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Medicine Year 2 > Repro Topic 6 - Kidney > Flashcards

Repro Topic 6 - Kidney Flashcards

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1
Q

How long is the PCT?

A

14 mm

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2
Q

What is the function of the PCT?

A
  • 70% reabsorption - microvilli increase surface area
  • Mostly active transport, almost everything moves with sodium (partially controlled by angiotensin II)
    • SGLT2 - active sodium and glucose reabsorption
    • Sodium and amino acid reabsorption
    • Sodium + sulphate/phosphate reabsorption
    • Sodium-hydrogen antiporter - sodium reabsorbed, hydrogen secreted
    • Basolateral Na+/K+ ATPase pumps sodium back into circulation
    • Aquaporin 1 - water movement due to osmotic gradient
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3
Q

How is H+ concentration maintained?

A
  • Acid-base balance
  • ECF and ICF equal, has to be kept within tight range
  • Typical western diet - net acid
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4
Q

How can kidney function be calculated?

A
  • MDRD formula used in labs
  • Cocheroft-Gault for prescribing - based on creatinine clearance
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5
Q

Describe the function of the kidney in erythropoietin production

A
  • Secreted from interstitial cells of the kidney
  • Filters blood, have cells sensitive to low pO2
  • Low pO2, increased EPO production, increased red blood cell mass, increased tissue pO2
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6
Q

What is the macula densa and what is its function?

A
  • Where thick ascending LH meets DCT - in contact with the glomerulus
  • Sensitive to sodium chloride concentration - increases blood flow in afferent arteriole and increases renein release from juxtaglomerular cells ( on afferent/efferent arterioles) if sodium chloride concentration is low
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7
Q

What triggers aldosterone release?

A

Angiotensin II or high serum K+ concentration

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8
Q

What causes metabolic alkalosis?

A

Low H+ or high bicarbonate

  • Volume depletion -
    • Gastric acid loss (vomiting)
    • Diuretics
  • Volume repleted type
    • Mineral corticoids
    • Hyperaldosteronism
    • Bartler’s syndrome
    • Cushing’s syndrome
    • Profoud K+ depletion
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9
Q

How does the kidney contrubite to acid-base balance?

A
  • Reabsorbs filtered bicarbonate - mostly in PCT (also thick ascending LH and DCT), carbonic anhydrase converts H+ and bicarbonate to H2O and CO2 to move into cells and be reabsorbed
  • Filters non-volatile acids e.g. sulphuric - uses PO4 or NH3 to fix H+, excreted into urine as H2PO4 or NH4
  • PCT synthesises ammonium, glutamine and amino acids
    • 1 bicarbonate ion returned to circulation for every H+ excreted as ammonium
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10
Q

How can uric acid stones be prevented?

A
  • Increase fluid consumption
  • Treat hyperuricaemia with xanthine oxidase inhibitors e.g. Allopurinol/rasburicase (gout treatment)
  • Alkalinise urine (pH > 6.0) - bicarbonate/citrate
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11
Q

Describe creatinine metabolism in the kidneys

A
  • Breakdown product of creatinine phosphate - muscle metabolism
  • Freely filtered at glomerulus
  • Not reabsorbed
  • Minimal tubular secretion
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12
Q

Describe the body fluid compartments

A

Intracellular fluid = 2/3

Interstitial and intravascular fluid (extracellular) = 1/3

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13
Q

What is the maximum/minimum urine production per day?

A

Minimum urine output = 0.4L per day

Maximum urine output = 12L per day

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14
Q

Why is maintenance of Ca2+ concentration important?

A

For normal muscle and nerve function

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15
Q

What are the causes of kidney disease?

A
  • Ineffective blood supply - low plasma volume (e.g. due to haemorrhage) or narrowed renal arteries
  • Glomerular disease
  • Interstitial disease - tubules
  • Obstructive uropathy
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16
Q

What is typically found on examination in renal stones?

A
  • Flank tenderness when balloting the kidneys
  • Signs of infection
  • Obesity
  • Hypertension
  • Gouty tophi - nodular masses, urate deposits
  • Diabetes mellitus
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17
Q

How is urine examined?

A
  • Visual inspection
  • Dipstick analysis
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18
Q

What are struvite renal stones composed of?

