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Primary Physiology > Renal physiology > Flashcards

Renal physiology Flashcards

1
Q

Arterial supply to kidney, subdivisions
Percentage of cardiac output at rest

A

Renal arteries, each dividing into 2 upper branches (supplying anterior and posterior upper poles) and lower branch (supplying lower pole). Then divide into interlobar, arcuate arteries interlobular arteries then afferent arterioles

Take 20% of resting Co

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2
Q

Blood vessels in kidneys distal to afferent arterioles

A

Glomerular capillaries
Efferent arterioles
Peritubular capillaries
Interlobular veins
Arcuate veins
Interlobar veins
Renal veins

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3
Q

Nervous supply to kidney

A

Autonomic T10-L1- travel with renal vessels
Some parasympathetic from vagus nerve
Nociceptive afferents T10-11

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4
Q

Layers of kidney external to internal

A

Capsule
Cortex
Medulla
Pelvis

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5
Q

Anatomy of a nephron

A

Knot of capiliaries from the afferent arteriole - glomerulus
Blind end of tubular system enveloping it - bowman’s capsule
Proximal tubule
Loop of Henle
Distal tubule
Collecting duct

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6
Q

Where in the kidney are nephrons found

A

Cortex with slight loop into medulla
25% have loop of henle that runs deep into medulla

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7
Q

Overall function of glomerulus

A

Produce an ultrafiltrate of plasma

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8
Q

What composes the glomerular filtration barrier

A

Fenestrated capillary endothelium
Glomerular basement membrane
Visceral epithelial cells of bowman’s capsule (podocytes)

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9
Q

Size of fenestrations in glomerular endothelium, function

A

60nm
Prevention of blood cells from contacting main filter

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10
Q

Main part of the glomerular filter?
Physiology and function

A

Basement membrane
Collagen and glycoproteins with strong negative charge
Allows passage of molecules according to size shape and charge

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11
Q

Anatomy and function of podocytes at bowman’s capsule

A

Encircling trabeculae with small processes (pedicels)
Pores between pedicels
Maintains basement membrane integrity and filtration selectivity

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12
Q

What is the composition of ultrafiltrate in the kidneys
What sizes of molecules included / excluded

A

Similar to plasma
Free of cells
Free of particles >70000 daltons
Reduced concentration of particles 7000-70000 daltons based on size and negative charge.
Particles <7000 pass through freely.

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13
Q

Term for nephrons that just pass into medulla
Term for nephrons that run deep into medulla

A

Cortical nephron
Juxtamedullary nephron

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14
Q

Where do collecting ducts drain

A

Renal papilla and calyces in medulla
Then into renal pelvis and on into ureter

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15
Q

Definition of stage 1 AKI

A

Cr increase of 26.4 micromol/L or by 150-200%
Urine output <0.5ml/kg/hr for >6hrs

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16
Q

Definition of stage 2 aki

A

Cr increase by 200-300%
Urine output <0.5ml/kg/hr for >12hrs

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17
Q

Definition of stage 3 AKI

A

Cr increase by 354.4 micro moles/L or by >300%
Urine output <0.3ml/kg/hr for >24hrs or anuric for 12hrs

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18
Q

GFR associated with each stage of CKD

A

1 >90
2 60-89
3 30-59
4 15-30
5 <15

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19
Q

Usual Glomerular filtration rate per day and per minute in L

A

180 L per day
Around 125 ml/min

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20
Q

What determins glomerular filtration

A

Size of molecules
Charge of basement membrane
Hydrostatic pressure gradient
Renal plasma flow
Colloid osmotic pressure gradient
Glomerular capillary coefficient
Blood pressure

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21
Q

Molecular weight of albumin

A

69000 daltons

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22
Q

What is the glomerular capillary coefficient
Value

A

Measure of resistance to flow of ultrafiltrate across the total glomerular surface
12.5ml/min/mmHg

