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renal 11-13 (s + p + t) Flashcards

1
Q

Why is urinalysis used as a basic clinical test and what for?

A
  • many drugs and their metabolites eliminated via the kidneys
  • for initial diagnosis of common conditions i.e. various types of renal disease
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2
Q

How do we use urine test strips for urinalysis?

A
  1. dip strip completely in fresh urine
  2. gently tap to remove excess urine
  3. dab back of strip on paper towel
  4. hold strip in horizontal position to prevent mixing of chemicals
  5. read at (timed) 30 seconds (bilirubin + glucose) by holding it over matchingcolour charton bottle
  6. read all tests at times specified by chart to find relevant values
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3
Q

How can we qualitatively assess urine?

A

colour and appearance e.g. may appear cloudy due to protein/blood

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4
Q

What is the normal range for osmotic pressure of urine?

Hint - digits of 300

A

300-600 mOsmol/l

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5
Q

State the normal expected results of urinalysis for:

a) glucose (mmol/L)
b) bilirubin (not a number)
c) ketones (s-m)
d) specific gravity (no units lots of zeroes)
e) blood (m-l)
f) pH (two whole numbers range)
g) protein (g/L)
h) urobilinogen (not a number but atypical indicator)
i) nitrite (not a number)
j) leukocytes (not a number)

A

a) 5.5mmol/L
b) positive
c) small-moderate
d) 1.000-1.015
e) moderate-large
f) 7-8.0
g) 0.3-1.0g/L
h) positive colours may be atypical
i) positive
j) positive

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6
Q

Which disease may be indicated by a urinalysis with a high glucose concentration?

(Hint - seen in juveniles)

A

type 1 diabetes

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7
Q

Which disease may be indicated by a urinalysis with a high protein concentration?

A

glomerulonephritis

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8
Q

Which disease may be indicated by high volumes of abnormally diluteurine?

(Hint - ‘insipidus’ is Latin for plain or tasteless)

A

diabetes insipidus

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9
Q

Which disease may be indicated by urine of a low pH?

Hint - to do with microorganisms and acid-producing flora

A

urinary tract infection (UTI)

ammonia-forming organisms can lead to a low pH

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10
Q

Which disease may be indicated by a urinalysis with a positive urobilinogen value?

(Hint - urobilinogen is produced in the liver)

A

hepatitis

indicates excess conjugated bilirubin in blood plasma which can only link to the liver

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11
Q

How does clean-catch MSU collection work?

A

(lean-catch midstream urine collection)

  1. washarea around urinary opening and start urination into the toilet
  2. stopmidstream
  3. let 1-2 ounces (30-60ml) flow into container
  4. finish urinating into toilet
  5. hand over sample to HCPs
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12
Q

What are the main causes of blood in the urine (haematuria)?

Hint - KILT G → hepatic, renal, general

A
  • kidney stones
  • infection
  • leakage from bladder area (harmless)
  • tumours in bladder/kidney
  • glomerulonephritis
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13
Q

What are the most common abnormal microscopic and microbiological constituents of urine which can indicate disease?

(Hint - RWcb)

A
  • RBC’s
  • WBC’s
  • casts (mucoprotein matrix structures)
  • bacteria
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14
Q

State some limitations of urinalysis.

Hint - +VE → n, -VE → p + g + k + b, S → pre pKa poly, quality vs quantity

A
  • potential of false positives forthe nitrite
  • potential of false negatives forthe protein, glucose, ketone (reacts with acetoacetic acid but not react with acetone), bilirubin (patients on large doses of chlorpromazine makes urine red)
  • SGTs (specific gravity tests) require a pKa change of certain pre-treated polyelectrolytes
  • qualitative analysis is subjective (i.e cloudiness and RBC’s can’t be seen with naked eye)
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15
Q

Define:

a) proteinuria
b) glucosuria
c) ketonuria
d) haematuria
e) hypersthenuria (Hint - water)
f) urobilinogenuria
g) hyposthenuria (Hint - SG)
h) bilirubinuria
i) nitrituria
j) pyuria

A 
presence of abnormal quantities of...
a) protein
b) glucose
c) ketone
d) blood
e) hypersthenuria → osmolality
f) urobilins
g) hyposthenuria → (low) specific gravity
h) conjugated bilirubin
i) nitrites 
j) pus 
... in the urine
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16
Q

Define nephrotic syndrome and where it often occurs.