A

Magnesium ammonium phosphate

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19
Q

Describe the mechanism of action of Thiazide diuretics

A
  • Inhibits NCC (Na+/Cl- symporter), inhibits reabsorption of sodium and chloride ions from the DCT
  • Also increase reabsorption of calcium ions
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20
Q

What drives the movement of ions in the Loop of Henle?

A

Countercurrent exchange multiplier

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21
Q

What pathologies can CT of the kidneys show?

A

Trauma, stones, tumour, infection, renal stones (location and type)

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22
Q

Describe lactic acidosis

A
  • Pyruvate converted to lactic acid which is converted to lactate, metabolised in liver/kidney
  • Acidosis due to hypoperfusion, low hepatic clearance (sepsis) or drugs e.g. metformin
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23
Q

What is the cause of acidosis?

A

High H+ or low HCO3-

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24
Q

In what type of patients are loop diuretics the diuretic of choice?

A

Those with impaired renal function

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25
How can cysteine stones be prevented?
* Increase fluid intake * Low protein/sodium diet * Alkalinise - bicarbonate/citrate
26
How are renal stones in the ureter treated?
* Small * Expectant management * Lower ureter - uteroscopic stone removal * Mid/upper - extracorporeal shock wave lithotripsy (ESWL) * Large (\>7mm) * ESWL * Uteroscopic stone fragmentation * Open surgery
27
What is the effect of impaired renal function on drug excretion?
Drugs will be excreted very slowly
28
What is the function of the glomerulus/Bowman's capsule?
* Blood through afferent arteriole into the glomerulus at high pressure - controlled by sympathetic nervous system and prostaglandins * Blood flows through glomerulus tufts, fluid filtered into Bowman's capsule to produce filtrate * Molecules and water pass through pass through glomerular basement membrane, negative charge repels proteins * Large molecules don't get through
29
How is ureteric stenting used in the treatment of renal stones?
* Allows drainage of obstructed kidney - alleviate pain * Dilate ureter - passage of stone? * Better ESWL and uteroscopic outcomes
30
How can calcium oxalate stones be prevented?
* Increase fluid * Low oxalate diet * Citrate * Thiazide diuretic?
31
Describe urea metabolism in the kidney
* Urea is by-product of amino acid metabolism in liver * Reabsorbed in inner medullary collecting ducts (passively) * Involved in countercurrent exchange and maintaining concentration gradient
32
Which drugs can cause renal papillary necrosis?
* Aspirin * NSAIDs
33
Can a low calcium diet be used to prevent calcium containing renal stones?
No - no good evidence
34
What kind of ion channels are present in the thick ascending limb of the loop of Henle?
* NKCC2 channel - active reabsorption of Na+, K+, Cl- (two chloride ions for every one sodium/potassium) * Blocked by loop diuretics - more Na+ excreted, more water excreted * Gradient maintained by basolateral Na+/K+ ATPase
35
What is the potential consequence of respiratory alkalosis?
Causes increased albumin binding to calcium, therefore lowers ionised calcium leading to tentany
36
What is the typical history of a patient with renal stones?
* Renal colic (flank pain) - moves loin to groin * Passage of stones * Haematuria * Infection * Family history, diet
37
Describe the components of acid-base balance
* Buffering * Ventilation - control of CO2 * Renal regulation of HCO3- and H+ secretion/reabsorption
38
In which drugs does enhancement of adverse effects occur in renal impairement?
* Digoxin * Potassium-sparing diuretics * Biguanides (metformin) - lactic acidosis * Sulphonylureas - hypoglycaemia
39
How does the kidney process lipid soluble drugs?
Lipid soluble drugs passively reabsorbed by diffusion - not usually excreted in urine
40
List the functions of the kidney
1. Removing metabolic waste from extracellular fluid - urea, acids 2. Controlling volume of extracellular fluid (and therefore blood pressure) 3. Maintaining optimal concentration of solutes in the extracellular fluid (Na+, K+, H+, Ca2+, Mg, Cl-, phosphate) 4. Extra functions e.g. erythropoietin production
41
Describe the venous drainage of the kidneys