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23
Q

What is the glomerular colloid osmotic pressure gradient

A

Glomerular capillary osmotic pressure - bowman’s capsule osmotic pressure
32 - 0
32mmHg

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24
Q

What determins colloid osmotic pressure in the glomerular capillaries

A

Colloid osmotic pressure in afferent arteriole
Filtration fraction
Renal plasma flow

Because as more fluid is filtered osmotic pressure will rise relatively

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25
Q

What is renal blood flow on average per min
Renal plasma flow on average per min
Glomerular filtration rate on average per min

A

1100ml/min
600ml/min
125ml/min (thus 20% of renal plasma flow is filtered)

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26
Q

How is filtration fraction calculated

A

GFR/renal plasma flow
120/600 = 0.2

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27
Q

What is the impact on filtration fraction and GFR of increased renal plasma flow

A

Higher renal plasma flow results in decreased filtration fraction. Because less is filtered glomerular oncotic pressure is lower so GFR increases.

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28
Q

What is the glomerular hydrostatic pressure gradient
Rough values in normal function

A

Glomerular hydrostatic pressure - bowman’s hydrostatic pressure
60-18 = 42mmHg

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29
Q

What determines glomerular hydrostatic pressure

A

Afferent and efferent arteriolar resistance

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30
Q

What is the effect of a decrease in glomerular hydrostatic pressure on gfr

A

Reduces as gradient lessens

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31
Q

What afferent arteriolar change result in decreased glomerular hydrostatic pressure? What drives this?

A

Constriction
Increased SNS stimulation
Circulating hormones - adrenaline, NA, endothelin

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32
Q

What artieriol changes result in increased glomerular hydrostatic pressure? What drives this?

A

Dilation of afferent arteriole:
Prostaglandins, NO

Constriction of efferent arteriole:
Angiotensin II

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33
Q

What is glomerular net filtration pressure?
Normal values

A

Hydrostatic pressure gradient - colloid osmotic pressure gradient
(60-18)-(32-0)
42-32
10mmHg

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34
Q

How would a renal stone or other obstruction impact on GFR via the glomerular pressure gradietn

A

Increase the hydrostatic pressure in bowman’s capsule

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35
Q

What is the impact of BP on GFR
Why

A

Very little in normal range due to auto regulation

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36
Q

What mediates renal auto regulation to Bp

A

Myogenic response of blood vessels - constriction as a result of stretching and relaxation as bP falls
Juxtaglomerular complex provides tuboglomerular feedback resisting changes in filtration rate on falling BP

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37
Q

What is the juxtaglomerular complex

A

Juxtaglomerular cells in the walls of the afferent and efferent arterioles and adjacent macula densa (epithelial cells around distal tubule)

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38
Q

How does the Juxtaglomerular complex respond to a drop in BP to maintain GFR

A

Low BP decreases GFR
Increased absorption of Na + Cl in loop of Henle
Less Na + Cl reaching macula densa
Renin released stimulating angiotensin I to II
Angiotensin II drives vasoconstriction of efferent arteriole increasing hydrostatic pressure and thus GFR
Macula densa also causes reduction in afferent arteriole resistance also increasing GFR

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39
Q

Why do high levels of angiotensin II not always result in maintained GFR

A

Overall reduction in glomerular blood flow thus increased colloid osmotic pressure due to increased filtration fraction

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40
Q

What else can activate the tubuloglomerular feed back mechanism

A

Filtration of Na or glucose - needs cotransport with Na for reabsorption thus less Na to macula densa

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41
Q

What is reabsorbed in the proximal tubule of the kidney?

A

100% amino acids and glucose
65% of other ions
20% phosphate
65% water

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42
Q

What happens to filtrate osmolarity in the proximal tubule

A

Stays roughly the same as plasma - 65% of ions and 65% water reabsorbed

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43
Q

What is secreted in the proximal tubule?

