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B1 > Kidneys > Flashcards

Kidneys Flashcards

1
Q

What are the 4 main functions of the kidneys?

A

Regulation of body fluid volume
Regulation of body fluid composition
Excretion of metabolic waste & toxins
Endocrine functions

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2
Q

What are the 4 key processes of the kidneys?

A

Filtration
Reabsorption
Secretion
All leading to urine formation and excretion

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3
Q

Outline the microstructure/components of the kidneys

A

Numerous uriniferous tubules and associated blood vessels:
nephron + collecting duct:
renal corpuscle + PCT + loop of Henle + DCT + collecting duct

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4
Q

What are the components of the renal corpuscle and what are the components of the filtration barrier?
What does filtration barrier limit passage of?

A

Renal corpuscle = glomerulus + bowman’s capsule

Fenestrated glomerular capillary endothelium
Negatively charged basement membrane
Podocytes with interdigitating foot processes

Limits passage of substances based on size, charge and shape

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5
Q

Outline the blood supply to the kidneys

A

Renal artery > Segmental arteries > Interlobar arteries > Arcuate arteries > Interlobular arteries which give off afferent arterioles to renal corpuscle

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6
Q

Blood to the kidneys passes through 2 capillary beds…

A

High pressure glomerular capillaries for filtration

Low pressure peritubular capillaries for reabsorption and secretion

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7
Q

Describe bowman’s capsule structure and function

A

Filters blood to form initial filtrate
Double walled cup surrounding glomerular capillaries
Outer parietal layer, simple squamous cells
Inner visceral layer, podocytes (modified simple squamous)

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8
Q

What happens in the PCT? What epithelium?

A

H20, Na+, Cl-, amino acids and glucose reabsorption
Secretion of drugs and waste molecules
Simple cuboidal with microvilli brush border

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9
Q

What’s the role of the loop of Henle? Outline the 3 parts

A

Generate hyperosmolar interstitium in medulla to concentrate urine

Thin descending limb - H20 permeable
Thin ascending limb - H20 impermeable
Thick ascending limb - H20 impermeable and active reabsorption of Na+

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10
Q

What happens in the DCT? Epithelium?

A

Variable H20 permeability dependent on ADH
Active reabsorption of Na+ and other solutes
Secretion of K+ and H+
Simple cuboidal cells

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11
Q

What part of the nephron is the JGA close to?

What are the 3 components of the JGA?

A

Distal tubule
Macula densa cells
Lacis cells
Granular cells in afferent arteriole

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12
Q

What’s the role of the collecting duct? Epithelium?

A

Final site for urine processing - regulates degree of urine concentration
H20 permeability controlled by ADH
Simple columnar cells

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13
Q

What are the different body fluid compartments? How much of body weight is roughly fluid?

A

In 70kg male 42L, 60% bodyweight

Different compartments separated by semi permeable membranes

Intracellular fluid - 28L (in cells)
Extracellular fluid - 14L
Extracellular fluid has 2 compartments: interstitial fluid surrounding cells and plasma which is non-cellular component of blood

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14
Q

What are the main cations and anions in ECF and ICF?

A

ECF: NA+ and Cl-

ICF: K+ and PO4-

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15
Q

Define the glomerular filtration rate and what is it determined by?

A

GFR = the volume of filtrate formed by all the nephrons in both kidneys per unit time

Determined by: glomerular capillary filtration coefficient (Kf) and net filtration pressure (NFP)

GFR = Kf x NFP

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16
Q

What does GFR Kf (filtration coefficient) represent?

How will this alter GFR in disease states?

A

The surface area available for filtration and the hydraulic conductivity (permeability) of the barrier

Changes in Kf aren’t major part of physiological regulation by may be affected in disease processes
Reduced number of nephrons will reduce surface area or reduce permeability and therefore decrease GFR

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17
Q

Define NFP (net filtration pressure) in the kidneys

A

The sum of pressures acting across the filtration barrier (starling forces)

Sum of hydrostatic pressures and sum of colloid osmotic pressures, typical NFP is 10mmHg

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18
Q

What’s the significance of hydrostatic and colloid osmotic (oncotic pressures) within the kidneys?