* Left and right renal veins * Leave hilum anterior to arteries, drain to inferior vena cava * Left is longer, passes anterior to abdominal aorta
42
What causes calcium-containing stone formation?
Primary hyperparathyroidism Hypercalcaemia Idiopathic hypercalciuria
43
How can struvite stones be prevented?
* UTI treatment * Bacteria increases urease enzymes - produce ammonium * E.g. proteous spp, staph spp, Klebsiella spp.
44
45
What is the function of the loop of Henle?
Reabsorbs 20% of Na+ and large amounts of water
46
Which drugs have decreased sensitivity in renal impairment?
* Diuretics * Urinary antibacterials
47
What is the physiological response to acidosis?
* Increased ventilation (shifts equilibrium) * Kidney - increased hydrogen secretion, increased bicarbonate reabsorption * Other buffers - haemoglobin, proteins, bone, PO4 - absorb H+
48
List the types of diuretics and give examples of each
* Loop e.g. Bumetanide, Furosemide * Thiazide e.g. Bendroflumethazide, Indapamide * Potassium sparing e.g. Amiloride, spironolactone
49
How are renal stones within the kidney treated?
* \<2cm - expectant management or offer extracorporeal shock wave lithotripsy (ESWL) * \>2cm or multiple - expectant management or percutaneous ultrasonic lithotripsy (PUL) * Large branched 'staghorn' stones - ESWL + PUL * Cysteine stones - PUL or open nephrolithotomy
50
What may be the consequence of maintaining [H+]?
May be at the expense of other abnormal blood chemistry e.g. [HCO3-], pCO2
51
Describe the release of anti-diuretic hormone
High serum osmolality and/or decreased stretch baroreceptors/atrial stretch causes increased ADH synthesis in the hypothalamus, released by the posterior pituitary
52
Describe secondary prevention of renal stones
* If multiple stones in 10 years * Increase fluid intake, increase citrate, stone-type specific advice
53
How can the cause of metabolic acidosis be determined?
* Use anion gap to identify likely cause * High anion gap - high acid production, chronic renal failure * Low anion gap - loss of bicarbonate = some cases of chronic renal failure, renal tubular acidosis
54
List drug induced glumerulonephropathies
* Membraneous * Castopril, Gold salts, heavy metals, penicillamine, phenytoin * Minimal change * NSAIDs (stop synthesis of prostaglandin for vasodilation of afferent arteriole) * Acute nephritis - penicillin
55
Describe the typical dialysis regime of a patient with chronic kidney disease
3x per week, 4/5 hours per session
56
How do the kidneys interact with the circulation?
* Baroreceptors (pressure) - carotid sinus, aortic arch, cardiac chambers, afferent arteriole of glomerulus * Detect changes, respond via sympathetic nervous system * If the ECF is depleted, baroreceptors detect change in BP, sympathetic stimulation causes afferent arteriole vasoconstriction to increase the volume of the ECF
57
What is the compensatory response to metabolic alkalosis?
Hypoventilation - increase pCO2
58
Define renal stones
* Also called renal calculus or nephrolithiasis * Solid concretion of crystal aggregate formed within the urinary space
59
What problems does impaired renal function cause in drug therapy?
Toxicity due to increased sensitivity or ineffective treatment due to decreased sensitivity * Impaired absorption * Impaired elimination * Renal dysfunction effect on hepatic drug elimination * Increased tissue sensitivity * Protein binding
60
What is the physiological response to increased sensed volume?
Natruiretic peptides (ANP, BNP) - opposite effect to angiotensin II
61
What is the function of the collecting tubules and how is it regulated?
* Collect and concentrate urine from the nephrons * Hormonal control - anti-diuretic hormone via AQP2 and aldosterone
62
What causes urate stone formation?
Hyperuricaemia
63
How is the action of rifampicin changed in impaired kidney function?
Metabolised by liver, half-life same in CKD
64
Which are the most common types of renal stones?
Calcium containing (phosphate or oxalate)
65
What is the function of the juxtaglomerular apparatus?
Maintain glomerular filtration rate
66
Describe the structure of the glomerular filtration barrier
* Specialised capillary endothelium - fenestrated * Glomerular basement membrane is collagen based * Podocytes (foot processes)
67
What is the first warning sign of acute tubular necrosis?
Oliguria
68
What is ENaC?
* Epithelial sodium channel - selectively permeable to sodium ions * Located in the apical membrane of polarised epithelial cells of the kidney, particularly in the collecting ducts