A

Organic acids, bases and drugs

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44
Q

How are amino acids and glucose reabsorbed in the proximal tubule

A

Na exchanged into blood on capillary membrane by NaKATPase
Cotransport of AA and glucose alongside sodium on luminal membrane

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45
Q

How is calcium reabsorbed in the PCT

A

Paracellular
Exchanged for Na at the capillary side then pulled into cells on the luminal side.

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46
Q

How is urea reabsorbed in the nephrons
How much in PCT
How does it continue all the way down?

A

Passive diffusion rate dependant on concentration gradient and permeability of membrane
50%
As water is reabsorbed concentration of urea increases relatively thus diffusion can continue

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47
Q

What is the tonicity of fluid in the loop of Henle with respect to plasma?

A

Isotonic on entering
Hypotonic on leaving

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48
Q

Given tubular fluid is hypotonic with respect to plasma at the end of loop of Henle how does the loh contribute to concentration of urine?

A

Manufacture of the countercurrent multiplier gradient

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49
Q

Segments of the loop of Henle

A

Thin decending
Thin ascending
Thick ascending

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50
Q

What occurs in the thick ascending limb of the loop of Henle
What osmotic difference does it generate in the medullary interstitium

A

Active reabsorption of NaCl and K via NaKCl2 synporters driven by NaKATPase on the basolasteral membrane.
200mosmols

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51
Q

What is the difference between the thin decending and thin ascending limbs of the loop of henle? What exchanges occur over whole loop.

A

Thin decending is permeable to water and ions. Thin ascending permeable to ions only.

Fluid in descending limb looses water becoming hyperosmolar to around 1200mosm/l due to the active extrusion of sodium by thick ascending limb. On ascending limb reabsorption of NaCl from tubule becoming more hypoosmolar eventually becoming slightly hypotonic, whilst increasing osmolarity of interstitium. Water cannot follow as impermeable. Overall hyperosmalar interstitium.

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52
Q

What percentages of ions are reabsorbed in the thick ascending limb of loh.

A

25% Na Cl K and bicarb
65% Mg

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53
Q

Characteristics of collecting duct

A

Relatively impermeable to water, urea and NaCl but water permeability can be increased by ADH leading to urine concentration

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54
Q

How is water reabsorbed in the nephron

A

Always following solute - never active

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55
Q

What routes can substances take from nephron lumen to blood?

A

Transcellular (across luminal cells, into intersitital space then into capillary)
Paracellular (between luminal cells into interstitial space then into capillary)

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56
Q

What are the types of aquaporin and where are they located?

A

AQA1 - PCT and thin descending limb apical and basal membranes, extra renal tissues
AQA2 - luminal membrane of collecting duct under ADH activation
AQA3 - basolateral membrane of collecting duct
AQA4 - brain - ? Hypothalamic osmoreception

57
Q

What is the maximum rate of tubular reabsorption termed?

A

Transport maximum

58
Q

Name a reabsorption that doesn’t have a transport maximum
Name 2 that do

A

Sodium reabsorption in the PCT

Do:
Glucose in PCT
Na in DCT

59
Q

Other than luminal transport of a substance what other factors can effect transport maximum?

A

Backflux (leakage back from interstitial fluid)
Peritubular capillary uptake

60
Q

What is the Peritubular capillary fluid reabsorption rate? How does it compare to GFR
What drives this reabsorption

A

124ml/min
125ml/min

Driven by colloid osmotic pressure (just outweighs reverse hydrostatic gradient)

61
Q

What occurs with Peritubular reabsorption as GFR increases
Why

A

Also increases,
Increased gfr leads to increased filtration fraction
Increased filtration fraction increases Peritubular colloid osmotic pressure this gradient favours reabsorption

62
Q

Why is inulin good for calculating gfr
How is it done

A

Filtered at glomerulous then neither secreted or reabsorbed

GFR = (urine concentration x flow rate) / plasma concentration

63
Q

How is creatinine handled in the kidneys

A

Filtered
Slight secretion
No reabsorption

64
Q

What is renal clearance?
Limitation

A

The theoretical volume of plasma from which a substance is removed by the kidneys per unit time (e.g. ml/min). This isn’t how it works - no one part of the plasma is completely cleared leaving the substance in the rest.