A

Hydrostatic pressure is that exerted upon the walls of the kidneys (glomerular capillaries) from the fluid within

Osmotic pressure is that exerted by proteins in glomerulus, exerting pull to stop fluid moving across

Higher hydrostatic pressure to drive net movement of fluid out of glomerular capillaries into bowman’s capsule

Most physiological regulation changes hydrostatic pressure (PG) as it depends on: arterial pressure, afferent and efferent arteriole resistance

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19
Q

What’s the link between afferent and efferent arteriole resistances in determining GFR?

A

Afferent arteriole dilation and efferent arteriole constriction increases GFR

Efferent arteriole dilation and afferent arteriole constriction reduces GFR

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20
Q

What vasoactive substances can regulate GFR and to what effect?

A

Dilating afferent arteriole and increasing hydrostatic pressure and therefore GFR:
Angiotensin II, prostaglandins and ANP

Reducing hydrostatic pressure by constricting the afferent arteriole and therefore reducing GFR:
NA, adenosine, endothelin

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21
Q

Briefly outline the two mechanism of autoregulation which prevent large changes in renal excretion of water and solutes across a range of systemic blood pressures

A

Myotonic autoregulation - ability of smooth muscle in afferent arterioles to respond to changes in vessel circumference by contracting/relaxing by Ca2+ channels activated by stretch

Tubuloglomerular feedback- uses JGA macula densa cells to respond to changes in NaCl concentration of own tubule lumen to alter resistance of afferent arteriole

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22
Q 
What clinical signs will renal dysfunction of the following lead to:
Regulation of body fluid volume?
Regulation of body fluid composition?
Excretion of metabolic waste and toxins?
Endocrine functions?
A

Hypertension/oedema

Electrolyte disorders
Acid base disorders

Uraemia
Drug toxicity

Anaemia
Renal bone disease

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23
Q

What investigations can be done for kidney disorders?

A

Urine - look at what’s being filtered/excreted
Blood - urea, creatinine, eGFR/GFR, Na+, K+
Imaging - ultrasound, CT, MRI, contrast studies
Biopsy

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24
Q

What are some indicators of renal decline?

A

Proteinuria - damage to filtration barrier, indicated by urine dipsticks
Haematuria
eGFR
Serum creatinine/urea

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25
Q

GFR is accepted as the best overall index of kidney function - how is it measured and what are the caveats?

A

Linked to surface area of body, age, sex and declines with increasing age
Hard to measure directly

Measured using renal clearance (volume of plasma from which a substance is completely cleared by kidneys per unit time)

For any substance that is only filtered (so fully enters urine) clearance = GFR

Can use inulin or radioisotopes but that’s technically difficult

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26
Q

Outline how creatinine clearance is used to calculate GFR

A

Creatinine is produced by the body, so easier to use than inulin/radioisotopes

Creatinine is breakdown of creatin (skeletal muscle component) as is freely filtered at glomerulus and not reabsorbed but a small amount is secreted meaning creatinine clearance will overestimate GFR = eGFR

Requires 24 hours urine collection so issues with compliance, time, reliability

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27
Q

What can you test in blood serum to assess kidney function? What would it indicate?

A

Serum urea and serum creatinine

If something that’s normally filtered by the kidneys builds up in the blood it indicates reduced GFR and therefore reduced renal function

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28
Q

Large proportion of AKI is drug induced. Why are the kidneys highly susceptible to drug induced damage?

A

Vascularity
Large surface area for binding/transport
Reabsorption of H20 from kidneys concentrates some drugs in the nephron
Main route of excretion for most drugs

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29
Q

Should consult BNF for drug dose adjustments in renal impairment or what other circumstances? Uses eGFR

A

Elderly patients >75 years
Toxic drugs
Patients of extreme weights

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30
Q

How does urine pH influence speed of drug excretion?

A

Most drugs are either weak acids or weak bases

In alkaline urine acidic drugs are more readily ionised, in acidic urine alkaline drugs are more readily ionised

Ionised substances are more soluble in water, so easier to be excreted by the kidneys

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31
Q

What is a diuretic and how do they work?

