renal Flashcards

1
Q

urinary system

A
  • 2 kidneys which produce urine from blood
  • urine travels down paired ureters
  • stored in urinary bladder
  • forced through urethra and expelled
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2
Q

function of kidneys

A
  • achieve electrolyte balance
  • regulate blood ph
  • remove waste
  • secrete hormones
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3
Q

cortical vs juxtamedullary nephron

A

cortical - shorter loop of henle, more abundant
juxtamedullary - longer loop of henle

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4
Q

afferent arteriole

A

carries blood to the glomerulus

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5
Q

glomerulus (glomerular capillaries)

A

filters protein free plasma into the tubular component

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6
Q

efferent arteriole

A

carries blood away from the glomerulus

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7
Q

peritubular capillaries

A

supply renal tissue, exchange of fluids

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8
Q

juxtaglomerular apparatus

A

produces substances involved in control of kidney function

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9
Q

Bowmans capsule

A

collects glomerular filtrate

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10
Q

proximal tubule

A

uncontrolled reabsorption and secretion
- have number of mitochondria to promote reabsorption

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11
Q

loop of henle

A

osmotic gradient in renal medulla
- ability of kidney to produce urine

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12
Q

distal tubule and collecting duct

A

controlled reabsorption of Na and H2O and secretion of K and H, fluid leaving collecting duct is urine

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13
Q

intercalated cells

A

secrete H/ HCO3 and reabsorb K

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14
Q

principal cells

A

reabsorb Na and H2O, secrete K

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15
Q

glomerular filtration

A
  • non discriminant filtration
  • entry of substances into bowmen’s capsule
  • protein free
  • fluid must pass through three layers of membrane
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16
Q

tubular reabsorption

A
  • selective movement of filtered substances from lumen to particular capillaries
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17
Q

tubular secretion

A

selective movement of non filtered substances from per tubular capillaries into lumen

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18
Q

3 layers of glomerular membrane

A
  1. glomerular capillary wall with pores
  2. basement membrane negatively charged
    - acellular
    - discourages filtration of small plasma proteins
  3. Bowmans capsule - slits between podocytes
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19
Q

three forces in glomerular filtration

A
  1. glomerular capillary blood pressure
  2. plasma colloid osmotic pressure
  3. Bowmans capsule hydrostatic pressure
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20
Q

glomerular capillary blood pressure

A
  • pressure exerted by blood
  • depends on heart contraction and resistance of blood flow
  • favours filtration
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21
Q

plasma colloid osmotic pressure

A
  • opposes filtration
  • concentration of H2O is higher in BC therefore H2O moves from BC to glomerulus
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22
Q

Bowmans capsule hydrostatic pressure

A

push fluid out of BC
- opposes filtration

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23
Q

arteriolar vasoconstriction/ dilation on GFR

A

vasoconstriction
- decrease in blood flow to the glomerulus
- decrease glomerular blood pressure
- decrease net filtration pressure
- decrease in GFR
vasodilation
- increase blood flow into glomerulus
- increase glomerular blood pressure
- increase net filtration pressure
- increase GFR

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24
Q

regulation of GFR

A

1 - auto regulatory mechanisms
2 - neural regulation
3 - hormonal regulation

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25
Q

auto regulatory mechanisms of regulation of GFR

A

tubuloglomerular feedback
- macula dense cells in distal tubule sense change in filtered Na
- ^ GFR and ^ Na - cells stimulate afferent arteriole to constrict = v GFR
- v GFR and v Na - cells stimulate afferent arteriole to vasodilate = ^GFR

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26
Q

neural regulation of GFR

A
  • sympathetic
  • stimulation = vasoconstriction = v renal blood flow = v GFR
  • stimulated when exercise, vBP, sever hypoxia
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27
Q

hormonal regulation of GFR

A

renin - angiotensin aldosterone system = ^ renal blood flow = ^GFR
release of renin = vBP, vNaCl

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28
Q

Na an Cl reabsorption

A
  • Na/K pump transports Na from tubular cell to interstitial fluid within lateral space
  • establishes concentration gradient for passive movement of Na from interstitial fluid to peritubular capillary
  • Na reabsorption responsible for passive reabsorption of Cl, H2O and urea
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29
Q