65
Q

What would renal clearance equal for inulin

A

GFR

66
Q

How can renal plasma flow be estimated (method and ideal substance)

A

Using a substance that is totally cleared from plasma in one pass through the kidneys
Must be filtered and secreted (as filtration only accounts for 20% renal plasma flow) must not be reabsorbed
RPF = urine concentration x urine flow / plasma concentration

67
Q

Example of substance that is nearly entirely secreted that can be used to calculate renal plasma flow

A

Para-aminohippuric acid

68
Q

What is the renal mechanism for controlling ECF osmolarity? What does it require

A

Controlling water reabsorption in DCT and collecting ducts

Generation of hypertonic medullary interstitium
Control of tubular permeability

69
Q

What solutes make the medullary interstitium hyperosmolar? Rough percentages?
Where is it most concentrated

A

NaCl and urea (40%)
Most concentrated at inner medulla - bottom of the loop (decreasing to outer medulla along a gradient)

70
Q

What is the term for the peritubular vessels accompanying the juxtamedullary loops of henle

A

Vasa recta

71
Q

How does the collecting duct aid in maintaining the hyper osmolarity of the medullary interstitium

A

Recirculating of urea
Facilitated diffusion of urea from medullary collecting duct to intersitium activated by ADH
Then re enters the descending/ ascending LOH
and so on

72
Q

What occurs in the vasa recta as it passes through the medulla

A

Decending limb looses water and gains solute as it moves through the concentrated intersitium becoming hyperosmotic. As it ascends and interstitial osmolality decreases then water enters and solute returns so osmolarity returns to normal

73
Q

How does ADH control water reabsorption in the kidneys?

A

Increasing osmolarity detected in hypothalamus
ADH synthesised and released
ADH binds to V2 receptors in distal tubules, cortical collecting tubules and medullary collecting ducts
G protein coupled mechanism leads to deposition of AQP2 channels on luminal side increasing permeability to water
Water is reabsorbed, osmolarity decreased, ADH secretion decreases

74
Q

Where is osmolarity change detected

A

Supraoptic and paraventicular nuclei of anterior hypothalamus
Third ventricle, organum vasculosum and lamina terminalis

75
Q

Where is ADH synthesised and released

A

Made in supraoptic and paraventricular nuclei of anterior hypothalamus. Transported in neurones of these nuclei to posterior pituitary where it is released.

76
Q

Other than high osmolarity what else triggers ADH release
Physiological and pathological

A

Physiological:
Hypovolaemia
Hypotension
Hypoxia
Nausea

Pathological:
Drugs eg opioids and chlorpromazine
Respiratory disease eg pneumonia
Head injury
Malignancy of lung, prostate, pancreas
Metabolic disease eg porphyria

77
Q

What is renal water clearance
Significance

A

Index of osmolarity and volume of urine vs plasma osmolarity
If urine hypoosmolar compared to plasma suggests filtered plasma is being diluted and thus patient is well hydrated or over hydrated
If urine hyperosmolar compared to plasma suggests under hydrated

78
Q

What is the primary determinant of sodium reabsorption (and thus renal control of sodium balance). What else plays a role

A

1o
Renin, angiotensin, aldosterone

2o
Starling forces in peritubular capilliaries
Neurological reflexes
ANP
Dopamine
Renal prostaglandins

79
Q

Where is renin synthesised and stored
Trigger for release

A

Granular cells of juxtaglomerular aparatus
Low sodium content

80
Q

effects of increased angiotensin 2 levels

A

Efferent arteriolar vasoconstriction causing:
Reduced peritubular hydrostatic pressure increasing sodium and water reuptake
Increased filtration fraction thus raised peritubular colloid oncotic pressure and increased reuptake