69
What does proteinuria indicate?
Consistent = glomerular disease One off = heavy exercise/infection
70
What is the response of the juxtaglomerular apparatus to decreased tubular flow?
Juxtaglomerular cells produce renin
71
Describe the acid-base balance equation
H+ + HCO3- \<--\> H2CO3 \<--\> H2O + CO2 HCO3- - buffer, absorbs H+, kidneys regenerate CO2 exhaled
72
List the ideal characteristics of drugs to be used in CKD
* Predominant hepatic/biliary elimination * Less than 25% excreted unchanged * No active metabolites * Wide therapeutic margin * Disposition unaffected by protein binding changes or by fluid balance changes * Response unaffected by tissue sensitivity changes * Not nephrotoxic
73
How is the tubular flow rate detected?
By the macula densa - detects changes in the DCT
74
What is the physiological response to reduced sensed volume?
Oliguria, concentrated urine, decreased Na+ concentration, K+ excretion
75
What is tested for in dipstick urinalysis?
* Protein (albumin) * Haemoglobin (indicates presence of blood) * pH * Ketones * Glucose * Bilirubin * Leukocytes, nitrites (inflammation/infection)
76
What are the clinical uses of thiazide diuretics?
Hypertension, oedema, hypercalcuria, nephrogenic diabetes insipidus
77
Describe the mechanism of action of loop diuretics
* Act on thick ascending loop of Henle - inhibits the NKCC2 channel * Inhibits sodium, potassium and chloride reabsorption - more water excreted * Acts by competing for the Cl- binding site * Also causes increased renin secretion, increased glomerular perfusion and so GFR * Inhibits magnesium and calcium reabsorption in the thick ascending limb
78
What kind of junctions are present between the cells of the PCT?
Tight junctions
79
What investigations should be done in suspected renal stones?
* Imaging - ultrasound (see acoustic shadow) * Serum and urine biochemistry - dipstick for protein, blood, leukocytes * Composition of stone - * Cysteine - low density * Struvite - low density * Calcium - high density
80
Describe examples of tubulo-interstitial diseases
* Congenital - autosomal dominant polycystic kidney disease, reflux nephropathy/chronic pyelonephritis, medullary cystic kidney disease, nephropthiasis, salt losing nephropathies (e.g. Bartler's syndrome) * Chronic nephrotoxic ingestion - analgesic nephropathy, lithium nephrotoxicity, chinese herb nephropathy, lead nephropathy * Autoimmune - sanoidosis, Sjogren's syndrome * Other - chronic bilateral recurrent caliculi, nephrocalcinosis, myeloma
81
What is respiratory acidosis?
High CO2 concentration, low pH
82
How can calcium phosphate stones be prevented?
* Increase fluid consumption * Citrate * Thiazide diuretic? - reduces calcium
83
What is the kidney's role in toxin metabolism?
* Metabolism of: * Insulin * Beta-2-microglobulin * Medicines
84
What kind of junctions are present between cells in the thin descending loop of Henle?
Loose junctions
85
What does ultrasound of the kidneys show?
Size, shape, location, structure, drainage/obstruction, blood flow, cysts
86
Describe the structure of the coverings of the kidney
Inner to outer: 1. Renal capsule - fibrous 2. Perirenal fat 3. Renal fascia - around kidney and adrenal gland 4. Pararenal fat
87
List diseases of the renal arterial supply which affect the main renal arteries
* Atherosclerotic renal artery disease * Fibromuscular dysplasia
88
What are the consequences of kidney failure?
* Excretion of solutes - high plasma concentration of urea/creatinine * Excretion of drugs - drug toxicity * Salt and water balance - extracellular fluid overload/depletion * BP control - hypertension * Electrolye balance - hyperkalaemia, hypokalaemia etc. * Acid-base balance - metabolic acidosis * Erythropoietin - anaemia * Vitamin D activation - hypocalcaemia and secondary hyperparathyroidism
89
Which drugs have the potential to cause Fanconi's syndrome?
Aminoglycosides, NSAIDs, paracetamol
90
Why is the kidney vulnerable to toxicity?
* Large blood flow * Drug and/or metabolites concentrate in renal medulla * Further concentration in tubular cells
91
What produces aldosterone?
Zona glomerulosa of adrenal cortex
92
What are the 'rules' which dictate the movement of ions/water in the loop of Henle?