H2O reabsorption

A
  • passively absorbed through length of tubule
  • osmotically follows reabsorbed Na
  • via aquaporins
  • AQP-1 in proximal tubule are always open
  • AQP-2 - regulated by vasopressin (ADH)
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30
Q

glucosuria

A
  • exceed threshold SGLTs become saturated and excess glucose is excreted
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31
Q

tubular maximum (Tm)

A
  • maximum absorption rate
  • when all carriers are occupied or saturated
  • cannot take additional passengers
  • any substance filtered beyond Tm is not reabsorbed and escapes in the urine
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32
Q

loop of henle - 3 sections and their roll

A
  1. descending limb
    - highly permeable to H2O
    - doesn’t actively reabsorb NaCl
  2. ascending thin limb
    - impermeable to H2O
    - permeable to NaCl
  3. ascending thick limb
    - impermeable to H2O
    - active reabsorption of NaCl
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33
Q

urea movement

A
  1. proximal tubule
    - mildy permeable to urea
  2. thin LOH
    - secretion of urea due to greater concentration then in the tubule
  3. thick LOH and DCT
    - highly impermeable to urea
  4. collecting ducts
    - highest permeability to urea
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34
Q

K secretion

A
  • filtered K is almost all reabsorbed in the proximal tubule
  • most K in urine is from controlled K secretion in the distal parts of the nephron
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35
Q

H secretion

A
  • regulating acid base balance in body
  • body fluids acidic = H secretion increase
  • low H in body fluids = decreased H secretion
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36
Q

blood tests to monitor kidney function

A
  • creatinine concentration vGFR = ^ creatinine levels
  • glomerular filtration rate
  • blood urea nitrogen
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37
Q

urine tests to monitor kidney function

A
  • urinalysis
  • creatinine clearance
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38
Q

renal clearance

A
  • volume of blood from which a substance is completely removed by the kidneys per unit time
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39
Q

what is creatinine

A
  • waste product from the normal wear and tear of muscles
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40
Q

blood urea nitrogen (BUN)

A
  • test that measures the amount of nitrogen in your blood that comes from urea
  • BUN rises if kidneys are not able to remove BUN from blood normally, dehydration, heart failure
  • BUN drop if liver disease / damage
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41
Q

angiotensin 2 affecting the kidney

A
  • due to hypotension, fall in NaCl or hypovolemia
  • afferent and efferent arteriole
  • ^afferent/vefferent constriction = v GFR
  • ^Na reabsorption to maintain fluid balance
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42
Q

atrial natriuretic peptide (ANP) affecting the kidney

A
  • released in response to atrial pressure
  • afferent/ efferent arteriol, DCT
  • afferent dilation and efferent constriction = ^GFR and ^Na filtration
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43
Q

aldosterone affecting the kidney

A
  • due to hypovolemia and hypotension and or hyperkalemia
  • distal and collecting duct
    ^Na uptake and K secretion into the urine = net fluid retention
44
Q

antidiuretic hormone (ADH) affecting the kidney

A
  • due to hypovolemia and hypotension and ^ plasma osmolality
  • distal and collecting ducts
  • ^ free H2O uptake from the collecting duct
45
Q

hypovolemia

A

decrease in blood volume

46
Q

atrial natriuretic peptide

A

produced in atrial cardiac muscle cells

47
Q

brain natriuretic peptide

A

produced primarily in ventricular cardiac muscle cells

48
Q

natriuretic peptide mechanism

A

ANP and BNP are markers for heart failure
- inhibit renin secretion
- inhibit aldosterone
- inhibit ADH release
overall effect = v blood volume and v BP

49
Q

ADH and water balance

A

dehydration
- osmoreceptors in the hypothalamus
- thirst
- drink = rehydration
- ^ ADH secretion
- ^ H2O reabsorption
= v urine volume - rehydration