Direct binding to PCT DCTand LOH stimulating nakatpase nahco3 synporter and NaH exchange

Triggers aldosterone release to cortical collecting tubule intracellular mineralocorticoid receptor stimulating Na K exchanger on basolateral wall

Systemic vasoconstriction

81
Q

Effects of nephrotic syndrome on extracellular and blood volume

A

Reduction

82
Q

Why does nephrotic syndrome cause ecf and blood vol to fall? Why does it cause oedema

A

Massive proteinurea
Reduction in reabsorption of fluid

Reduction in capillary colloid oncotic pressure so oedema along with raas activation retaining salt and water

83
Q

Renal response to increased blood volume

A

Reduced raas
Sodium and water excretion

84
Q

Long term response to high salt and water intake
In health
In HTN

A

Increased ability to excrete salt and water!
In HTN with renal pathology obtunded ability to respond so salt causes water retention and further bp increase

85
Q

H+ concentration at pH
7.0
7.4
7.8

A

100nmol/L
39.8nmol/L
15nmol/L

86
Q

What is a buffer system

A

Weak acid and conjugate base of that acid
Minimises changes in pH when an acid or base is added to it

87
Q

Why does the body need buffers

A

Deranged pH significantly effects enzyme function
Body trends towards acidic due to production of H+ in metabolism

88
Q

Examples of blood buffer systems with weak acid and conjugate base

A

CO2/bicarbonate
Hb (HbO2 and Hb-)
Plasma proteins (H+protein and protein-)
Phosphate (h2po4- and hpo42-)

89
Q

Examples of extracellular buffer systems

A

CO2/bicarb
Proteins
Phosphate

90
Q

Examples of intracellular buffer systems

A

Proteins
Phosphates
Bicarbonate
Organic phosphates

91
Q

What is the Henderson hasselbach equation

A

Ph = pK + log [base]/[acid]

92
Q

How can Henderson hasselbach be applied to the bicarbonate buffer?

A

pH = 6.3 + log [HCO3-]/[H2CO3] = 6.3 + log [HCO3-]/[CO2] ~ 6.3 + log 25/2 ~ 7.39

93
Q

Role of kidneys in ph control

A

Conservation of bicarb and regeneration of additional bicarb:
Reabsorption of filtered bicarb
Generation of bicarb by co2 reabsorption
Secretion of H in exchange for Na
Secretion of H along with ammonia or phosphate
Metabolism of glutamine

94
Q

Where is filtered bicarb reabsorbed

A

85% pct
10% thick ascending loh
5% DCT and collecting duct

95
Q

How is filtered bicarb reabsorbed in the pct

A

Extrude h ion in exchange for na reabsorption
H + bicarb to h2co3 then with carbonic anhydrates to co2 and h2o
Co2 reabsorbed through luminal membrane, combines with h2o to h2co3 with carboinc anhydrase
This breakers back down to bicarb and h + (extruded as in step 1)
Bicarb then transported to plasma in synport with reabsorbed na.

96
Q

How is h+ excreted in the kidneys?

A

In exchange for Na
Then either buffered with bicarb causing bicarb reabsorption or buffered with ammonia or phosphate

97
Q

What is the anion gap

A

Difference between measured anions and cations

AG = na - bicarb - cl

98
Q

How does does glutamine play a role in management of pH

A

Metabolised by kidneys to nh4 and glutamate.
Nh4 in gradient to ammonia which is secreted and acts as buffer to allow h excretion
Glutamate metabolised via steps to co2 and water and thus a source of bicarb

99
Q

Causes of normal anion gap acidosis

Why?

