Week 3 Flashcards
(189 cards)
1
Q
What are the main functions of the kidney?
A
Filter metabolic waste
Control fluid volume
Maintain electrolyte balance
2
Q
How many litres of water are in the body?
A
42L (60% weight)
3
Q
What are the body fluid compartments?
A
Intracellular
Extracellular - intravascular, extravascular (interstitial)
4
Q
In what direction do oncotic and hydrostatic pressure push fluid?
A
Oncotic - inwards
Hydrostatic - outwards
5
Q
What percentage of the cardiac output do the kidneys receive?
A
20%
6
Q
What are the 3 main processes which occur in the nephron?
A
Glomerular filtration
Tubular reabsorption
Tubular secretion
7
Q
What is glomerular filtration?
A
Filtering of blood into tubule forming the primitive urine (glomerular filtrate)
8
Q
What is tubular reabsorption?
A
Selective absorption of substances from tubule to blood
9
Q
What is tubular secretion?
A
Secretion of substances from blood to tubular fluid
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
11
Q
What particles are not filtered by the kidney?
A
Haemoglobin, albumin, RBCs
12
Q
What is a normal glomerular filtration rate?
A
100ml/min (144L/day)
13
Q
What particles are filtered by the kidney?
A
Glucose, water, urea, amino acids, salt
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
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
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
17
Q
Which part of the nephron is responsible for fine tuning?
A
DCT
18
Q
What parts of the nephron are responsible for altering urine concentration?
A
LoH and CD
19
Q
What is the plasma osmolality?
A
300 mosmoles/kg
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
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
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
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
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
25
What happens when the macula densa senses increased and decreased tubular flow?
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
26
What is the role of natriuretic peptides in sensing body fluid volume?
Produced in response to increased volume and oppose effects of angiotensin II - pressure natriuresis
27
Give examples of acidic and alkaline foods
Acidic - white bread, alcohol, sugar, meat, fish, nuts
| Alkaline - asparagus, melon, avocado, fruit, vegetables
28
What is the carbonic acid/bicarbonate buffer equation?
H + HCO3 (bicarbonate) →← H2CO3 (carbonic acid) →← H2O + CO2
29
What is the concentration of H ions which enter the body each day?
70 mmol
30
How does the kidney participate in acid-base balance?
Reabsorbs filtered bicarbonate, filters non-volatile acids (e.g. sulphuric), PCT synthesises ammonium from H
31
How is calcium concentration regulated by the kidney?
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
32
How is the kidney involved in activation of vitamin D?
2nd hydroxylation of vitamin D occurs in the kidney
33
How is erythropoietin regulated by the kidney?
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
34
What are the features of extracellular fluid overload?
Tissue and pulmonary oedema, hypertension, increased JVP
| Needs diuretic
35
What are the features of extracellular fluid depletion?
Dry mucous membranes, reduced skin turgor, hypotension, decreased JVP
Needs saline
36
What features does a substance need to have in order to use it in measuring GFR?
Completely filtered
Not reabsorbed or secreted
(e.g. inulin - gold standard but cumbersome and expensive)
37
What 2 substances are almost perfect for measuring GFR?
Creatinine, cystatin C
38
What is creatinine and why is it used for measuring GFR despite incomplete filtration and some tubular secretion?
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
39
What is the equation for calculating creatinine clearance (GFR)?
Clearance = (urine volume x [urine creatinine] / [plasma creatinine]) / 1440*
*Timed urine collection over 24 hours
40
If GFR is high, will creatinine concentration be high or low?
Low
41
What factors is creatinine concentration dependent on?
Muscle mass, age, sex
42
What is the MDRD 4-variable formula?
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
43
What are the limitations of eGFR?
Not accurate:
- >60ml/min
- <18 years of age (separate paediatric formula)
- immediate changes
44
What are the ways in which urine can be examined?
Inspection
Dipstick
Microsopy
Biochemistry
45
What urine tests can be done using a dipstick?
Albumin, blood, pH, ketones, glucose, bilirubin, leukocytes, nitrites
46
What does a positive urine test for protein indicate?
Glomerular disease
47
Why is spot urine protein concentration not enough to quantify proteinuria and what is done instead?
Varies with degree of urine dilution
| Ratio of protein to creatinine is used instead
48
What might urine microscopy tell us?
Confirmation of non-visible haematuria
| Specific abnormalities
49
What might urine electrolytes and osmolality tell us?
Kidney response to changes in fluid volume
Cause of acid-base disorder
Identification of stone-forming tendency
50
What eGFR value indicates kidney dysfunction/damage/disease?
<60 ml/min
51
How is kidney injury/disease defined?
Reduced eGFR and detection of urine protein with/without blood
52
What do AKI and CKD stand for?
Acute kidney inury and chronic kidney disease
53
What causes AKI or CKD?
Ineffective blood supply, glomerular disease, tubulo-interstitial disease, obstructive uropathy
54
What is oliguria and what is it a sign of?