* Thick ascending loop is impermeable to water, actively transports Na+, K+ and Cl-, providing a concentration gradient (fluid in intersitium becomes more concentrated that in thick ascending LH) * Thin descending LH - freely permeable to salt and water * Interstitium becomes concentrated due to movement of ions out of thick ascending LH, water moves out of thin descending LH into interstitium * Specialised blood vessel - vasa recta - winds around loop to take water from interstitium, doesn't wash away concentration gradient
93
What are the clinical uses of loop diuretics?
Oedema, acute renal failure, hypertension, hypercalcaemia
94
Describe the classification of chronic kidney disease
1. Kidney damage with normal or raised GFR, GFR \> 90 2. Kidney damage with mildly impaired GFR, GFR 80-60 3. Moderately impaired GFR, GFR 30-59 4. Severely impaired GFR, GFR 15-29 5. Established renal failure, GFR \<15 or on dialysis
95
List causes of metabolic acidosis
* Extra acid - lactic acidosis, ketoacidosis * Failure to excrete acid - renal tubular acidosis * Loss of HCO3 - stool (diarrhoea) or urine (renal tubular acidosis)
96
What is the function of the DCT?
* 5% sodium reabsorption * Main channel = NCC * Active Na+ and Cl- reabsorption, maintained by basolateral Na+/K+ ATPase * Blocked by Thiazide diuretics - more Na+ excreted, more water secreted * No hormonal control
97
How should drug prescription be altered if there is reduced elimination due to impaired renal function?
* Modify dose - decrease dose or increase dose interval (in drugs with 50% renal clearance and low therapeutic index) * Loading dose? * Monitor drug concentration
98
What are the effects of ADH?
* Increased thirst * Collecting duct AQP2 channel insertion * Vasoconstriction * = increased fluid retention, decreased serum osmolality, increased BP
99
Which organs contribute to drug metabolism?
Kidney and liver
100
Give examples of drugs whose action is affected by renal impairment
* Gentamicin, vancomycin * Antibiotics, metabolised fully in kidney * Toxicity and dosing altered in decreased kidney function * Take into accound gender, age, weight, height
101
How is K+ concentration maintained?
* Low plasma volume or increased plasma K+- renin-angiotensin system activated, K+ excreted * High or low potassium affects muscles and nerves - cardiac arrhythmias/paralysis
102
Why does hypocitraturia cause renal stone formation?
* Citrate is protective - prevents stone formation * Inhibits stone formation - increased by low Na+ diet, decreased by acidosis * Forms complexes with calcium * Increases activity of macromolecules which inhibit CaOx aggregation * Alkalinising effect - inhibits urate and cysteine stones
103
Where is aspirin secreted in the nephron?
PCT - weak acid (salicylic acid)
104
Define medullary sponge kidney
Congenital disorder of kidneys characterised by cystic dilation of collecting tubules of one or both kidneys - predisposes to stone formation
105
Describe the distribution of ions across the body fluid compartments
Sodium, calcium, chloride, bicarbonate = mostly ECF Potassium, magnesium, phosphate, sulphate = mostly ICF
106
What is the physiological response to respiratory acidosis?
Renal retention of HCO3-
107
What urinary environment predisposes to renal stones?
Renal tubular acidosis (type 1 diabetes) Hypocitraturia
108
Which drugs can cause interstitial nephritis?
* DCT and CT * NSAIDs * Penicillins * Sulphonamides * Thiazides * Vancomycin
109
What effect do NSAIDs have on renal function?
* Inhibit prostaglandins - for afferent arteriole dilation (maintenance of glomerular capillary pressure) * Present with fluid overload (oedema) and renal failure
110
What is the compensatory response to respiratory alkalosis?
Renal secretion of HCO3-
111
Which drugs can cause nephrogenic diabetes insipidus?
Lithium (affects CTs)
112
What are the clinical uses of potassium sparing diuretics?
K+-conservation, oedema, hyperaldosteronism, hypertension
113
What is the normal appearance of the kidneys on ultrasound?
* \<9cm is abnormal, \>1cm cortex normal * Should be less echobright than liver * Blood flow - renal artery/vein
114
What is metabolic acidosis?
Low bicarbonate ion concentration - low pH
115
What is the typical life-long effects of chronic kidney disease?
* Dialysis, transplant * Transplant can eventually fail so require dialysis again until new transplant can be found * Increasing cardiovascular risk (strokes, MI) throughout life, even with transplant
116
Where is the highest osmotic gradient in the loop of Henle?