A

Diarrhoea
Renal tubular acidosis
Nacl administration

Bicarb loss is compensated for by Cl increase

100
Q

Why does diarrhoea cause normal anion gap acidosis

A

Gastric secretions more na than Cl thus when lost and nacl replaced to maintain na Then cl rises

101
Q

Causes of raised anion gap acidosis

A

Methanol
Uraemia
DKA
Paracetamol
Infection
Lactate
Ethylene glycol
Salicylates

102
Q

Types of renal tubular acidosis and features

A

Type 1 - DCT unable to secrete h+
Causes - hereditary, obstruction, toxins, autoimmune
Urine ph remains high despite acidaemia
Forms renal stones
Hyperaldosteronism causes k loss

Type 2 - impaired reabsorption of bicarb proximally
Hereditary, Fanconi syndrome, Vit d deficiency
Metabolic acidosis with inappropriately high urinary bicarb
Hypokalaemia

Type 4 - deficit in DCT cation exchange with h+ and k+ retention
Hyperkalaemia
Low aldosterone (addisons, adrenalectomy) aldosterone blockers eg acei or arbs

103
Q

Where is most potassium reabsorbed in the nephron? How much?

A

90% in pct and ascending loh

104
Q

Where is k secretion regulated in the nephron
How?

A

DCT and collecting duct principle cells
Increased aldosterone increases na reabsorption by inducing synthesis of luminal na channels. This increases basal NaKATPase increasing k gradient from cell to lumen. Aldosterone also increases NaKATPase. Finally aldosterone increases luminal k channels increasing membrane permeability to k

105
Q

What does increased filtrate flow do to potassium reabsorption

A

Proximal sodium retention due to diuretics result in more sodium for uptake at principle cells increasing k excretion and also more dilute k in urine (as more water) thus increase concentration gradient favouring k excretion.

106
Q

Factors that effect renal k secretion in DCT

A

Concentration of k in tubular cells
Activity of basal NaKATPase
Potassium perimability of the cell
Filtrate flow rate - faster flow equals lower k thus bigger gradient

107
Q

Where and how much ca is reabsorbed in the nephron

A

99%
65% in pct
Rest in thick ascending loh and DCT/collecting tubule

108
Q

How is most calcium reabsorbed from nephron

A

Paracellular diffusing through tight junctions

109
Q

How is calcium reabsorption controlled in the kidney

A

Parathyroid hormone and Vit d (calcitriol) stimulation of trancellular ca reuptake
Performed via basolateral caATPase and na ca counter transport and luminal ca channels

110
Q

Where in the kidney is phosphate reabsorbed
How is it controlled

A

80% pct
10% DCT

Under pth control via Transcellular transporters (luminal na phos cotransporter)

111
Q

What is the hormonal response to hypocalcaemia

A

Detected by parathyroid gland
Increased pth production
Stimulation of 25hydroxycholecalciferol to 1,25dihydroxycholcalciferol

112
Q

Actions of 1,25dihydroxychoelcalciferol

A

Increase renal reabsorption of ca and phos
Increase intestinal reabsorption of ca and phos
Increase bone mineralisation

113
Q

Actions of pth

A

Increase renal ca reabsorption
Increase renal phos excretion
Increase formation of 1,25dihydroxychoelcalciferol
Increase calcium release from bones

114
Q

effect of renal disease on calcium metabolism

A

Failure of hydroxylation of 25hydroxychoelcalciferol
Causes hypocalcaemia
Increased pth levels (secondary hyperparathyroidism)
Increased calcium release from bones causing osteomalacia
Increased phosphate renal excretion causing hypophosphataemia

115
Q

What is tertiary hyperparathyroidism

A

Secondary hyperparathyroidism that overdoes it and starts releasing pth autonomously independent of ca level causing effects seen in secondary but also with hypercalcaemia

116
Q

What is primary hyperparathyroidism

A

Innapropriate release of pth causing hypercalcaemia often secondary to cancer

117
Q

What is nephrotic syndrome

A

Proteinurea >3500mg per 24 hrs
Hypoalbuminaemia
Oedema
Hypercholestrolamia

118
Q

What is nephritic syndrome

A

Haematuria
Hypertension
Acute renal failure
Possible oedema

119
Q

What makes tubular cells vulnerable to hypoxia

A

Highly metabolically active
Supplied by peritubular capillaries which are second capillary bed.
Control of GFR (efferent constriction) reduces flow

120
Q

What can lead to acute tubular necrosis

A

Hypoxia
Hypotension
Myoglobin casts (rhabdomyolysis)

121
Q

What may cause acute tubular necrosis in anaesthetic practice?