Reduced urine output
| Impending acute tubular necrosis; kidneys are sensitive to other insults when oliguric
55
What risk is increased by chronic kidney disease?
Cardiovascular risk
56
What is the National Kidney Foundation classification of chronic kidney disease?
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)
57
What imaging modalities are used to image the kidney?
X-ray, ultrasound, CT, MRI, radioisotope, angiography
58
What is the most commonly used modality to image the kidney and what information can it give?
Ultrasound
| Size, shape, location, number, structure, drainage/obstruction, blood flow
59
Which kidney is more superior?
Left
60
What ultrasound findings are normal for kidneys?
>10cm length
>1cm cortex
Less bright than liver
61
When imaging the kidneys, what is CT useful for?
Trauma, stones, tumours, infection
62
What needs to be considered when using contrast-enhancing CT imaging for the kidney?
Potential nephrotoxicity; risk:benefit must be assessed, may be able to use pre-hydration
63
When imaging the kidneys, what is MRI useful for?
Soft tissue pathology; tumours, infection
64
What needs to be considered when using Gd-contrast MRI for the kidney?
Nephrogenic systemic fibrosis
65
When imaging the kidneys, what is isotope scanning useful for?
Structure, perfusion, excretion, renal function
66
What is the basic mechanism by which kidney stones/crystals form?
Too much solute, not enough solution
67
What is a kidney stone?
A solid concretion of crystal aggregate formed within the urinary space
68
What does cystolithiasis mean?
Stone in the bladder
69
What are the main risk factors for kidney stones?
Male, family history, BMI >27, dehydration, UTI, immobility, obesity and metabolic syndrome
70
What factors decrease the risk of kidney stones?
Vegetarian diet, high fruit and fibre
71
What is the composition of kidney stones and their prevalence?
```
Calcium oxalate/phosphate (80%)
Magnesium ammonium phosphate/struvite (5-10%)
Uric acid (5-10%)
Cystine (1-2%)
Mixed
```
72
How would a patient with kidney stones present?
Flank tenderness, signs of infection, obesity, hypertension, gout tophi (uric acid crystals), diabetes
73
What is nephrocalcinosis?
Deposition of calcium salts in renal parenchyma
| Normally calcium phosphate
74
What is medullary sponge kidney?
A congenital disorder of the kidneys characterised by cystic dilatation of the collecting tubules, predisposing to stone formation
Normally calcium phosphate or oxalate
75
What conditions can predispose a patient to calcium kidney stones?
Primary hyperparathyroidism, hypercalcaemia, hypercalciuria
76
What conditions can predispose a patient to oxalate/urate/cysteine kidney stones?
Hyperoxaluria, hyperuicaemia, cystinuria
77
What conditions can cause a pro-calculus urinary environment?
Hypocitraturia, renal tubular acidosis (type 1)
78
What is the normal pH of urine?
4.6-8.0
79
At what pH do calcium, struvite, uric and cysteine stones precipitate?
Calcium and struvite - >7.0
| Uric and cysteine - >6.0
80
How are stones in the kidney treated?
<2 cm - manage, extracorporeal shock wave lithotripsy
| >2 cm/multiple - manage, percutaneous ultrasonic lithotripsy
81
How are stones in the ureter treated?
Small (<7 mm) - allow 2-4 weeks to pass; ureteroscopic removal, ESWL
Large (>7 mm) - ESWL, ureteroscopic stone fragmentation, open surgery
82
What are ureteric stents used for?
Draining obstructed kidney to relieve pain, dilating ureters to facilitate stone passage, facilitating ESWL and ureteroscopic procedures
83
What secondary prevention is there for kidney stones?
Monitor with periodic imaging
Citrate
Stone-specific advice
84
What secondary prevention advice should be given regarding calcium phosphate kidney stones?
```
Increase fluids (>2L/day) treat cause, consider citrate or thiazide
No good evidence for low calcium diet
```
85
What secondary prevention advice should be given regarding calcium oxalate kidney stones?
```
Increase fluids (>2L/day), low oxalate diet, consider citrate or thiazide
No good evidence for low calcium diet
```
86
What secondary prevention advice should be given regarding uric acid kidney stones?
Increase fluids (>2L/day), xanthine oxidase inhibitors (treat hyperuricaemia), treat cause, alkalinise urine to pH > 6.0 (bicarbonate/citrate)
87
What secondary prevention advice should be given regarding cysteine kidney stones?
Increase fluids (>2L/day), reduce protein and sodium in diet, alkalinise urine to pH > 7.0 (bicarbonate/citrate)
88
What secondary prevention advice should be given regarding struvite kidney stones?
Debulk where possible, aggressive treatment of UTI
89
What is the most important inhibitor of kidney stone formation and how does it achieve this?
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
What is Tamm-Horsfall protein?
Macromolecule in urine which inhibit calcium oxalate aggregation
91
What is the anatomical position of the kidneys?
Obliquely in a paravertebral gutter at the level of the upper 3 lumbar vertebrae (left extends to the 11th rib)
92
What are the posterior relations of the kidneys?
