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Reproduction, Nephrology and Urology > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What are the main functions of the kidney?

A

Filter metabolic waste
Control fluid volume
Maintain electrolyte balance

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2
Q

How many litres of water are in the body?

A

42L (60% weight)

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3
Q

What are the body fluid compartments?

A

Intracellular

Extracellular - intravascular, extravascular (interstitial)

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4
Q

In what direction do oncotic and hydrostatic pressure push fluid?

A

Oncotic - inwards

Hydrostatic - outwards

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5
Q

What percentage of the cardiac output do the kidneys receive?

A

20%

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6
Q

What are the 3 main processes which occur in the nephron?

A

Glomerular filtration
Tubular reabsorption
Tubular secretion

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7
Q

What is glomerular filtration?

A

Filtering of blood into tubule forming the primitive urine (glomerular filtrate)

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8
Q

What is tubular reabsorption?

A

Selective absorption of substances from tubule to blood

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9
Q

What is tubular secretion?

A

Secretion of substances from blood to tubular fluid

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10
Q

What is the glomerular filtration barrier?

A

Size-selective sieve with specialised capillary endothelium, glomerular basement membrane and podocyte foot processes which allows filtration of extracellular fluid

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11
Q

What particles are not filtered by the kidney?

A

Haemoglobin, albumin, RBCs

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12
Q

What is a normal glomerular filtration rate?

A

100ml/min (144L/day)

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13
Q

What particles are filtered by the kidney?

A

Glucose, water, urea, amino acids, salt

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14
Q

What are the main epithelial features of the proximal convoluted tubule?

A

Basolateral Na/K ATPase
Cl enters, creating an osmotic gradient for water to be reabsorbed
Basolateral membrane infoldings rich in mitochondria
Apical membrane has microvilli and aquaporins

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15
Q

What are the main epithelial features of the collecting duct?

A

Principle cells and intercalated cells working side-by-side
Principle cell - Na/K ATPase, epithelial Na channels, K moves into lumen
Intercalated cell - H ions move into lumen due to negative charge created by Na entering the cells

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16
Q

What are the main epithelial features of the thick ascending loop of Henle?

A

Na/K ATPase
NKCC transporter
K leaks into lumen creating a positive charge so Ca and Mg move paracellularly to interstitium

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17
Q

Which part of the nephron is responsible for fine tuning?

A

DCT

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18
Q

What parts of the nephron are responsible for altering urine concentration?

A

LoH and CD

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19
Q

What is the plasma osmolality?

A

300 mosmoles/kg

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20
Q

What is the basic mechanism of the countercurrent exchange multiplier?

A

Thick ascending limb is impermeable to water (but not Na) - dilute tubule contents and concentrated interstitium
Concentrated interstitium encourages water to leave in the thin descending limb
Increased efficiency
Vasa recta do not wash away the gradient

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21
Q

What does ADH do to the nephron?

A

Stimulates insertion of aquaporins in the CD and DCT when fluid volume is sensed to be low which causes water and salt conservation, leading to concentrated urine production

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22
Q

How does the kidney interact with the systemic circulation?

A

Baroreceptors detect reduced pressure → brain increases sympathetic activity and ANP/BNP produced → heart pumps harder → constriction of afferent arteriole → reduced blood to kidneys and reduced filtration = protects
extracellular fluid volume → pressure increased

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23
Q

What is the juxta-glomerular apparatus?

A

Specialised structure formed by the distal convoluted tubule and the glomerular afferent arteriole
Functions to regulate blood pressure and filtration rate of the glomerulus

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24
Q

What is the macula densa and how does it function?

A

Region of specialised cells lining the distal convoluted tubule which monitors NaCl concentration and tubular flow

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25
Q

What happens when the macula densa senses increased and decreased tubular flow?

A

Increased tubular flow → sensed by macula densa → adenosine produced → afferent arteriolar
constriction
Decreased tubular flow → sensed by macula densa → granular cells produce renin → RAAS activation

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26
Q

What is the role of natriuretic peptides in sensing body fluid volume?

A

Produced in response to increased volume and oppose effects of angiotensin II - pressure natriuresis

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27
Q

Give examples of acidic and alkaline foods

A

Acidic - white bread, alcohol, sugar, meat, fish, nuts

Alkaline - asparagus, melon, avocado, fruit, vegetables

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28
Q

What is the carbonic acid/bicarbonate buffer equation?