(Hint - the said syndrome ‘itis’ and in the part inside the bowman’s capsule)

A
  • syndromecomprising signs of nephritis → kidney disease involving inflammation
  • often occurs in glomerulus (glomerulonephritis)
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17
Q

Define nephrotic syndrome.

(Hint - caused by damage to which blood vessels?)

A
  • kidneydisorder causing protein to pass into urine

- caused by damage to small clusters of blood vessels in kidneys which filter waste from blood

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18
Q

Define acellular casts.

A

clumping of substances which are not cells (hyalinecasts are solidified mucoproteins secreted from tubular cells of nephrons)

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19
Q

What are kidney stones, what are the different types and why may they form?

A

• 75% are calcium stones and remainder are struvite, urate or cysteine
• very common and form due to:
- genetic factors (metabolic abnormality) e.g. cysteinuria
- environmental factors - heat, dehydration, medications e.g. calcium

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20
Q

What is cysteinuria?

A
  • inherited abnormality where there is a defect in cysteine transport from tubular lumen to tubular cells
  • leads to increased urinary cysteine
  • cysteine not very soluble, most often found in young people
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21
Q

What is proteinuria a marker of and what can affect its detection by dip-stix screening tests?

A
  • a marker and cause of kidney damage → >300mg/24 hrs is abnormal (spot Protein Creatinine Ratio, PCR)
  • can be reduced by certain BP drugs
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22
Q

What is the guidance for BP thresholds in renal patients?

Hint - normal limit “less than,” protein/diabetic limit, agents available for

A
  • should be <140/90
  • <130/80 if proteinuria/diabetes
  • many agents available to lower BP
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23
Q

In which four ways can renal function be assessed and which is the best method?

(Hint - the usual G, CI clearance and then plasma c levels)

A
  • plasma creatinine - but this a flawed marker
  • creatinine clearance - involves 24-hour urine collection
  • inulin clearance (gold standard)
  • glomerular filtration rate (GFR)
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24
Q

Which two treatments can offered for renal problems to control BP?

(Hint - pye and peri)

A
  • pyelolithotomy → lengthy procedure clamping of renal artery where thousands of cysteine stones removed
  • peritoneal dialysis → used to manage post-op developed renal failure
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25
Q

How can cystinuria be treated and managed so more stones won’t form?

(Hint - treatment: have 5L altogether, sodium bicarb to reduce acid and penicillin with amines + management: low protein, low NaCl, capto meds, pH dipper to keep urine high)

A 
• treatment:
- 4L fluid/day
- wake up overnight to drink 1L water
- sodium bicarbonate to alkalinise urine
- penicillamine
• management:
- low protein, low salt diet
- captopril (ACE inhibitor)
- pH dispstix at home to keep urine alkaline
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26
Q

Which other surgical treatments can be offered for stones?

Hint - scopy and stent, nephro blocking, the most common using igh frequency waves lithotr

A

• ureteroscopy + ureteric stent
• nephrostomy (opening between kidney and skin to drain blocked urine)
• lithotripsy (high frequency waves to break stone down)
- not useful for cysteine stones
- some stones large and can’t be extracted via ureter
- so, nephrostomy + crushing of stones
- some stones → episodes of renal obstruction
- ongoing hypertension

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27
Q

What is a JL reciprocal creatinine vs time plot?

Hint - can be used to estimate something

A

graph used to predict estimated renal function (RF)

NB: negative correlation and eRF decreases over time

28
Q

What are the signs and symptoms associated with advanced renal failure?

(Hint - can’t eat, feel sick, feel tired, scratchy, can’t catch breath, heart infection)

A
  • loss of appetite
  • nausea
  • fatigue
  • itchiness
  • breathlessness
  • pericarditis
29
Q

What is ESRF (end-stage renal failure), its types of symptoms and treatments?

(Hint - when the values for something are very low, symptoms → two grouped symptoms and one usually seen in starved children, treatment → keeping body fluid clean, new kidneys, prep for body accepting new organs, surgery)

A
  • renal function declined to negligible levels, eGFR <15ml/min, stage 5 CKD (chronic kidney disease)
    • symptoms → uraemic symptoms, GI symptoms/fluid overload, malnutrition
    • treatment → dialysis, renal transplant (cadaveric/live-related), major surgery, pre-transplant work-up and immunosuppressive drugs
30
Q

What is chronic kidney disease (CKD), its GFR thresholds (in males and females) and its complications?

