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Year 2 > ILO WEEK 7 & 8 > Flashcards

ILO WEEK 7 & 8 Flashcards

Renal

1
Q

Give an account of the role of the kidneys in controlling the volume of extracellular fluid, metabolic waste removal and electrolyte homeostasis

A

The role of the kidney is to:

  • Remove metabolic waste from the extracellular fluid (urea, acids)
  • Controlling the volume of extracellular fluid ( close link to blood pressure)
  • Maintaining optimal concentration of vital solutes in the extracellular fluid (Na, K, Ca, Mg, Cl, Phos)
  • A few other functions have evolved as a result of kidneys unique physiology

Controls the volume by ADH and aqua poring; rest of the water follows sodium!

Metabolic waste; things reabsorbed and actively excreted from the body;

Loop of Henle

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2
Q

Describe the composition of the nephron and explain the function of each component

A
  1. Glomerulus -> ultrafiltration; podocytes; leaky capillaries; pressure difference
  2. Proximal convoluted tubule -> active reabsorption; most occurs here-> all glucose and amino acids; lots of electrolytes and water
  3. Loop of Henle -> concentration; creating environment for water reabsorption ( descending water only; ascending electrolytes only) Sodium potassium chloride channels
  4. Distal convoluted tubule -> small reabsorption only; same as in proximal but just adjusting
  5. Collecting duct; collecting all; ADH water reabsorption
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3
Q

Understand the other main functions of the kidneys, including activation of vitamin D, toxin metabolism and regulation of erythropoietin

A
  1. Vit D activation -> last stage of Vit D activation
  2. Regulation of erythropoein -> makes erythropoein -> making red blood cells
  3. Blood pressure regulation; macula densa; renin;angiotensin; aldosterone
  4. Toxin metabolism
    Some of toxin metabolism occurs in the kidney ( medicines; degoxin)
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4
Q

Juxta-glomerular apparatus and blood flow

A

Juxta-glomerular apparatus:
Maintains GFR in face of increases or decreases in blood flow to the kidney

Macula densa - senses tubular flow; next to glomerulus

Increases tubular flow:
Sensed by macula densa
Macula densa produces adenosine -> afferent arteriolar constriction

Reduced tubular flow:
Sensed by macula densa; reduction in flow
Granular cells produce renin (green)

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5
Q

Describe the common causes and classification of kidney disease

A

Defined by reduced eGFR and detection and qualification of urine protein +/- blood

Once defined a combination of history, examination and investigation is employed to identify aetiology

AKI (Acute Kidney Injury); CKD (Chronic Kidney Disease)

Common causes:

  • Ineffective blood supply (reduced effective plasma volume or narrowed renal arteries) mostly AKI
  • Glomerular diseases
  • Tubulo-interstitial diseases
  • Obstructive uropathy most AKI
  • For CKD -> Following acute kidney injury
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6
Q

Oliguria

A

Warning od impending acute tubular necrosis

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7
Q

List what is measured by semiquantitative urinalysis

A
  • Inspection
  • Dipstick testing
    Microscopy and quantification of detected protein
  • Depending on clinical situation- urine biochemistry (sodium, potassium, chloride, urea, osmolality)

Check:

  • Protein/Albumin
  • Haem
  • pH
  • Ketones
  • Glucose
  • Bilirubin
  • Leucocyte
  • Nitrites

Blood:

  • visible haematuria
  • non-visible (seen with a microscope)

Protein:
Measuring, need 24h sample

No normal values for electrolytes

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8
Q

How proteinuria and Haematuria are quantified

A

Blood:

  • visible haematuria
  • non-visible (seen with a microscope)

Protein:
Measuring, need 24h sample
need a ratio with creatine

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9
Q

Identify patients with kidney injury by eGFR, serum creatine, dipstick urinanalysis and urine quantification

A
  • > eGFR <60 ml/min
  • > Rise in serum creatine within the eGFR> 60mL/min range
  • > Anion gap
  • > Blood and proteins
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10
Q