A

H + HCO3 (bicarbonate) →← H2CO3 (carbonic acid) →← H2O + CO2

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29
Q

What is the concentration of H ions which enter the body each day?

A

70 mmol

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30
Q

How does the kidney participate in acid-base balance?

A

Reabsorbs filtered bicarbonate, filters non-volatile acids (e.g. sulphuric), PCT synthesises ammonium from H

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31
Q

How is calcium concentration regulated by the kidney?

A

Low Ca sensed by parathyroid gland → increased PTH secretion → kidney increases Ca reabsorption from the glomerular filtrate
Resorption of bone by PTH will increase blood phosphate which is also excreted by the kidneys

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32
Q

How is the kidney involved in activation of vitamin D?

A

2nd hydroxylation of vitamin D occurs in the kidney

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33
Q

How is erythropoietin regulated by the kidney?

A

Secreted from kidney interstitial cells
Kidney very sensitive to tissue hypoxia (as capillaries at the end of LOH are already hypoxic) which stimulates EPO to increase RBCs

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34
Q

What are the features of extracellular fluid overload?

A

Tissue and pulmonary oedema, hypertension, increased JVP

Needs diuretic

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35
Q

What are the features of extracellular fluid depletion?

A

Dry mucous membranes, reduced skin turgor, hypotension, decreased JVP
Needs saline

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36
Q

What features does a substance need to have in order to use it in measuring GFR?

A

Completely filtered
Not reabsorbed or secreted
(e.g. inulin - gold standard but cumbersome and expensive)

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37
Q

What 2 substances are almost perfect for measuring GFR?

A

Creatinine, cystatin C

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38
Q

What is creatinine and why is it used for measuring GFR despite incomplete filtration and some tubular secretion?

A

Normal product of muscle metabolism; plasma concentration depends on muscle mass, recent protein intake and kidney function
Filtration and secretion cancel each other out and it is produced at a constant rate

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39
Q

What is the equation for calculating creatinine clearance (GFR)?

A

Clearance = (urine volume x [urine creatinine] / [plasma creatinine]) / 1440*

*Timed urine collection over 24 hours

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40
Q

If GFR is high, will creatinine concentration be high or low?

A

Low

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41
Q

What factors is creatinine concentration dependent on?

A

Muscle mass, age, sex

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42
Q

What is the MDRD 4-variable formula?

A

Equation for GFR estimation which takes into account the factors which affect creatinine concentration to avoid overestimation - serum creatinine, age, sex and correction for black African American race
Expressed as ml/min/1.73m3 - corrected for body surface area

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43
Q

What are the limitations of eGFR?

A

Not accurate:

  • > 60ml/min
  • <18 years of age (separate paediatric formula)
  • immediate changes
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44
Q

What are the ways in which urine can be examined?

A

Inspection
Dipstick
Microsopy
Biochemistry

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45
Q

What urine tests can be done using a dipstick?

A

Albumin, blood, pH, ketones, glucose, bilirubin, leukocytes, nitrites

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46
Q

What does a positive urine test for protein indicate?

A

Glomerular disease

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47
Q

Why is spot urine protein concentration not enough to quantify proteinuria and what is done instead?

A

Varies with degree of urine dilution

Ratio of protein to creatinine is used instead

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48
Q

What might urine microscopy tell us?

A

Confirmation of non-visible haematuria

Specific abnormalities

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49
Q

What might urine electrolytes and osmolality tell us?

A

Kidney response to changes in fluid volume
Cause of acid-base disorder
Identification of stone-forming tendency

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50
Q

What eGFR value indicates kidney dysfunction/damage/disease?

A

<60 ml/min

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51
Q

How is kidney injury/disease defined?

A

Reduced eGFR and detection of urine protein with/without blood

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52
Q

What do AKI and CKD stand for?

A

Acute kidney inury and chronic kidney disease

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53
Q

What causes AKI or CKD?

A

Ineffective blood supply, glomerular disease, tubulo-interstitial disease, obstructive uropathy

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54
Q

What is oliguria and what is it a sign of?

A

Reduced urine output

Impending acute tubular necrosis; kidneys are sensitive to other insults when oliguric

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55
Q

What risk is increased by chronic kidney disease?

A

Cardiovascular risk

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56
Q

What is the National Kidney Foundation classification of chronic kidney disease?