50
Q

ADH / vasopressin

A
  • secreted from posterior pituitary gland
  • key role = maintain osmolarity
  • hypo-osmotic
  • regulates aquaporin
  • controls H2O reabsorption
    more ADH = more AQP2 open
50
Q

substances that affect ADH levels

A

adrenaline ^ ADH
nicotine ^ ADH
alcohol v ADH
caffeine V ADH

51
Q

diabetes insipidus

A

condition where this is an excessive production of dilute urine

52
Q

central diabetes insipidus

A

lack of ADH in the body due to brain unable to respond to ^ osmolality

53
Q

nephrogenic diabetes insipidus

A

V2 ADH receptor mutations
- aquaporin 2 gene mutations

54
Q

renal clearance formula

A

(urine flow x urine concentration) / plasma concentration

55
Q

molarity

A

concentration measuring the number of moles of a solute per litre of solution

56
Q

osmolarity

A

concentration of a solution expressed as the total number of solute particles per litre

57
Q

osmolality

A

measure of different solutes in plasma per kg

58
Q

tonicity

A
  • isotonic, hypotonic, hypertonic
  • measure of osmotic pressure gradient between two solutions
59
Q

hypotonic

A

water diffuses into cell and swells

60
Q

hypertonic

A

water diffuses out of cell and shrinks

61
Q

regulation of ECF volume

A
  • extracellular fluid
  • long term control of arterial BP
    v ECF volume = v BP
    ^ ECF volume = ^ BP
  • maintenance of salt balance
62
Q

regulation of ECF osmolality

A
  • prevention of osmotic movement between ECF and ICF
    ^ ECF osmolarity (hypertonicity) = H2O leaves the cell = cell shrinks
    v ECF osmolarity (hypotonicity) = H2O enters the cells = cell swells
  • maintained by free H2O balance
63
Q

causes of hypertonicity

A
  • dehydration
  • insufficient H2O intake
  • excessive H2O loss
  • diabetes insipidus
64
Q

causes of hypotonicity

A
  • overhydration
  • renal failure
  • H2O rapidly ingested
  • excess synthesis of ADH
65
Q

blood pH regulation

A

^H (acidosis) = v pH
v H (alkalosis) = ^pH

66
Q

lines of defence against changes in H

A
  1. chemical buffer = instantaneous
  2. respiratory system = mins to hours
  3. kidneys = maintain acid base balance by adjusting urinary output, hours to days
67
Q

H2CO3 : HCO3‐ buffer system

A
  • primary ECF buffer against non carbonic acid changes
  • able to resist change
68
Q

protein buffer system

A

primary ICF buffer also buffers ECF

69
Q

haemoglobin buffer system

A

primary ICF buffer against carbonic acid changes

70
Q

phosphate buffer system

A

filtered urinary buffer
ICF buffer
- consists of NaH2PO4
- donates H when v H
- accept H when ^H

71
Q

ammonia buffer system

A

secreted urinary buffer

72
Q

respiratory system and blood pH regulation

A

^H - stimulation of respiratory centre in brain - ^ pulmonary ventilation - ^ removal of CO2
vH - v pulmonary ventilation - ^ acid forming CO2 accumulate in blood - restoration of H towards normal

73
Q

kidneys and blood pH regulation

A
  1. H excretion
  2. HCO3 excretion
  3. ammonia secretion
74
Q

acidosis

A

-pH below 7.35
- increase H
- acidemia
- H2CO3 increased

75
Q

alkalosis

A
  • pH above 7.45
  • decrease H
  • alkalaemia
  • HCO3 increased
76
Q

causes of acidosis

A

metabolic
- diarrhoea
- a lot of exercise
- aspirin
- type 1 diabetes
respiratory
- hypercapnia
- lung disease
- holding breath

77
Q

causes of alkalosis

A

metabolic
- vomiting
- ingestion of alkaline drugs
respiratory
- excessive loss of CO2
- hypocapnia
- anxiety
- fever
- aspirin intoxication

78
Q

metabolic acidosis pathophysiology

A
  • HCO3 decreases because of excess ketones
  • body compensates by hyperventilation decrease H2CO3 and kidneys conserve HCO3
79
Q

respiratory acidosis pathophysiology

A
  • hypoventilation retains H2CO3 the lungs are the problem
  • body compensates by kidneys conserving HCO3
80
Q

metabolic alkalosis pathophysiology

A
  • HCO3 increases because of excess infection of sodium bicarbonate
  • body compensates by hypoventilation to increase H2CO3 and kidneys eliminate HCO3
81
Q

respiratory alkalosis pathophysiology

A
  • decrease in H2CO3 due to hyperventilation
  • body compensates by kidney eliminating HCO3
82
Q

tests to diagnose renal problems

A
  • albuminuria
  • pathological abnormalities
  • structural abnormalities
  • blood urea nitrogen
  • blood pressure
83
Q

acute renal failure

A
  • sudden onset
  • often reversible
84
Q

signs and symptoms of acute kidney failure

A
  • decrease urine
  • fluid retention
  • shortness of breath
  • confusion
  • sometimes insidious
85
Q