A

A substance that promotes the formation and excretion of urine, mainly by promoting renal excretion of sodium (natriuresis)

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32
Q

Why is it sometimes a good idea to combine loop diuretics or thiazides, with potassium sparing diuretics?

A

Eg co-amilofruse or co-amilozide
Prevents large losses of K+ but must beware of K+ retention
Loop diuretics increase amount of NaCl delivered to distal nephron

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33
Q

What is an ICIQ-IU form and what does it tell you?

A

Structured incontinence questionnaire - how much urine you leak, when and how much it bothers the patient
Allows you to establish the degree of urinary frequency and at night which can be indicative of underlying problems eg diabetes

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34
Q

What’s the definition of osmosis? What are osmoles?

A

Movement of water across a semi-permeable membrane from an area of low solute concentration to a region of high solute concentration

Osmoles = number of osmotically active particles in a solution

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35
Q

What’re the main osmotically active electrolytes in ECF and ICF?

A

ECF Na+

ICF K+

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36
Q

Where is EPO produced and what’s its role?

A

By interstitial cells in cortex and outer medulla
It’s a growth factor that stimulates production of RBC precursors in bone marrow (proerythroblasts from haemoatopoetic stem cells)
Released in hypoxic situations

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37
Q

What type of anaemia will kidney disease result in and why?

A

Normocytic normochromic anaemia

Reduced kidney function will reduce production/release of EPO for RBC production

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38
Q

What’s the role of the kidneys in vitamin D activation? What’s the implication of this in kidney disease?

A

Kidney produces enzyme 1a-OHase which converts 25(OH)D -> 1,25(OH)2D (calcidiol->calcitriol) the active form for absorption

Patients with renal failure = develop renal bone disease as unable to produce the enzyme and unable to absorb sufficient Ca2+ from diet

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39
Q

Why is reabsorption favoured in the peritubular capillaries (after blood leaves efferent arteriole)?

A

Lower hydrostatic pressure + higher colloid osmotic pressure = reabsorption, rather than filtration is favoured

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40
Q

Why is it important that renal blood flow and GFR are relatively constant across a range of blood pressures? Which pressures?

A

80-180 mmHg

To prevent large changes in renal excretion of water and solutes

41
Q

What are the caveats to using creatinine for eGFR as a measure of kidney function? (think about different muscle mass)

A

Rate of creatinine production varies between individuals
Age, sex, malnutrition, amputation, muscle wasting and ethnicity all affect muscle mass

Normal muscle mass will show marked increase in serum creatinine levels in kidney disease

Increased muscle mass will show increased creatinine, even though kidney function may be normal

Reduced muscle mass will show ‘normal’ serum creatinine even though kidneys may be diseased, therefore not picking it up

42
Q

What’s urea and what effect does it have on GFR?

What are blood urea levels affected by?

A

Nitrogen containing metabolic waste product from protein metabolism
Filtered but partially reabsorbed, therefore will underestimate GFR

High protein diets, increased catabolism, GI bleed and some drugs all increase serum urea

43
Q

Why should you compare serum urea to serum creatinine?

A

If both are increased then likely there’s renal impairment (fall in GFR)
If urea is higher, likely: dehydration, GI bleed, catabolic state (trauma, infection, surgery, cancer), high protein diet

44
Q

What are MDRD and CKD-EPI?

A

Modifications to eGFR equations
MDRD - modification of diet in renal disease
CKD-EPI - CKD epidemiology (NICE recommended)

45
Q

What are two qualities of tubular reabsorption?

A

Quantitatively large and highly selective, allowing independent regulation of solute excretion

46
Q

Which particular channel/transporter maintains the concentration gradient for reabsorption throughout the nephron?

A

Na+/K+ ATPase on basal membrane of tubular epithelial cells

47
Q

Where does the majority of reabsorption occur? What are the properties of this part of the nephron to facilitate this?