A
  1. Kidney damage with normal/increased GFR (>90)
  2. Mildly impaired (60-89)
  3. Moderatly impaired (30-59)
  4. Severely impaired (15-29)
  5. Renal failure (<15)
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57
Q

What imaging modalities are used to image the kidney?

A

X-ray, ultrasound, CT, MRI, radioisotope, angiography

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58
Q

What is the most commonly used modality to image the kidney and what information can it give?

A

Ultrasound

Size, shape, location, number, structure, drainage/obstruction, blood flow

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59
Q

Which kidney is more superior?

A

Left

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60
Q

What ultrasound findings are normal for kidneys?

A

> 10cm length
1cm cortex
Less bright than liver

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61
Q

When imaging the kidneys, what is CT useful for?

A

Trauma, stones, tumours, infection

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62
Q

What needs to be considered when using contrast-enhancing CT imaging for the kidney?

A

Potential nephrotoxicity; risk:benefit must be assessed, may be able to use pre-hydration

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63
Q

When imaging the kidneys, what is MRI useful for?

A

Soft tissue pathology; tumours, infection

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64
Q

What needs to be considered when using Gd-contrast MRI for the kidney?

A

Nephrogenic systemic fibrosis

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65
Q

When imaging the kidneys, what is isotope scanning useful for?

A

Structure, perfusion, excretion, renal function

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66
Q

What is the basic mechanism by which kidney stones/crystals form?

A

Too much solute, not enough solution

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67
Q

What is a kidney stone?

A

A solid concretion of crystal aggregate formed within the urinary space

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68
Q

What does cystolithiasis mean?

A

Stone in the bladder

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69
Q

What are the main risk factors for kidney stones?

A

Male, family history, BMI >27, dehydration, UTI, immobility, obesity and metabolic syndrome

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70
Q

What factors decrease the risk of kidney stones?

A

Vegetarian diet, high fruit and fibre

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71
Q

What is the composition of kidney stones and their prevalence?

A 
Calcium oxalate/phosphate (80%)
Magnesium ammonium phosphate/struvite (5-10%)
Uric acid (5-10%)
Cystine (1-2%)
Mixed
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72
Q

How would a patient with kidney stones present?

A

Flank tenderness, signs of infection, obesity, hypertension, gout tophi (uric acid crystals), diabetes

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73
Q

What is nephrocalcinosis?

A

Deposition of calcium salts in renal parenchyma

Normally calcium phosphate

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74
Q

What is medullary sponge kidney?

A

A congenital disorder of the kidneys characterised by cystic dilatation of the collecting tubules, predisposing to stone formation
Normally calcium phosphate or oxalate

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75
Q

What conditions can predispose a patient to calcium kidney stones?

A

Primary hyperparathyroidism, hypercalcaemia, hypercalciuria

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76
Q

What conditions can predispose a patient to oxalate/urate/cysteine kidney stones?

A

Hyperoxaluria, hyperuicaemia, cystinuria

77
Q

What conditions can cause a pro-calculus urinary environment?

A

Hypocitraturia, renal tubular acidosis (type 1)

78
Q

What is the normal pH of urine?

A

4.6-8.0

79
Q

At what pH do calcium, struvite, uric and cysteine stones precipitate?

A

Calcium and struvite - >7.0

Uric and cysteine - >6.0

80
Q

How are stones in the kidney treated?

A

<2 cm - manage, extracorporeal shock wave lithotripsy

>2 cm/multiple - manage, percutaneous ultrasonic lithotripsy

81
Q

How are stones in the ureter treated?

A

Small (<7 mm) - allow 2-4 weeks to pass; ureteroscopic removal, ESWL
Large (>7 mm) - ESWL, ureteroscopic stone fragmentation, open surgery

82
Q

What are ureteric stents used for?

A

Draining obstructed kidney to relieve pain, dilating ureters to facilitate stone passage, facilitating ESWL and ureteroscopic procedures

83
Q

What secondary prevention is there for kidney stones?

A

Monitor with periodic imaging
Citrate
Stone-specific advice

84
Q

What secondary prevention advice should be given regarding calcium phosphate kidney stones?

A 
Increase fluids (>2L/day) treat cause, consider citrate or thiazide
No good evidence for low calcium diet
85
Q

What secondary prevention advice should be given regarding calcium oxalate kidney stones?