A

Muscle trauma (eg pressure, electrocution)
Meds (muscle relaxants, statins)
Drugs (cocaine, ecstasy, amphet)
Metabolic emergencies (dka, hypothyroid)
Infection
Autoimmune muscle disease (poly/dermatomyositis)

122
Q

What is acute tublointersitial nephritis?
Causes

A

Inflammation - with eosinophilia, oedema, necrosis, fibrosis and atrophy
Often a drug reaction (can be infection)
Linked drugs include
NSAIDs
Aspirin
PPI
h2 antagonists
Diuretics
Penicillin, gentamicin, erythromycin

123
Q

When does acute kidney rejection occur post transplant

A

1-12 weeks

124
Q

What causes acute cellular rejection of kidney?

A

Alloantigens presented to cd4 cells producing cytokines stimulating B cell antibody release opsinoising graft cells resulting in
Phagocytosis
Complement
Platelet activation and thrombus formation
Neutrophil infiltration.

125
Q

Causes of chronic tubulointersitial nephritis

A

Infection
Toxins
Malignancy
Radiotherapy
Long term drugs eg lithium, immunosuppression
Autoimmune

126
Q

Triggers for renal stone formation

A

Excess substrate
Stagnation
Acidity
Forign bodies

127
Q

Types of renal stone

A

Triple phosphate - calcium ammonium and magnesium
Uric acid - uricosuria esp with acid urine
Calcium oxate - hypercalciuria with hyperoxaluria
Cystine - cystinuria

128
Q

What is the micturation reflex

A

Reflex from bladder to sacral spine
As bladder stretches increased reflex frequency and duration
When overcomes inhibitory signals from higher centres then relaxation of external sphincter, and contraction of detrusor

129
Q

What nerves are involved in micturation reflex

A

Afferents - parasympathetic splanchnic nerves
Efferent - parasympathetic nerves to detrusor and pudendal nerve to urogenital diaphragm (external sphincter)

130
Q

What occurs to micturation reflex with damage to sacral spinal cord

A

Retention and overflow incontenance

131
Q

What happens to micturation reflex with damage to higher centres

A

Loss of inhibitory signals so frequent micturation

132
Q

Mechanism and example of loop diuretic

A

Nak2cl inhibition in thick ascending loop of Henle
Furosemide

133
Q

Mechanism and example of thiazide diuretic

A

Inhibition of nacl cotransport in DCT
Bendroflumethiazide

134
Q

Mechanism and example of aldosterone antagonist

A

Inhibition of aldosterone in collecting tubules - na excretion and k retention
Spinonlactone

135
Q

Mechanism and example of renal sodium channel blocker

A

Inhibition of luminal na channels
Amiloride

136
Q

Mechanism and example of carbonic anhydrase inhibitor

A

Inhibits bicarb reabsorption
Acetazolamide

137
Q

Mechanism and example of osmotic diuretic

A

Increases osmolarity of tubular fluid
Mannitol

138
Q

Drugs used in suppression of immune response to transplant

A

Alentuzumab - anti cd52 antibody - lymphocyte depletion
Methylpred - corticosteroid - anti inflammatory
Tacrolimus, cyclosporin - calcineurin inhibitor - cytokine blockade
Basilisimab, daclizumab - anti cd25 antibody for induction - cytokine blockade
Mycophonalte, azothiaprine - inhibition of lymphocyte dna synthesis - anti proliferation

Primary Physiology (15 decks)

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