A

Proximal tubule (PCT)
Plenty of mitochondria for energy
H20 permeable so can follow solute reabsorption
Filtrate is isosmotic
Main site of glucose and amino acid reabsorption

48
Q

What’s the mechanism of glucose and amino acid reabsorption?

A

In PCT
SGLT2 sodium glucose co-transporters on luminal side move glucose against its concentration gradient
GLUT transporters on basal membrane allow facilitated diffusion into interstitial fluid

Amino acids are co-transported with Na+ on luminal side then diffuse through basal membrane

49
Q

What causes osmotic diuresis?

A

Finite number of SGLT2 transporters
If glucose concentration in filtrate increases the transport maximum (Tm) will be reached meaning no more glucose can be reabsorbed so the rest will be lost, with H20 following in the urine

50
Q

How are H+ ions excreted?

A

Secreted by NHE (sodium, hydrogen exchanger) on luminal membrane into the tubule lumen to be lost in filtrate

Important for HCO3- reabsorption in the PCT

51
Q

Outline reabsorption in the loop of Henle

A

Thin descending limb: H20 permeable but no active reabsorption or secretion
Thin ascending limb: H20 permeable, no active reabsorption or secretion = dilutes filtrate

52
Q

How does the thick ascending limb contribute to dilution of filtrate in the tubule lumen?

A

H20 impermeable but actively reabsorbs/secretes Na+ and other solutes = H20 unable to follow therefore luminal fluid becomes hypo-osmotic

Na+ reabsorption by Na+/K+/2Cl- cotransporter
Paracellular diffusion of positive electrolytes due to positive charge of lumen

53
Q

What co-transporter is on the luminal membrane of the early distal tubule?

A

Na+/Cl- co-transporter to further dilute tubule lumen fluid

54
Q

What are the similar functional characteristics of the distal convoluted tubule and the cortical collecting duct?

A

Permeability to H20 is controlled by ADH hormone

Principal cells Na+ reabsorption and K+ secretion (ENaC)
Intercalated cells K+ reabsorption and H+ secretion

55
Q

What are ENaCs and how is their activity controlled?

A

Epithelial sodium channels, found on luminal side of DCT/Collecting duct epithelial cells

Aldosterone (activated by angiotensin II to indirectly regulate bp) unregulated number of ENaC and Na+/K+ ATPase activity

56
Q

What hormones can regulate tubular processes?

A

Aldosterone (increases reabsorption in CD)
ADH (increases reabsorption in DCT and CD)
ANP (reduced NaCl reabsorption on DCT and CD)
Angiotensin II (increases reabsorption in PCT, DCT and CD)
PTH (increase Ca2+ reabsorption and reduces PO4 reabsorption in PCT and DCT)

57
Q

What’s pressure diuresis/natriuresis? What’s is good for?

A

Ability of kidney to increase urine output (diuresis) / increase Na+ excretion (natriuresis) in response to increases in arterial blood pressure

Simple way to control bp/Na+ to maintain blood volume over a wide range of pressures

58
Q

What does the JGA secrete, in response to what?

A

Granular cells in the juxtaglomerular apparatus secrete Renin in response to low ECF or low NaCl, to increase Na+ reabsorption and therefore H20 reabsorption and restore ECF volume

59
Q

What are the 3 main triggers for Renin release?

A

Low afferent arteriole pressure
Low [NaCl] in early distal tubule
Activation of sympathetic nerves that supply JGA

60
Q

Where is Aldosterone secreted from and how does it mediate its effects?

A

Zone glomerulosa in the adrenal cortex in response to increased Angiotensin II or increased extracellular [K+]

Binds to intracellular mineralocorticoid receptors in principal cells, to up regulate expression/activity of ENaC and Na+/K+ ATPase

61
Q

Where is Atrial Natriuretic Peptide secreted from and in response to what?