A 
Increase fluids (>2L/day), low oxalate diet, consider citrate or thiazide
No good evidence for low calcium diet
86
Q

What secondary prevention advice should be given regarding uric acid kidney stones?

A

Increase fluids (>2L/day), xanthine oxidase inhibitors (treat hyperuricaemia), treat cause, alkalinise urine to pH > 6.0 (bicarbonate/citrate)

87
Q

What secondary prevention advice should be given regarding cysteine kidney stones?

A

Increase fluids (>2L/day), reduce protein and sodium in diet, alkalinise urine to pH > 7.0 (bicarbonate/citrate)

88
Q

What secondary prevention advice should be given regarding struvite kidney stones?

A

Debulk where possible, aggressive treatment of UTI

89
Q

What is the most important inhibitor of kidney stone formation and how does it achieve this?

A

Citrate
Reduces calcium saturation of urine by forming soluble complexes with ions and inhibiting crystal formation; increase activity of molecules which inhibit calcium oxalate aggregation, alkalinisation inhibits urate and cysteine stones

90
Q

What is Tamm-Horsfall protein?

A

Macromolecule in urine which inhibit calcium oxalate aggregation

91
Q

What is the anatomical position of the kidneys?

A

Obliquely in a paravertebral gutter at the level of the upper 3 lumbar vertebrae (left extends to the 11th rib)

92
Q

What are the posterior relations of the kidneys?

A

Diaphragm, posterior abdominal wall muscles, subcostal/iliohypogastric/ilioinguinal nerves

93
Q

What are the anterior relations of the right and left kidneys?

A

Right colic flexure

Left colic flexure

94
Q

What are the relations of the hilum of the right and left kidneys?

A

Right - duodenum

Left - pancreas

95
Q

What type of arteries are the segmental branches of the renal artery?

A

End arteries

96
Q

What are the anatomical features of the left renal vein?

A

Longer than the right; receives the left gonadal and left suprarenal veins

97
Q

What type of membrane lines the ureter?

A

Mucous membrane

98
Q

By what movement does urine pass through the ureter?

A

Peristalsis

99
Q

At what points is the ureter constricted, therefore making it susceptible to stone obstruction?

A

As it crosses the brim of the lesser pelvis and as it passes through the bladder wall

100
Q

What structure crosses the ureter in the pelvis in males and females?

A

Males - vas deferens

Females - uretetic artery

101
Q

What feature allows the bladder to expand when filled with urine?

A

Retropubic space is filled with loose areolar tissue

102
Q

Which ligament anchors the bladder neck to the pubis?

A

Puboprostatic ligament

103
Q

What does the bladder rest on?

A

Pelvic diaphragm

104
Q

What is the trigone?

A

Smooth-walled triangular area of the bladder which has the opening of a ureter at each upper corner and the opening to the urethra at the apex

105
Q

Why do the ureters pass through the bladder wall obliquely?

A

Ensures that an increase in urine and pressure in the bladder will compress the ureters to prevent reflux

106
Q

Which muscle lies on the medial side of the kidneys?

A

Psoas major

107
Q

Which muscles lie on the lateral side of the kidneys?

A

Quadratus lumborum and transversus abdominis

108
Q

What do the adrenal/suprarenal glands produce?

A

Cortex - corticosteroids and androgens

Medulla - adrenaline and noradrenaline

109
Q

What effect does contraction of the psos major have on the hip and thigh?

A

Hip - flexion

Thigh - flexion and lateral rotation

110
Q

What do medullary rays consist of?

A

The collecting ducts draining the nephron

111
Q

What type of epithelium is present in the Bowman’s capsule?

A

Simple squamous

112
Q

What type of epithelium is present in the PCT?

A

Cuboidal

113
Q

What are juxtaglomerular cells?

A

Specialised smooth muscle cells in the wall of the afferent arteriole which contain secretory granules of renin

114
Q

When do the kidneys begin to form in embryological development?

A

Week 4

115
Q

What are the 3 main components of the male urethra?

A

Prostatic, membranous, spongy

116
Q

What renal factors affect drug elimination?

A

Glomerular filtration
Tubular secretion
Diffusion
Protein binding

117
Q

What is gentamicin?

A

Glycoside antibiotic

Almost exclusively excreted by the kidney; not well tolerated in dysfunction (PCT nephrotoxicity)

118
Q

How is rifampicin affected by kidney dysfunction?