(Hint - potential for change and how many stages and defining measurement, only a 10 ml/min difference between M and F, symptoms → BAMAH)

A

• CKD → irreversible renal impairment with 1-5 stages defined by eGFR
- GFR of 130 ml/min M and 120 ml/min F)
• complications → bone disease, anaemia, malnutrition, acidosis, hypertension

(management is a Low Clearance Clinic → complicated, multi-disciplinary, time-consuming and repetitive)

31
Q

What is renal anaemia (high morbidity and mortality) and how can it be treated?

(Hint - anaemia due to a shortage of a kidney hormone)

A
  • anameia due to lack of erythropoetin

- easy but expensive to treat with recombinant epo

32
Q

What is renal bone disease and in which four ways can it be managed?

(Hint - less Ca → more P → more thyroid h → renal bye bye, management → PABD - lower P and Ca, increased active it D)

A 
- hypocalcaemia (lacking activated vit D), hyperphosphatemia (reduced excretion of phosphate) → leading to hyperparathyroidism + renal osteodystrophy
• management:
- phosphate binders
- activated vit D replacement
- beware high calcium-phosphate products
- dietary restriction of phosphate
33
Q

What are the two options for dialysis?

A
  • peritoneal dialysis (bag)
  • haemodialysis (machine and filter)
    (pros and cons for each)
34
Q

How do we prepare patients for dialysis?

Hint - ash s or AV fist

A
  • ‘ash split catheter’ - a hemodialysiscatheter connecting to multi-holed cylindrical tips in a central vein
  • ‘arteriovenous fistula’- an abnormal connection between an artery and vein surgically created for hemodialysis treatments
35
Q

What is the dietary advice to renal patients?

Hint - have P, K, NaCl, AAs, H2O, ATP

A

consume food including → phosphate, potassium, salt, protein, water, energy

36
Q

How often is hospital haemodialysis and what problems may it create?

A
  • 3 x week for 4 hours (started early 2002)

- problems related to sessions → lifestyle and work limitations

37
Q

Why may a kidney transplant be rejected?

Hint - r and i and o tion, miscellanous, moderate hyd, transplant b

A
  • rejection
  • infection
  • obstruction
  • others e.g. drugs, intercurrent illness
  • moderate hydronephrosis on USS
  • nephrostomy placed but no improvement
  • transplant biopsy
38
Q

What can the differential diagnosis of hypertension plus hypokalaemia imply and what is this caused by?

(Hint - mineral high BP, by too much aldo keeping salt in the body)

A
  • mineralocorticoid hypertension

- hyperaldosteronism causing salt and water retention

39
Q

What can mineralocorticoid hypertension be caused by?

Hint - c1-ah2-grh(r) → L syndrome

A

• Conn’s syndrome - primary hyperaldosteronism
• Adrenal Hyperplasia - secondary hyperaldosteronism
• Glucocorticoid-remediable hyperaldosteronism
- liquorice/carbenoxolone ingestion
- apparent mineralocorticoid excess → Liddles syndrome

40
Q

How can liquorice lead to increased cortisol-driven mineralocorticoid activity (not under feedback control)?

(Hint - inhibition of a g. acid and hence a b-h-dehydrogenase)

A
  • contains Glycyrrhizic acid
  • inhibits enzyme 11 β-hydroxysteroid-dehydrogenase

(see notes for diagram)

41
Q

What can hyporeninaemic hypoaldosteronism result from?

Hint - L syndrome, congenital AH, L excess

A
  • Liddles syndrome
  • congenital adrenal hyperplasia
  • liquorice excess
42
Q

What is Liddles Syndrome and how its it treated?

Hint - genetic but not sex-linked and about CDs → NaK, amil antibiotic

A
  • rare autosomal-dominant abnormality of collecting tubules → increase in Na⁺ reabsorption + K⁺ secretion
  • treatment → amiloride therapy
43
Q

What is renal endocrine hypertension?

Hint - R- I- E → C, L etc…

A
  • renal artery stenosis
  • intrinsic renal disease
  • endocrine → Conns, Liddles and other rare entities
44
Q

What is transplant artery stenosis?

Hint - creatinine levels, high BP, b ryhmes with fruit, flash pulm. swelling

A
  • occurs in up to 12% of transplants, usually near anastomosis → post-anastomosis following rejection
  • rise in creatinine (gradual)
  • hypertension
  • bruit (murmur of arteries)
  • flash pulmonary oedema
45
Q

How can renal disease be investigated and managed?

Hint - scans → U, M but no I, a, treatment → a-plasty

A
  • USS (doppler)
  • MRA (magnetic resonance angiogram)
  • angiography
  • treatment by angioplasty
46
Q

How does oedema (excessive accumulation of fluid in intercellular spaces of tissue) develop?