A

Atrial muscle fibres in response to atria stretch (increased blood vol)
Inhibits Na+ and H20 reabsorption in the kidney

62
Q

What’s the normal range for extracellular K+

A

3.5 - 5.3 mmol/L

63
Q

Outline hypokalaemia

A

When extracellular [K+] is below normal range
Caused by: reduced dietary intake, diuretics, severe diarrhoea, altered body distribution
Symptoms: muscle weakness and cardiac arrhythmias
Treatment: find underlying cause and K+ supplements

64
Q

Outline hyperkalaemia

A

When extracellular [K+] is above normal range
Caused by: excessive intake, inadequate loss (kidney disease, aldosterone deficiency, insulin deficiency - diabetes), acidosis
Symptoms: cardiac arrhythmias, tall T waves on ECG
Treatment: find underlying cause, restrict intake, calcium gluconate, insulin

65
Q

What drives K+ into cells? What increases extracellular K+ to rise?

A 
Into cells:
Insulin
Aldosterone
B-adrenergic stimulation
Alkalosis
Increase extracellular:
Cell lysis
Insulin deficiency 
Aldosterone deficiency (Addison's disease)
B-adrenergic blockade
Acidosis
Increased extracellular fluid osmolarity
Strenuous exercise
66
Q

What 3 factors determine the rate of K+ secretion (and excretion)?

A

Na+/K+ ATPase activity
[K+] gradient between blood, lumen and principal cell
Permeability of luminal membrane to K+

67
Q

What 4 factors regulate K+ secretion/excretion?

A

Plasma [K+]
Aldosterone
Tubular flow rate

[H+] increased, reduces Na+/K+ ATPase activity therefore reducing K+ secretion

68
Q

Which type of cell reabsorbs K+ when intracellular levels are depleted?

A

Intercalated cells in the DCT and collecting duct

Principal cells secrete K+, intercalated reabsorb it

69
Q

What are signs and symptoms of hypovolaemia?

A 
Dizziness on standing (postural hypotension)
Thirst
Confusion
Low JVP
Weight loss
Reduced urine output
Dry mucous membranes
70
Q

What are signs and symptoms of hypervolaemia?

A 
Oedema/ankle swelling
Breathlessness
Raised JVP
Weight gain
Hypertension
71
Q

As well as body fluid volume, why must osmolarity be regulated?

A

To avoid excessive movements between cell compartments and cell swelling and dehydration

72
Q

What’s the obligatory urine volume?

A

The minimum volume of urine that needs to be produced each day to excrete waste solutes, usually 0.5L a day

73
Q

What’s the equation for osmoles of urine excreted/day?

A

Osmoles excreted = urine osmolarity x urine output

74
Q

What’s polyuria and oliguria?

A

Polyuria - increased urine volume (increased water ingestion, inability to concentrate urine, diabetes or due to increased solute excretion: diuretics and glycosuria)

Oliguria - reduced urine volume due to reduced water or solute excretion (due to dehydration, low ECF vol, poor renal perfusion)

75
Q

Where is ADH produced and released from?

A

Supraoptic and paraventricular nuclei in the hypothalamus

Released from posterior pituitary by exocytosis

76
Q

How does ADH increase water reabsorption?

A

ADH released into bloodstream
Binds to Vasopressin 2 receptor on basal membrane
Inside cell: ATP -> cAMP -> PKA = phosphorylation of vesicles with inactive water channels
Vesicles fuse with apical membrane and AQP2 (active water channels) allow reabsorption of water

77
Q

What does the osmotic potential of the kidney depend on and how?

A

Urea and NaCl - high concentration of these drives H20 reabsorption

78
Q

How does urea contribute to the osmotic gradient of the kidneys?

A

It’s recirculated and because some areas have higher permeability it becomes trapped within the medullary interstitium

79
Q

What is the counter current mechanism? What 4 things contribute to it and what’re the 2 results?