Management of Chronic Kidney Disease

A
  • > Dialysis
  • > Kidney transplant
  • > Increased cardiovascular risk
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11
Q

Describe the various methods available to image the kidneys and bladder and understand the risks associated with some of these methods

A
  • Plain X-ray
    (useful for radio-opaque stones
  • Ultrasound
    (no radiation; gains information about kidney size; shape; location; obstruction and renal blood flow)
  • CT
    ( Useful for trauma, stone, tumour, infection) (popular)
    Contrast enhanced imaging Blood supply and neighbouring structures; (IV iodinated contrast -> potentially methatoxic)

NEED to weight up benefits and potential nephrotoxicity; sometimes really needed

  • MRI
    Soft tissue evaluation; contrast can be toxic
  • Radioisotope scanning
    tracer needed
    information on: structure; perfusion; excretion; differential renal function
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12
Q

Understand how kidney stones/ crystals form, and the different types that exist

A

Crystals too much solute for the solution:
- calcium; Oxalate; Urate; Cysteine
Not enough solution: filtrate, urine
They form in urinary space

Classification:
By location:
- kidney/ nephrolithiasis
- ureter/ ureterolithiasis
- bladder/ cystolithiasis

By composition:

  • calcium- phosphate/ calcium-oxalate
  • urate/ cysteine/ struvite

Risk factors:
- male; 50% have a genetic component; positive family history
rise in obesity+ metabolic syndrome (DM/ HBP) have caused an increase in uric acid stones

Composition:
- Calcium containing (80%)
Calcium OXalate; Calcium Phosphate
Magnesioum ammonium Phosphate
Uric Acid; Cysteine; Mixed stones

HIGH SOLUTE STATES? LOW PREVENTER STATES

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13
Q

Understand the role of serum/ urine biochemistry and imaging in diagnosing kidney stones

A

pH Urine -> may be helpful in guiding diagnosis/ treatment:
Calcium stones pH >7.0
Struvite pH >7.0
Uric acid + cystine pH <6.0

High solute states: High calcium; High Oxalate/ Urate/ Cysteine/ Pro-calculi
CITRATE IS PROTECTIVE

Serum biochemistry tests: calcium, Phosphate, PTH, Urate, Bicarbonate

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14
Q

Discuss the common treatments for kidney stones

A

<2 cm expectant management or offer extracorporeal shock wave lithiotripsy
>2 cm or multiple stones -> expectant management ultrasonic litrotripsy
Large branched stones may require pul and eswl
Cysteine stones pul or open nephrolithotomy

Stones in ureter:

  • small have a good chance of paddage
  • allow time to pass
  • lower ureter - ureteroscopic stone removal
  • mid-upper ureter eswl
  • large stones -> >7mm eswl; ureteroscopic stone fragmentation
  • open surgery

IN ALL increase fluid! In some change the diet: (low oxalate; reduce protein/ sodium)

Citrate inhibitor of stone formation; can be increased by low Na diet

Struvite (Magnesium Ammonium Phosphate) -> Debulk where possible; Aggressive treatment of UTI (made by worms)

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15
Q

Functions of the kidney and consequence of failure in thees

A
  • Excretion small solutes -> consequence -> increased plasma concentration (e.g. urea, creatine)
  • Excretion of drugs -> drug toxicity
    (Done by filtration and tubular secretion)
  • Salt & water balance -> extracellular fluid overload or depletion
    Blood pressure control -> Hypertension
    ( Pressure natriuresis renin/angiotensin system, ADH, countercurrent mechanism, ANP/ BNP)
  • Electrolyte balance -> Hyperkalaemia, hypokalaemia
  • Acid base balance -> Metabolic acidosis
    ( Filtration then tubular cell membrane ‘pumps’)
  • Erythropoein -> Anaemia
  • Vit D activation -> Hypocalcaemia and secondary hyperparathytoidis
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16
Q