A

It’s not - metabolised by the liver

119
Q

How is vancomycin affected by kidney dysfunction?

A

Much more prolonged half-life

120
Q

What adjustments to dosing can be made in renal dysfunction and for which drugs would this need to be done?

A

Decrease dose and increase dose interval

Drugs with at least 50% renal clearance and a low therapeutic index (e.g. digoxin, lithium)

121
Q

What drugs will a patient with kidney dysfunction become more sensitive to?

A

Opiates, morphine, antihypertensives

122
Q

What drugs will a patient with kidney dysfunction become less sensitive to?

A

Diuretics, urinary antibacterials

123
Q

How are the adverse effects of metformin and sulphonylureas enhanced in renal dysfunction?

A

Metformin - increased risk of lactic acidosis

Sulphonylureas - provoked hypoglycaemia

124
Q

Why are the kidneys vulnerable to toxic drug effects?

A

Large blood flow

Drugs/metabolites concentrate in renal medulla and tubular cells

125
Q

What types of renal impairment are caused by drugs?

A

Acute tubular necrosis - NSAIDs, aminoglycosides, paracetamol
Fanconi’s syndrome - tetracyclines
Glomerulonephropathy - captopril, NSAIDs, penicillin
Crystalluria - methotrexate, sulphonamides
Renal tubular acidosis - acetazolamide, lithium
Interstitial nephritis - furosemide, penicillin, thiazides
Nephrogenic diabetes insipidus - lithium
Renal papillary necrosis - aspirin

126
Q

What do ACE inhibitors do and when are they used?

A

Prevent normal efferent arteriole vasoconstriction due to angiotensin II; antihypertensive
Used in diabetic nephropathy, proteinuric renal disease and cardiovascular disease
Can be nephroprotective or cause renal problems

127
Q

How do NSAIDs work and what are their effect on the kidney?

A

Inhibit prostaglandins which normally causes afferent arteriole dilation to maintain glomerular capillary pressure

128
Q

What is acute interstitial nephritis and what symptoms does it cause?

A

A cause of acute renal failure resulting from immune-mediated tubulointerstitial injury initiated by medications (antibiotics, anticonvulsants, diuretics, PPIs)/infection
Raised eosinophils, rash

129
Q

Give the main features of loop diuretics

A

Site of action - thick ascending LOH (inhibit NKCC)
Used for - oedema, acute renal failure, hypertension, hypercalcaemia
E.g. bumetanide, furosemide
Duration - 4-6 hours
Useful in renal failure - yes (high dose)
Absorption speed - fast
Side effects - metabolic alkalosis, GI upset, hypersensitivity reactions, ototoxicity

130
Q

Give the site of action, uses and examples of thiazide diuretics

A 
Site of action - DCT (Na/Cl)
Used for - oedema, hypertension, hypercalcuria (renal stones), nephrogenic diabetes insipidus 
E.g. bendrofluamethazide, indapamide 
Duration - 12-24 hours 
Useful in renal failure - no 
Absorption speed - slow
131
Q

Give the site of action, uses and examples of K sparing diuretics

A

Site of action - DCT and CD (mineralocorticoid receptor/Na channel antagonist)
Used for - K conservation, oedema, hyperaldosteronism, hypertension, HF, cirrhosis
E.g. amiloride, spironolactone
Duration - 12-24 hours
Useful in renal failure - no, dangerous, hyperkalaemia
Absorption speed - slow

132
Q

What amino acids metabolised from food create acid and alkali loads?

A

Acid - lysine, arginine, methionine, cysteine

Alkali - glutamate, aspartate

133
Q

What factors affect/threaten acid-base homeostasis?

A 
CO2 from aerobic respiration 
Metabolism of food
Anaerobic respiration 
Loss of alkali in stool 
Loss of acid in vomit
134
Q

What are the 3 main components of acid-base regulation?

A

Buffering
Ventilation
Renal regulation

135
Q

What is a normal H ion concentration?

A

40 nmoles/L

136
Q

What is a normal blood pH?

A

7.4

137
Q

What is the consequence of buffering/compensatory repsonse?

A

H+ can be normal in the presence of an acid-base disturbance at the expense of other blood chemistry (e.g. HCO3, pCO2)

138
Q

What are buffers?

