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37
Q

urine formed in the kidneys and secreted is the sum of___

A

glomerular filtration - tubular reabsorption + tubular secretion

38
Q

T/F in general, tubular reabsorption is more vital for determining excretion rate

A

true

39
Q

T/F tubular reabsorption is highly selective, glomerular filtration is nonselective

A

true

40
Q

steps for reabsorption of a substance

A
  1. transported across the tubular epithelial membrane
  2. through the interstitial fluid
  3. through the peritubular capillary membrane
  4. into the blood
41
Q

travel of water and solutes

A
  1. transcellular route - thru cell membranes
  2. paracellular route - bet. cells thru tight junctions
  3. travel thru peritubular capillary walls into the blood
42
Q

movement of solute against an electrical gradient

A
  1. primary active transport - coupled with hydrolysis of ATP

2. secondary active transport - coupled indirectly to the energy source gradient

43
Q

osmosis

A

diffusion from an area of low solute concentration to an area of high solute concentration (from the luminal membrane into the cell - proximal tubular membrane)

44
Q

how is sodium moved to the medullary interstitium

A

the cell membrane on the basolateral surface has a sodium-potassium ATPase system (hydrolysis of ATP)
Active transport of sodium and potassium from inside the cell to the interstitium (causes the -70 millivolt negative charge in the cell)

45
Q

how is sodium moved from the intercellular fluid into the peritubular capillary

A

passive process - sodium, water and other substances are reabsorbed by ultrafiltration (driven by osmotic gradient)

46
Q

where are sodium glucose co-transporters (SGLT2 & SGLT1)

A

located in brush border - transport glucose into the cell against a concentration gradient.
SGLT2 - early part of prox. tub. - 90% glucose reabsorbed
SGLT1 - late part of pro. tub - 10% of glucose reabsorbed

47
Q

what is the normal transport maximum for glucose

A

375 mg/min

48
Q

what is gradient time transport

A

some substances that are passively absorbed do not demonstrate a transport maximum. the rate depends on :

  1. electrochemical gradient
  2. permeability of the membrane to the substance
  3. time the fluid containing the substance remains in the tubule
49
Q

T/F sodium does not exhibit a transport maximum

A

true.

50
Q

T/F maximum transport capacity of the basolateral sodium potassium ATPase pump is greater than the actual rate of sodium reabsorption

A

true

51
Q

Principles of sodium gradient time transport

A
  1. the greater the concentration of sodium in the proximal tubule, the greater the reabsorption rate
  2. the slower the flow rate of tubular fluid, the greater the amount of sodium that can be reabsorbed
52
Q

t/f the osmosis of water can only occcur across te tubular membrane if it is permeable to water, no matter how large the osmotic gradient is

A

true

53
Q

65 % of the filtered water and sodium are reabsorbed in the proximal tubule, before reaching the loop of Henle

A

high active and passive reabsorption
highly metabolic epithelial cells
large surface area for reabsorption (brush border - luminal surface) intercellular and basilar channels (basolateral surface)

54
Q

t/f co-transporters (Na+ transported with glucose or amino acids

A

true

55
Q

t/f counter-transport mechanisms (Na+ reabsorption - hydrogen ion secretion into the tubular lumen)

A

true

56
Q

t/f sodium potassium ATPase pump - primary way to reabsorb sodium, chloride and water

A

true

57
Q

Proximal tubule reabsorption (1st and 2nd part)

A
  1. first half of tubule - sodium, glucose, amino acids and water are rapidly reabsorbed
  2. second half of tubule - low conc. of glucose and amino acids - left with a high conc. of chloride ions (favors passive diffusion of chloride ions
58
Q

t/f proximal tubule is highly permeable to water

A

true

59
Q

proximal tubular secretion

A
  1. organic acids and bases (bile salts, oxalate, urate and catecholamines
  2. drugs and toxins
  3. rapid excretion from the body
60
Q

primary function of the descending loop of henle

A

allow for simple diffusion - thin epithelial membrane, no brush border, few mitochondria - highly permeable to water, moderately permeable to urea and sodium, 20% of water is absorbed here

61
Q

thin ascending loop of henle

A

impermeable to water, impermeable to most other solutes except sodium and chloride (via diffusion) takes advantage of high concentrations

62
Q

thick ascending loop of henle

A

thick epithelial cells, brush border, high metabolic activity - active reabsorption of sodium, chloride and potassium - about 25 % of these substances are absorbed here as well as calcium, bicarbonate and magnesium