Describe how the nephron controls excretion of sodium and potassium

A

Potassium is mostly intracellular
Sodium and Chloride are in the interstitium

The kidney can only alter what it has filtered
Afferent arteriole Central nervous system
Efferent -> Angiotensin II constricting
+ ALL other mechanisms that control filtration

Then tubular reabsorption (active via channels) (passive down conc. gradient or osmotic gradient)
Tubular secretion -> In distal conv. tubule

Excretion = (Filtration - Reabsorption) + Secretion

17
Q

Explain how the kidney controls water reabsorption and secretion

A

Water follows sodium
Lots reabsorbed in the proximal conv. tubule;
In the loop of Henle; water leaved in the descending limb

The in distal and collecting duct; special system for further water reabsorption ADH; AQUAPORINS -> going down conc. gradient due to the loop of HENLE

18
Q

Describe how the countercurrent multiplier system concentrates filtrate in the loop of Henle

A

Descending -> only water permeable passive process
Ascending -> sodium, potassium, chloride permeable; Osmolality highest at the bottom; then electrolytes lost as it goes up -. Ends up being diluted at the top? all electrolytes are outside

19
Q

Understand how the countercurrent mechanism functions in the Vasa Recta

A

Vasa Recta is the vessel that appears in the juxtamedullary nephrons;
They flow in the opposite direction to the loop of Henle; but alongside it. It does not wash away the gradient as it flows in the opposite direction; It moves water into the ascending and electrolytes into the descending loop

20
Q

Understand the channels involved in electrolyte transport

A

Na+K+ ATPase and NaH antiporter (in PCT)

NKCC2 (Thick Ascending Loop of Henle)

NCC (DCT) (Na+ 2Cl-)

Aquaporins (Collecting Duct)

ENaCl (Cortical collecting duct)

IS THERE MORE?

21
Q

List the mail hormones involved in regulating renal function and understand how they act

A

Angiotensin II; Aldosterone; Renin -> Blood pressure; Contract on the afferent and efferent arterioles to go increase the flow (Maintain)

ADH and aquaporins -> open channels to allow passive passage of water out of the tubule

22
Q

Understand the mechanism involved in renal excretion of drugs

A

Drug elimination:

  1. Glomerular filtration; doses should be reduced if less filtration
  2. Tubular secretion
  3. Diffusion (non-ionic) - related to pH of urine/pKa of the drug ( important in aspirin)
  4. Protein-blinding ( in low serum albumin; more free and being filtered free fraction - rate of filtration
23
Q

Describe how impaired kidney function has an effect on drug metabolism and clearance

A

Problems:

  1. Toxicity
  2. Ineffective treatment

Relevant factors:

  1. Impaired drug absorption
  2. Impaired elimination
  3. Effect of renal dysfunction on hepatic drug metabolism
  4. Increased tissue sensitivity
  5. Protein binding
Impaired renal function:
Altered pharmacokinetics:
- decreased elimination
- decreased protein binding
- ALtered drug effect
Worsening of the existing condition
Enhancement of adverse effects
24
Q

Explain the dose adjustment options necessary in patients with compromised kidneys

A

Decreased elimination:
- Modify dose or monitor drug concentration

  • decreased dose -> decreased peak concentration
  • Increased dose interval -> decrease trough concentration (less exposure)
    Both -> more uniform serum concentration
    GOOD EXAMPLE: Gentamicin
25
Q

Understand the mechanism and clinical presentation of nephrotoxicity

A

Mechanisms:

  • Pre-renal acute kidney injury (diuretics)
  • Glomerular damage
  • Nephrotic syndrome (immune complex)
  • Lupus syndrome
  • Tubular damage
  • Acute interstitial nephritis (immunological)
  • Acute Tubular necrosis (direct toxicity)
  • Anelgesic Nephropathy
  • Uretic obstruction (analgesics)

Clinical presentation:

  • Acute kidney Injury ( interstitial nephritis/ ATN)
  • Chronic Renal Failure (nearly all, esp alengesics/ NSAIDs)
  • Nephrotic syndrome ( gold, penicilamine)
  • Lupus-like syndrome (hydralazine)
  • Nephrogenic DIaebtes Insipidus (lithium)
  • Fluid overload (NSAIDs)
  • Uraemia
26
Q

Understand the use and misuse of diuretics

A

Use:
- Loop diuretics (e.g. furosemide, bumetanide):
Inhibit Na/K/2Cl co-transporter in TALH
Increase K/Mg/Ca excretion
Metabolic alkalosis
Ototoxicity in high doses
Used when oedema is a problem -> heart failure, need a shift of fluid also in kidney failure, some in hypertension, get rid of calcium

  • Thiazide diuretics (e.g. bendroflumethiazide, metolazone, chlorothiazide)
    Act on Na/C; cotransporter in DCT
    Less potent
    Used in hypertension; some in oedema but less
    Retain calcium; also nephrogenic diabetes
    Increased K/Mg excretion
    Can be used to reduce hypercalcuria (renal stones)
    Ineffective in kidney damage
  • Potassium spiring diuretics (spironolactone, amiloride):
    Spironolactone- mineralocorticoid receptor antagonist
    Useful for hyperaldosterone states (heart failure, cirrhosis)
    Amiloride- sodium channel blocker- blocks eNaC in collecting duct
    May be combined with loop to reduce K loss
    In hypokalaemic; K low; Used along side the others also in excess of aldosterone
    Get dangerous in kidney damage; concentration of K
Side effects:
- Non-specific
- GI upset
- Hypersensitivity reactions
- Thrombocytopenia
Many others!
Cardiac arrhythmia; Muscle weakness; Hyperkalaemia; Otottoxicity
27
Q

Understand the mechanism by which chronic obstruction of bladder outflow can lead to back pressure, dysfunction and damage to the kidneys

A

Causes:

  • Benign Prostatic Hyperplasia
  • Bladder Stones
  • Kidney Stones
  • Bladder tumours
  • Causes back-flow up the ureters and buildup of urine; ureters become diluted and lose their peristaltic function -> urine can only flow down the ureters by the force of gravity
  • Dilation of renal pelvis and calyces known as HYDRONEPHROSIS -> untreated hydronephrosis can lead to progressive atrophy of the kidneys -> leads to kidney impairment
28
Q

Outline the causes of chronic kidney disease and explain in brief the treatments given to the patient

A

Causes:

  • Can be multifactorial
  • Diabetes mellitus
  • Interstitial diseases
  • Hypertension
  • Glomerular disease

Clinica features:

  • Increased urea and creatine
  • Hypertension, proteinuria and anaemia
  • Most patients tend to be asymptomatic until GFR falls below 30 mL/min/1.73m2
  • Tiredness, breathless, anaemia, anorexia, weight loss, nausea, vomiting, then deep respiration in metabolic acidosis

Effects:

  • Increased risk of Cardiovascular disease
  • Metabolic bone disease ( calcium and phosphate metabolism -> osteoporosis; Osteitis Fibrosa Cystica; Osteomalacia)
  • Impaired conversion of Vit D in the renal tubules; decreased Ca2+ absorption in the intestines
  • Increased risk of bleeding
  • Immune dysfunction

MANAGEMENT:

  • ANTIHYPERTENSIVE TREATMENT -> slows the rate of decline
  • Reduction of proteinuria -> ACE inhibitors; Angiotensin receptor blockers
  • Dietary/ Lifestyle interventions -> reduce protein consumption, ensure sufficient caloric intake with limited intake of phosphate and potassium, stop smoking, control weight and do exercise
  • Treatment of Anaemia (EPO)
  • Maintaining fluid/ electrolyte balance -> give them sodium; if hyperkalaemia -> potassium-sparing diuretics should be stopped
  • Treatment of bone disease
29
Q

Ideal characteristics of drugs in kidney impairment

A

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

30
Q

Hormonal control of Vasa Recta

A

Vasopressin

Year 2 (8 decks)

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