A

Weak acids partially dissociated in solution

139
Q

What is the CO2-HCO3 buffering system equation?

A

CO2 + H2O H2CO3 HCO3 + H

pH = 6.1 + log ([HCO3]/[CO2])

140
Q

What type of acid is CO2 and what does this mean?

A

Volatile

Can be eliminated from the body as a gas - 12-13000 mmol/day exhaled

141
Q

What acids are fixed and cannot be exhaled (converted to CO2) and what implications does this have?

A

Dietary and anaerobic respiration

In order to get rid of the extra H+, more HCO3 is consumed and then more needs to be generated

142
Q

What organs are responsible for CO2 and HCO3 regulation?

A

CO2 - lungs

HCO3 - kidneys

143
Q

How do the kidneys regulate acid-base balance?

A

Reabsorb filtered HCO3

Secrete fixed acid - titrate buffer (PO4) in urine, secrete NH4 into urine

144
Q

How much HCO3 is filtered daily?

A

> 4000 mmol/day

All of it

145
Q

Where is HCO3 reabsorbed in the kidneys and what does failure of this cause?

A

PCT (and thick ascending limb and DCT)

Metabolic acidosis

146
Q

What is the daily amount of fixed acid?

A

70 mmol/day

147
Q

What mechanism of fixed acid excretion is regulatable?

A

Secretion of NH4

PO4 is relatively fixed

148
Q

How is fixed acid excreted by the kidneys?

A

Tubular cells generate a new HCO3 which is absorbed with a H+ and binds to PO4 or is fixed with NH3 which is excreted as NH4 in urine

149
Q

Where does NH4 originate from in order to buffer H+?

A

Glutamine is metabolised to HCO3 and NH4+ in the PCT

NH4+ becomes NH3 in the interstitium and enters the tubule to joins with H+, forming NH4 which is excreted in urine

150
Q

How much H+ is excreted via titration of phosphate and excretion of ammonium daily?

A

Phosphate - 40 mmol/day

Ammonium - 50-100 mmol/day (can be increased)

151
Q

What is glutamine metabolism stimulated by?

A

Acidosis stimulated transport and oxidation of glutamine

152
Q

What is the difference between efficiency of renal and respiratory compensation?

A

Renal compensation may be complete but there is a limit to how hard patients are able to breath which can limit compensation

153
Q

What is acidosis and acidaemia?

A

Acidosis - abnormal HCO3
Acidaemia - decreased pH (increased H+)
More patients will be acidotic

154
Q

What would happen to H+, pCO2 and HCO3 in metabolic acidosis?

A

H+ - increased or normal
pCO2 - decreased (compensation)
HCO3 - decreased

155
Q

What would happen to H+, pCO2 and HCO3 in respiratory acidosis?

A

H+ - increased or normal
pCO2 - increased
HCO3 - increased (compensation)

156
Q

What would happen to H+, pCO2 and HCO3 in metabolic alkalosis?

A

H+ - decreased or normal
pCO2 - increased (compensation)
HCO3 - increased

157
Q

What would happen to H+, pCO2 and HCO3 in respiratory alkalosis?

A

H+ - decreased or normal
pCO2 - decreased
HCO3 - decreased (compensation)

158
Q

How is an acid-base disorder diagnosed?

A

Initial clinical assessment - history, examination, investigation
Acid-base diagnosis - blood-gas and other results
Clinical diagnosis - collate information

159
Q

What are the causes of metabolic acidosis?

A

Addition of extra acid (metabolism, ingestion)
Failure of acid excretion (renal tubular acidosis)
Loss of HCO3 (stool or urine)

160
Q

What is the primary abnormality and compensatory mechanism in metabolic acidosis?

A

Abnormality - decreased HCO3

Compensation - fall in pCO2 (increased respiration)

161
Q

What are the systemic effects of metabolic acidosis?

A

CV - arrhythmia, decreased contractility, vasodilation
Respiratory - increased ventilation (Kussmaul’s breathing)
Metabolic - protein wasting, bone resorption
Other - neutrophilia

162
Q

What is the anion gap and what is its normal value?

A

The difference between measured cations (Na+ and K+) and anions (Cl- and HCO3-) in blood
(Na) - (Cl + HCO3)
6-12 mmol/L

163
Q

What information does the anion gap give?