(Hint - more salt in than out so water follows into body fluid)

A
  • when NaCl intake exceeds output

- extra Na⁺ retained causes water retention and expansion of ECF volume (oedema)

47
Q

How do diuretics reduce oedema?

A
  • prevent Na⁺ entry into tubular cells so more is excreted
  • increase in tubular Na⁺ is matched by increase in water as it is osmotically obliged to follow Na⁺ decreasing ECF volume (reduces oedema)
48
Q

How can diuretics treat hypertension (i.e. thiazine)?

Hint - reduces volumes reducing pressure

A
  • plasma ECF compartment volume reduced via diuretic-mediated losses of Na⁺ and water in urine
  • decreases hydrostatic pressure on vessel walls by plasma → reduces BP and excess fluid and Na⁺-related hypertension
49
Q

Why do diuretics not work as well during renal failure?

A
  • mechanisms of diuretic action depend on inhibiting processes in healthy nephrons so effect reduced
  • reduced renal blood flow limits diuretic delivery
50
Q

How does mannitol cause a diuresis?

Hint - sits in the tubule’s fluid making it more osmo. (salty) so more water is drawn out

A
  • increases osmolality of tubular fluid by remaining trapped within it
  • so osmotically-obliged water is drawn out into tubular fluid
51
Q

How does acetazolamide increase bicarbonate excretion?

Hint - CA enzymes and Na⁺ meaning more HCO₃- out

A
  • inhibits CA → increases HCO₃- ions in tubular fluid → increase amount of (accompanying) Na⁺ in tubular fluid
  • in distal tubule, Na⁺ reabsorbed, but not HCO₃- → increased HCO₃- excretion
52
Q

How do loop diuretics cause a diuresis and which conditions can this lead to?

(Hint - high-ceiling or potassium-wasting → block the co-transporter of all 3 ions, less conc. ability, less normal 2+ ions reabsorbed, lead to → too much K and Mg but not Ca)

A
  • disrupt medullary hypertonicity by blocking Na⁺/K⁺/2Cl- co-transporter in apical membrane of TAL of loop of Henle
  • reduces maximal concentrating ability of urine by NaCl reabsorption
  • also site of normal Ca2⁺ and Mg2⁺ reabsorption so increase
  • can lead → hypokalaemia and hypomagnesaemia, but not hypocalcaemia (Ca2⁺ reabsorption continues in significant amounts distally to TAL)
53
Q

How does bumetanide cause increased K⁺ excretion?

Hint - inhibits NKC transporter so ions can come into tubule, so more K out

A
  • inhibits luminal Na⁺/K⁺/2Cl- co-transporter which brings these ions into tubule cells
  • means more K⁺ present in tubular fluid and hence urine
54
Q

What can irresponsible prescribing of loop diuretics cause?

Hint - too little bananas in life

A

hypokalaemia

55
Q

How do thiazides prevent kidney stones?

Hint - less excretion of uri and Ca so can’t form stones in ureters

A
  • increase reabsorption of uric acid and Ca2⁺ in proximal tubule so excretion is reduced → no longer participate in kidney stone formation within the collecting system
56
Q

How does spironolocatone act to spare potassium?

classed as “potassium-sparing” → aldo increases Na⁺ IN and K⁺ and H⁺ OUT

A
  • a competitive antagonist for aldosterone sites (so inhibits it)
  • aldosterone increases reabsorption of Na⁺ and secretion of K⁺ and H⁺ in collecting duct
  • still increased Na⁺ and water (diuretic action) in urine but decreased K⁺ and H⁺ → means more K⁺ retained
57
Q

Should amiloride be given to hyperkalaemic patients? Explain.

A
  • a potassium-sparing diuretic
  • no, in hyperkalaemia, would be dangerous to further increase K⁺ levels in body
  • amiloride inhibits luminal Na⁺ channels in CD of nephron which drive secretion of K⁺ and H⁺ into urine
  • a weaker Na⁺ gradient for movement of ions by basolateral Na-K ATPase so luminal H⁺ and K⁺ secretion inhibited
  • H⁺ and K⁺ levels decreased in urine and increased in plasma
58
Q

How does triamterene cause a diuresis (increased urine production)?

(Hint - about Na⁺ channels of cd and dt and K⁺ and H⁺ into urine, K⁺-sparing or not and how is it best used?)