Tip of the loop - increases down descending then decreases up ascending
117
Which drugs can cause renal tubular acidosis?
* Proximal CT - acetazolamide * Distal CT - amphotericin B, lithium
118
How can you tell that the kidneys are not functioning?
Low estimated glomerular filtration rate (eGFR) - below 60ml/min High creatinine within eGFR \>60ml/min range
119
What is the term for blood in the urine at what does it indicate?
* Haematuria * Visible (frank/gross) haematuria or microscopic haematuria * Source can be anywhere in urinary tract
120
Describe examples of glomerular diseases
* Diabetic glomerulopathy - thickening of tubules, damage to glomerular basement membrane, protein gets through * Acute glomerular disease - inflamed tissue, basement membrane damage * Cresentic glomerulonephritis e.g. antiglomerular basement membrane disease
121
What effect do ACE inhibitors have on renal function?
* Associated with reduced renal function * Bilateral renal artery stenosis * Especially with NSAIDs, diuretics or when dehydrated/septic * Prevent Angiotensin II production - unable to maintain glomerular capillary pressure (no vasoconstriction of efferent arteriole)
122
What is the volume of extracellular fluid dependent on?
Salt intake, water intake, salt and water losses
123
Describe examples of obstructive uropathy
* Bladder outflow - prostate hyperplasia, urethral stricture * Vesico-ureteric junction - bladder/cervical cancer * Uterus - ureteric calculi, retroperitoneal fibrosis
124
What causes respiratory acidosis?
Hypoventilation, leads to build up of CO2
125
How does ADH cause AQPII activation?
* ADH binds to V2 receptor * Activates cAMP on vesicles containing pre-formed AQPII * AQPII inserts on membrane - pure water channel, water pumped back into circulation via AQPI
126
Describe the structure of the nephron
* Afferent arteriole into glomerulus, surrounded by Bowman's capsule * Proximal convoluted tubule * Loop of Henle * Thick descending, thin descending * Thin ascending, thick ascending * Distal convoluted tubule * Collecting duct
127
What causes reduced sensed volume by the juxtaglomerular apparatus?
* ECF depletion * Haemorrhage * Vasodilation * Heart failure
128
How is proteinuria quantified?
Using creatinine:protein ratio in urine
129
What pathologies can be seen on MRI of the kidneys?
Tumour, infection, cysts, renal vasculature, fistulas, stenosis
130
What effect does aldosterone have?
* ENaC insertion in cortical collecting duct, sodium reabsorption and potassium excretion (maintained by basolateral Na+/K+ ATPase) * Uses renal outer medullary potassium channel (ROMK) to pump potassium out * Site of action of potassium sparing diuretics - blocks mineralocorticoid receptor that aldosterone binds to - no ENaC insertion = water loss, high K+ as not excreted
131
How long is the DCT?
1mm
132
What kind of channels are present in the thin descending loop of Henle?
AQP1 - no hormonal control
133
What is the response of the juxtaglomerular apparatus to increased tubular flow?
* Produces adenosine * Efferent arteriole constriction, Na+/water reabsorbed
134
What is the action of each class of diuretics in renal failure?
* Loop = effective * Thiazide = ineffective * K-sparing = dangerous
135
What causes respiratory alkalosis?
Hyperventilation - low pCO2
136
Describe the anatomical position of the kidneys
* Retroperitoneal, T12-L3 * R lower due to liver * Adrenal glands immediately superior * Morrison's pouch between R kidney and liver
137
Describe the mechanism of action of potassium-sparing diuretics
* Block ENaC, more sodium ion excretion so more water excretion * Antagonist for aldosterone - prevents synthesis of proteins produced in response to aldosterone * Prevents sodium reabsorption and potassium/hydrogen ion secretion in the late distal tubule and collecting duct
138
How are renal stones classified?
* By location * Kidney - nephrolithiasis * Ureter - ureterolithiasis * Bladder - cystolithiasis * By composition * Calcium phosphate * Calcium oxalate * Urate * Cysteine * Struvite * Uric acid * Mixed
139
What are the side effects of Thiazide and Loop diuretics?
* Non-specific - GI upset (nausea, vomiting), hypersensitivity reactions (rash), thrombocytopaenia * Metabolic - hypokalaemia, urate retention, glucose intolerance * Specific - ototoxicity (high dose loop)
140
What does radiosotope scanning of the kidneys show?
Structure, perfusion
141
Define acute and chronic kidney disease