63
Q

distal tubule - macula densa

A

first portion of distal tubule - part of juxtaglomerular complex - provides feedback control or GFR

64
Q

5% of the filtered load of sodium is reabsorbed in the early distal tubule

A

sodium chloride co-transporter moves sodium chloride from the tubular lumen into the cell

65
Q

late distal tubule and cortical collecting tubule

A

composed of principal cells - sodium reabsorption, potassium secretion
intercalated cells -bicarbonate and potassium ion reabsorption
both segments are impermeable to urea
permeabiltiy of these segments to water is dependent on ADH (vasopressin)

66
Q

medullary collecting duct

A

reabsorb around 10% of filtered water - final output of water and solutes in the urine
urea transporters - urea is reabsorbed into the medullary interstitium

67
Q

Pressure natriuresis and pressure diuresis

A

natriuresis - Na+ excretion in urine

diuresis - water excretion to regulate BP

68
Q

increase in arterial pressure:
increase in urinary excretion of sodium
increase in urinary excretion of water T/F

A

true

69
Q

osmolarity of filtrate at beginning of prox. tub 300mOsm/L
osmolarity of filtrate at the end of prox tub 300mOsm/L
osmolarity of plasma 300mOsm/L
stays isotonic

A

see figure on page 158

70
Q

T/F thick and thin ascending segments of the loop of henle are not permeable to water

A

true

71
Q

cortical collecting tubule

A

high ADH - tubules become permeable to water

low ADH - tubules are impermeable to water

72
Q

forming concentrated urine in the inner medullary collecting ducts

A

high concentration of urea

diffusion of urea into the renal medulla - facilitated by urea transporters, active transporters by ADH

73
Q

vasa recta and their special features preserve the high solute concntration in the renal medulla

A

vasa recta are countercurrent exchangers (minimizes washout of solutes from the interstitium

74
Q

when sodium increases 2mEq/L above normal there is a desire to ingest fluid

A

thirst - an area along the anteroventral wall of the third ventricle that promotes ADH also stimulates thirst

75
Q

if kidneys can not maintain balance of extracellular fluid what happens

A
systemic adjustments will be made:
1. change in blood pressure
2. change in circulating hormones
3. change in sympathetic nervous system
this comes at all $cost$
76
Q

kidney damage results in

A
  1. impaired sodium excretion

2. electrolye and fluid imbalance = cardiac insufficiency = death within days

77
Q

when we increase fluid intake how do we maintain blood volume

A
  1. slight change in blood volume = marked increase in cardiac output
  2. slight change in cardiac output = marked increase in blood pressure
  3. slight change in blood pressure = marked increase in urine output
78
Q

sympathetic nervous system control of renal excretion

A

an extensive decrease in blood volume (hemorrhage) will activate sympathetic nerve activity - signals that kidneys need to hold on to salt and fluid
constriction of renal arterioles = decrease in GFR
stimulation of renin release

79
Q

angiotensin II

A

most powerful controller of sodium excretion

80
Q

aldosterone

A

increase sodium and water reabsorption in the cortical collectiing tubules - increased potassium excretion

81
Q

ADH vasopressin

A

increased ADH:
increased reabsorption of fluid
maintain excretion of sodium

82
Q

other stimulations that increase ADH secretion

A

nausea, hypoxia, drugs

83
Q

Atrial Natriuretic Peptide ANP

A

high circulating fluid levels => release of ANP => increase in GFR and decrease in tubular reabsorption of sodium

84
Q

regulation of potassium balance

A

insulin is important to help uptake of potassium into the cells after a meal

85
Q

T/F increased potassium intake stimulates aldosterone production

A

true

86
Q

T/F b-adrenergic stimulation causes increased secretion of catecholamines

A

true

87
Q

metabolic acidosis increases extracellular potassium levels

A

loss of potassium from the cells

reduce activity of the ATPase pump

88
Q

T/F cell lysis results from severe hyperkalemia - release of potassium in the extracellular compartment

A

true

89
Q

T/F prolonged exercise causes release of potassium from the muscles

A

true

90
Q

factors that shift potassium into cells

A
insulin
aldosterone
b-adrenergic stimulation
alkalosis
deficiency of above shift potassium out of cells
91
Q

T/F principal cells in the late distal and collecting tubules secrete potassium for excretion

A

true

92
Q

a person is considered to have acidosis if the pH of the atrial blood is below 7.4

A

a person is considered to have alkalosis when the pH increases above 7.4