A

Identification of the cause of metabolic acidosis
If the gap is increased, another molecule outwith the 4 which are being measured is involved
E.g. lactic acidosis, ketoacidosis, poisoning

164
Q

What adjustments need to be made to the anion gap if albumin is decreased?

A

Decreased anion gap by 2.5 for every 10 g/l fall in albumin

165
Q

How would you check if the respiratory compensation of a patient with metabolic acidosis is adequate?

A

pCO2 should fall 0.125kPa (from 5) for every 1mmol/L fall in bicarb (from 25)
If pCO2 has not fallen sufficiently, there may be a co-existing respiratory acidosis

166
Q

How does acidosis due to chronic renal failure progress?

A

Initially - normal AG gap (decreased renal NH4 excretion); titratable acid excretion preserved (increased PO4 excretion and decreased reabsorption)
Eventually - high AG (accumulation of PO4 and other anions)

167
Q

How does lactic acidosis occur?

A

Lactic acid produced by glycolysis - metabolism of pyruvate
LA buffered by HCO3 to lactate and metabolised in liver/kidney
LA production is greater than renal excretion of H+
Acidosis occurs due to hypoperfusion and reduced hepatic clearance - sepsis, drugs (metformin), liver failure, poisoning (cyanide, aspirin)

168
Q

What is the primary abnormality and compensatory response in metabolic alkalosis?

A

Abnormality - decreased H+ and increased HCO3

Compensation - increased pCO2 (hyperventilation)

169
Q

What are the main causes of metabolic alkalosis?

A

Inability to excrete HCO3
Volume depletion - gastric acid loss (vomiting), diuretics
Volume repletion - mineralocorticoids, hyperaldosteronism, Cushing’s, profound K depletion

170
Q

Why does HCO3 excretion fail to occur in maintained metabolic alkalosis?

A

HCO3 is reabsorbed in the kidneys with Na, especially when there is a Cl deficiency

171
Q

Outline the mechanisms of volume, chloride and potassium depletion in metabolic alkalosis

A

Volume depletion - Na reabsorption drives HCO3 absorption (promoted by aldosterone)
Chloride depletion - HCO3 reabsorption in DCT requires Cl secretion (decreased Cl with cause increased HCO3 reabsorption)
Potassium depletion - unknown; H secretion requires K reabsorption, when retaining K, H will be excreted

172
Q

What is the treatment for metabolic alkalosis?

A

Fluid resuscitation - 0.9% NaCl

Treat cause

173
Q

Describe respiratory acidosis

A

Hypoventilation
Increased pCO2 with compensatory HCO3 retention
H+ buffered intracellularly with later renal compensation

174
Q

Describe respiratory alkalosis

A

Hyperventilation

Decreased pCO2 with compensatory HCO3 excretion

175
Q

What happens to Ca in acute alkalosis?

A

Increased binding of Ca to albumin causes a fall in free ionised Ca, leading to tetany

176
Q

How is concentration of H+ found from pH using a calculator?

A 
pH = -log[H+]
[H+] = 10^-pH
177
Q

What is the most important vehicle for H+ excretion?

A

NH4+ as it is regulatable and produced by glutamine metabolism

178
Q

What conditions can be investigated using dipstick urinalysis?

A

Kidney function
UTIs
Diabetes mellitus
Liver disease

179
Q

What needs to be checked before doing a urinalysis?

A

Patient details
Expiry date on container
Visual inspection of sample

180
Q

How long should a dipstick be submerged in urine during urinalysis?

A

2 seconds

181
Q

What might leukocytes in a urine sample mean?

A

Infection
Inflammation
Tumour

182
Q

What might nitrites in a urine sample mean?

A

UTI (nitrates usually present)

183
Q

What might urobilinogen in a urine sample mean?

A

Haemolytic anaemia (usually in stool)

184
Q

What might blood in a urine sample mean?

A

Infection
Stone
Trauma
Glomerulopathy

185
Q

What might specific gravity in a urine sample mean?

A

Diabetes insipidus (concentration measurement)

186
Q

What might ketones in a urine sample mean?

A

Ketoacidosis

Diabetes mellitus

187
Q

What might glucose in a urine sample mean?

A

Diabetes mellitus

188
Q

What might protein in a urine sample mean?

A

Albumin >300 mg/L

189
Q

Would a normal urinalysis rule out renal pathology?

A

No

Further tests and renal imaging required

Reproduction, Nephrology and Urology (4 decks)

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