A
  • inhibits Na⁺ channel in apical membrane of late DT and CD causing urinary retention of water
  • K⁺ and H⁺ secretion driven by electrochemical gradient generated by Na⁺ reabsorption, so their transport into urine is reduced
  • is K⁺-sparing, so best with another diuretic to prevent hyperkalaemia
59
Q

When were diuretics first used?

A
  • anti-microbial agent sulphanilamide found useful in reduction of oedema in patients with CHF (increase in renal excretion of Na⁺)
  • modern diuretics developed to lessen side effects “water tablets”
60
Q

How do the controls of the kidneys prevent hypertension and oedema in a healthy individual?

A
  • kidneys control ECF volume by adjusting NaCl and H₂O excretion
  • thus, body maintains BP at expense of ECF volume
  • when NaCl intake exceeds output, oedema develops
  • Na⁺ reabsorption driven by basolateral Na⁺-K⁺ ATPase which ensures low intracellular Na⁺, allowing Na⁺ influx down electrochemical gradient on luminal side of tubule
61
Q

Where do all diuretics, except spironolactone, exert their effects and how do they act?

(Hint - mannitol acts according to renal blood flow and at the cup of the bowman’s capsule)

A
  • from luminal side of nephron (enter tubule fluid)
  • mannitol filtered at glomerulus whereas other diuretics (except spironolactone) tightly-bound to proteins and therefore not filtered
  • bound diuretics reach luminal side of nephron via secretion across proximal tubule (on organic acid/base secretory pathway)
  • means decreased renal blood flow/renal failure can reduce diuretic effect as can drugs which compete for secretory pumps
62
Q

Briefly describe osmotic diuretics (i.e. mannitol).

Hint - metabolism and filtration at glomerulus

A
  • non-metabolisable

- freely filtered at glomerulus

63
Q

Describe Carbonic anhydrase (CA) inhibitor diuretics (i.e. mannitol).

(Hint - less HCO₃- in so Na⁺ follows and water follows → but overtime less effect)

A
  • weak diuretic agents which cause reduced HCO₃- reabsorption
  • Na⁺ in proximal tubule fluid, accompanies HCO₃- out → increase in urinary HCO₃-, K⁺, and water excretion
  • effectiveness reduced with continued therapy as plasma [HCO₃-] falls, reducing amount in urine
64
Q

Describe Loop Diuretics or “high ceiling” diuretics (sulphonamide derivatives i.e. frusemide and bumetanide).

A
  • blocking of the Na⁺/K⁺/Cl- co-transporter in TAL of loop of Henle
  • responsible for concentrating/diluting urine and Ca2⁺ and Mg2⁺ reabsorption
  • increase urinary water, Na⁺, K⁺, Ca2⁺, and Mg2⁺
  • dilation of venous and renal system
  • effects mediated by PGs and rapidly-absorbed from gut
65
Q

Describe Distal convoluted tubule diuretics (i.e. thiazides and thiazide-like drugs).

A
  • mild diuretic action by inhibiting Na⁺ and Cl- transport in cortical TAL to reduce Na⁺ and water excretion
  • results in increased absorption and reduced excretion of Ca2⁺ and uric acid by proximal tubule
66
Q

Describe potassium-sparing diuretics spironolactone and amiloride/triamterene

(Hint - spironolactone → competes for aldo + amiloride/triamterene → basic and just Na⁺ channels and hence K⁺ too)

A
  • spironolactone → competitive antagonist of aldosterone (weak diuretic) which blocks aldosterone-stimulated Na⁺ reabsorption and K⁺ and H⁺ excretion in late DT and CD
  • acts from peritubular side of tubule and which reabsorbs modest amounts of Na⁺
  • amiloride/triamterene → weak diuretic which inhibits Na⁺ channel in apical membrane of late DT and collecting duct
  • K⁺ and H⁺ secretion in nephron segment driven by electrochemical gradient (generated by Na⁺ reabsorption) so presence in urine reduced
67
Q

Name some causes of diuretic resistance.

Hint - most often → haven’t solved first problem, high salt diet, won’t listen, won’t absorb

A

(most common)
- incomplete treatment of primary disorder
- continuation of high Na⁺ intake
- patient non-compliance
- poor absorption
(next most common)
- volume depletion:
• decreases filtration of diuretics + access to tubule lumen
• increases proximal tubule fluid reabsorption, limiting fluid delivery to more distal nephron sites where it acts
• increases serum aldosterone which enhances Na⁺ reabsorption
(uncommon)
- non-steroidal anti-inflammatory drugs (NSAIDs) can reduce renal blood flow
- metabolic acidosis can limit efficacy

CRR (11 decks)

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