3 causes of acute renal failure

A
  1. pre renal
  2. intra renal
  3. post renal
86
Q

pre renal cause of acute renal failure

A

hypo - perfusion - inadequate blood supply

87
Q

intra renal cause of acute renal failure

A

acute tubular necrosis
acute interstitial necrosis
vascular damage

88
Q

post renal cause of acute renal failure

A

obstructions due to oedema, tumour kidney stone, clot etc

89
Q

chronic renal failure

A

due to complications of systemic or renal diseases
- kidney is smaller in size, granular surface

90
Q

signs and symptoms of chronic renal failure

A
  • fatigue and weightloss
  • muscle twitches and cramps
  • itching
  • chest pain
  • hypertension
91
Q

common causes of chronic renal failure

A
  1. diabetes mellitus
  2. hypertension
  3. autoimmune disorders
92
Q

factors advancing renal failure

A
  1. tubular protein reabsorption
  2. increased angiotensin 2 activity
93
Q

urination

A

when pelvic floor muscles are contracted, relaxing the pelvic floor allows passage or urine

94
Q

urinary retention

A

inability to empty the bladder completely

95
Q

causes of urinary retention

A

obstructive problem eg enlarged prostate or kidney stones
non obstructive such as weakened bladder

96
Q

urinary incontinence

A

accidental or involuntary loss of urine from the bladder

97
Q

Describe the effect of increasing the afferent radius on glomerular filtration rate and glomerular pressure.

A

increase glomerular pressure, increasing the filtration rate

98
Q

Describe the effect of decreasing the efferent radius on glomerular filtration rate and glomerular pressure.

A

increase glomerular pressure increase filtration rate

99
Q

Describe the effect of increasing the efferent radius on glomerular filtration rate and glomerular pressure.

A

decrease glomerular pressure and filtration rate

100
Q

Mrs Jones was diagnosed with hypertension. Her GP advised her to minimise her salt intake. Why do you think a decrease in her salt intake could reduce her blood pressure?

A

less salt therefore less water reabsorption therefore reducing blood pressure
more salt = ^ concentration gradient = ^ water reabsorption =decrease in urine output = ^ blood pressure

101
Q

Does ADH favour the formation of dilute or concentrated urine?

A

ADH made in hypo and released from anterior pituitary gland
ADH binds to B2 receptors
B2 trigger response to open aquaporins #2
sends signal to increase expression making more aquaporin #2
this happens in distal convoluted tubule and collecting duct of principle cells
concentrated urine
facilitates reabsorption of water

it favours concentrated urine

101
Q

Describe the possible pathophysiological changes that may take place in patients with decreased ADH secretion

A

decrease ADH means a decrease in water reabsorption in kidneys
- diabetes insipidus
- central as ADH is produced in the posterior pituitary
- increased dilute urine output
- Hypernatremia with increased urine output = increased sodium = increased thirst

102
Q

Describe the possible pathophysiological changes that may take place in patients with decreased Aldosterone secretion?

A

decreased aldosterone affects absorption of sodium
- hypoaldosternism
- decrease urination of K+ and increase urination of Na+ excretion
- increase K+ levels in the blood, Hyperkalemia
- decrease Na+ in the blood, Hyponatremia

103
Q

You eat an entire bag of salty popcorn while watching a two-hourmovie. You have nothing to drink. Describe the homeostatic reflexes that occur while you are eating and watching the movie.

A

reabsorb water towards the salt
- osmo receptors in hypothalamus pick up salt levels
- swell when low salt and shrink when high salt
- trigger release of ADH, binds to B2
- return of water through aquaporin
- decrease aldosterone secretion to eliminate Na

sodium content increases which stimulates the release of ADH, which then promotes water reabsorption, decreasing urine and triggers the sensation of thirst

104
Q
A