A

= method by which medullary interstitium is concentrated

Hairpin arrangement of loop of Henle
Fluid moving in opposite directions in the LoH limbs
Different H20 permeabilities of the 2 limbs
Ability of Na+/K+/2Cl- cotransporter to actively transport against its gradient

= dilute filtrate and large increase in [NaCl] in medulla to increase osmotic gradient

80
Q

Outline Syndrome of Inappropriate ADH

A

Causes: pneumonia, meningitis, small cell lung carcinoma
Effects: inappropriate water reabsorption (low plasma osmolarity and low serum Na+, may cause cerebral oedema) and urine really concentrated
Treatment: restrict fluid intake, ADH inhibitors

81
Q

Outline Diabetes Insipidus

A

Too little ADH = inability to effectively reabsorb H20
Causes: Cranial DI (don’t produce ADH - trauma, surgery, infections) or Nephrogenic DI (renal tubules insensitive to ADH)
Effects: polyuria, thirst and polydipsia, low urine osmolarity, high serum Na+
Treatment: adequate fluid intake, synthetic ADH if cranial DI, drugs to sensitise tubules to ADH in nephrogenic DI

82
Q

Define AKI

A

Acute Kidney Injury = significant deterioration in renal function, which is potentially reversible over a period of hours/days

83
Q

Outline 3 causes of AKI - which is the most common?

A

Pre-renal failure (85%) - renal hypo perfusion (sepsis, hypovolaemia, renal artery stenosis, drugs like ACEi/NSAIDs)

Intrinsic renal failure - primary renal disease, secondary renal disease, interstitial nephritis, secondary acute tubular necrosis

Post-renal failure - obstruction/blockage of the kidneys (stone/tumour)

84
Q

What are important clinical features to look for in AKI?

A

Fluid status: JVP, oedema, peripheral perfusion, tissue turgor, mucous membranes/tongue, pulse rate/rhythym/volume

Signs of sepsis: fever, tachycardia, tachypnoea

85
Q

What should you look for in a urine dipstick for renal dysfunction?

A 
Microscopic haematuria
Proteins
Leucocytes
Nitrites
Urine vol output
86
Q

What are some ECG changes of hyperkalaemia?

A

Peaked T waves
Prolonged P-R interval
Prolonged QRS duration
Loss of P waves

87
Q

What are some common risk factors for AKI?

A 
Age
Co-morbidity
Medication
Previous CKD
Hypovolaemia
Sepsis
Biochemistry
Urinalysis
Weight
Nurtitional status
88
Q

What’re the basic differences between AKI and CKD?

A

AKI: reversible lasting hours/days
CKD: irreversible lasting months/years (>90d)

89
Q

When is CKD classified as kidney failure?

A

GFR<15 (dialysis and organ replacement required)

90
Q

What are complications of CKD?

A 
Cardiovascular disease
Hypertension
Anaemia
Bone-mineral metabolism
Poor nutritional and functional status
Progression of CKD -> kidney failure
91
Q

How is CKD measured?

A

Test renal excretory function - albuminuria/proteinuria

92
Q

How is significant CKD progression defined?

A

25% decrease in GFR over 12 months

93
Q

What are risk factors for CKD progression?

A 
Hypertension
DM
Albuminuria
Cardiovascular disease
Smoking
Ethnicity
NSAIDs
94
Q

What are socpop factors associated with renal replacement therapy?

A 
Geographical distance from house
Space/cleanliness of house for home therapy
Work
Family/social support
Mobility
Nutritional status
95
Q

What are 4 types of renal replacement therapy?

A

Haemodialysis (home, satellite, hospital)
Peritoneal dialysis
Transplantation
Conservative care

96
Q

What are types of organ transplant?

A

Deceased donor transplant
Brain dead donation
Live donation

97
Q

How will eGFR be different to that expected in someone with:
Amputation/muscle wasting disorder/malnutrition

Bodybuilder taking creatine supplements

A

Amputation = incorrectly high eGFR (massively overestimated)

High muscle mass/supplements = underestimates eGFR

= eGFR calculation doesn’t take things like this into account

98
Q

What’s Diabetes Insipidus? What are the two categories and their causes?

A

DI = too little ADH = inability to reabsorb H20 from distal nephron either due to inadequate production (cranial DI) or insensitivity (nephrogenic DI)

Cranial DI: head trauma, tumour, infection
Nephrogenic: electrolyte imbalance (high Ca2+, low K+)

99
Q

What are effects of large losses of H20 in urine?

A

Polyuria
Increased thirst
Low urine osmolarity = dilute
High plasma osmolarity (serum Na+)

B1 (19 decks)

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