Acute - 1-2 weeks Chronic - 3+ months
142
How is CT of the kidney enhanced?
* Contrast enhanced - perfusion/excretion * Potentially nephrotoxic, weigh up risk vs benefit * Avoid if GFR \< 30mL/min * Risk lowered by pre-hydration
143
Which drugs can cause damage to the PCT, loop of henle and collecting ducts?
Methotrexate, sulphonamides, omeprazole
144
Describe the systemic effects of metabolic acidosis
* Symptoms related to cause * CVS - arrhythmias, reduced cardiac contractility, vasodilation * Respiratory - increased ventilation (Kussmaul's breathing) * Metabolic - protein wasting, resorption of Ca2+ from bone
145
What is the functional unit of the kidney?
Nephron
146
List the processes which occur in the nephron
1. Glomerular filtration - blood filtered to glomerular filtrate 2. Tubular reabsorption (into the blood) 3. Tubular secretion - blood to tubular fluid
147
How do the kidneys compensate for ineffective blood supply?
* Baroreceptors detect low blood supply, causes sympathetic outflow * Efferent arteriole constriction due to reduced sensed bloodflow at macula densa * Renin production by juxtaglomerular cells - conversion of angiotensin to angiotensis I to angiotensin II (by angiotension converting enzyme - ACE), constriction of afferent arteriole, increased aldosterone production by the adrenal cortex (lowers potassium concentration) * Baroreceptors cause ADH production in hypothalamus, release in posterior pituitary - thirst and renal water reabsorption
148
List diseases of the renal arterial supply affecting small renal arteries
* Hypertension * Nephrosclerosis * Accelerated phase hypertension * Vasculitides
149
List abnormal urine characteristics which can be seen on visual inspection and what they indicate
* Frothy = protein * Red = blood, drugs (e.g. rifampicin) * Brown = myoglobin * Cloudy = infection
150
Describe the arterial supply of the kidney
* Right and left renal arteries, from the abdominal aorta (L1-L2, just below the origin of the superior mesenteric artery) * Right is longer, crosses the inferior vena cava posteriorly * Within the kidneys: * Renal arteries * Segmental arteries * Interlobar arteries * Arcuate arteries * Interlobular arteries * Afferent arteriole * Capillary network (glomerulus) * Efferent arteriole form peritubular network - supplies nephron tubules * Inner 1/3 of cortex and medulla supplied by vasa recta
151
Define acidaemia and acidosis
Acidaemia = high [H+] Acidosis = H+ normal, other ion imbalances e.g. HCO3-
152
Describe the gross structure of the kidney
* Parenchyma = outer cortex and inner medulla * Medulla forms medullary pyramids - apex of pyramids drains to the minor calyces via the renal papillae * Minor calyces drain to major calyces, which drain to the renal pelvis * Renal hilum = where the vessels and ureters enter/exit
153
What causes oxalate stone formation?
Primary/secondary hyperoxaluria Hypocitraturia
154
Which drugs have increased sensitivity in impaired renal function?
* CNS depressants - opiates (respiratory depression) * Antihypertensives
155
What is the normal response to low serum Calcium?
* Increased parathyroid hormone (PTH) secretion * Increased calcium ion reabsorption in the kidneys * Increased hydroxylated vitamin D - increased GI calcium absorption * Calcium ion release from bone resorption
156
How can renal stones be distinguished by pH?
Calcium \>7.0 Struvite \>7.0 Uric acid/cysteine \<6.0
157
What are the risk factors for renal stones?
* Gender - male * Family history * High BMI * Immobile/sedentary * Dehydration * Urinary tract infections * Protective factors - vegetarian, diet high in fruit/fibre
158
List the disorders of renal ion channel dysfunction and how they are treated
* PCT - Fanconi's syndrome, use acetazolamide diuretic (carbonic anhydrase inhibitor) * NKCC2 - Bartler's syndrome, use loop diuretics * NCC - Gitelman's syndrome, use thiazide diuretics * ENaC - Liddle's syndrome, use amiloride (potassium-sparing) diuretics
159
Describe the functions of the parts of the nephron in terms of drug excretion
* Glomerulus - filtration of all LMW drugs * PCT - active tubular secretion of acid, bases and digoxin * DCT - passive tubular reabsorption * CT - water soluble drugs and metabolites * Drugs very heavily bound to plasma proteins e.g. albumin not filtered out - only free fraction filtered

Medicine Year 2 (41 decks)

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