Diaphragm, posterior abdominal wall muscles, subcostal/iliohypogastric/ilioinguinal nerves
93
What are the anterior relations of the right and left kidneys?
Right colic flexure
| Left colic flexure
94
What are the relations of the hilum of the right and left kidneys?
Right - duodenum
| Left - pancreas
95
What type of arteries are the segmental branches of the renal artery?
End arteries
96
What are the anatomical features of the left renal vein?
Longer than the right; receives the left gonadal and left suprarenal veins
97
What type of membrane lines the ureter?
Mucous membrane
98
By what movement does urine pass through the ureter?
Peristalsis
99
At what points is the ureter constricted, therefore making it susceptible to stone obstruction?
As it crosses the brim of the lesser pelvis and as it passes through the bladder wall
100
What structure crosses the ureter in the pelvis in males and females?
Males - vas deferens
| Females - uretetic artery
101
What feature allows the bladder to expand when filled with urine?
Retropubic space is filled with loose areolar tissue
102
Which ligament anchors the bladder neck to the pubis?
Puboprostatic ligament
103
What does the bladder rest on?
Pelvic diaphragm
104
What is the trigone?
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
Why do the ureters pass through the bladder wall obliquely?
Ensures that an increase in urine and pressure in the bladder will compress the ureters to prevent reflux
106
Which muscle lies on the medial side of the kidneys?
Psoas major
107
Which muscles lie on the lateral side of the kidneys?
Quadratus lumborum and transversus abdominis
108
What do the adrenal/suprarenal glands produce?
Cortex - corticosteroids and androgens
| Medulla - adrenaline and noradrenaline
109
What effect does contraction of the psos major have on the hip and thigh?
Hip - flexion
| Thigh - flexion and lateral rotation
110
What do medullary rays consist of?
The collecting ducts draining the nephron
111
What type of epithelium is present in the Bowman's capsule?
Simple squamous
112
What type of epithelium is present in the PCT?
Cuboidal
113
What are juxtaglomerular cells?
Specialised smooth muscle cells in the wall of the afferent arteriole which contain secretory granules of renin
114
When do the kidneys begin to form in embryological development?
Week 4
115
What are the 3 main components of the male urethra?
Prostatic, membranous, spongy
116
What renal factors affect drug elimination?
Glomerular filtration
Tubular secretion
Diffusion
Protein binding
117
What is gentamicin?
Glycoside antibiotic
| Almost exclusively excreted by the kidney; not well tolerated in dysfunction (PCT nephrotoxicity)
118
How is rifampicin affected by kidney dysfunction?
It's not - metabolised by the liver
119
How is vancomycin affected by kidney dysfunction?
Much more prolonged half-life
120
What adjustments to dosing can be made in renal dysfunction and for which drugs would this need to be done?
Decrease dose and increase dose interval
| Drugs with at least 50% renal clearance and a low therapeutic index (e.g. digoxin, lithium)
121
What drugs will a patient with kidney dysfunction become more sensitive to?
Opiates, morphine, antihypertensives
122
What drugs will a patient with kidney dysfunction become less sensitive to?
Diuretics, urinary antibacterials
123
How are the adverse effects of metformin and sulphonylureas enhanced in renal dysfunction?
Metformin - increased risk of lactic acidosis
| Sulphonylureas - provoked hypoglycaemia
124
Why are the kidneys vulnerable to toxic drug effects?
Large blood flow
| Drugs/metabolites concentrate in renal medulla and tubular cells
125
What types of renal impairment are caused by drugs?
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
What do ACE inhibitors do and when are they used?
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
How do NSAIDs work and what are their effect on the kidney?
Inhibit prostaglandins which normally causes afferent arteriole dilation to maintain glomerular capillary pressure
128
What is acute interstitial nephritis and what symptoms does it cause?
A cause of acute renal failure resulting from immune-mediated tubulointerstitial injury initiated by medications (antibiotics, anticonvulsants, diuretics, PPIs)/infection
Raised eosinophils, rash
129
Give the main features of loop diuretics
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
Give the site of action, uses and examples of thiazide diuretics
```
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
Give the site of action, uses and examples of K sparing diuretics
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
What amino acids metabolised from food create acid and alkali loads?
Acid - lysine, arginine, methionine, cysteine
| Alkali - glutamate, aspartate
133
What factors affect/threaten acid-base homeostasis?
```
CO2 from aerobic respiration
Metabolism of food
Anaerobic respiration
Loss of alkali in stool
Loss of acid in vomit
```
134
What are the 3 main components of acid-base regulation?
Buffering
Ventilation
Renal regulation
135
What is a normal H ion concentration?
40 nmoles/L
136
What is a normal blood pH?
7.4
137
What is the consequence of buffering/compensatory repsonse?
H+ can be normal in the presence of an acid-base disturbance at the expense of other blood chemistry (e.g. HCO3, pCO2)
138
What are buffers?
Weak acids partially dissociated in solution
139
What is the CO2-HCO3 buffering system equation?
CO2 + H2O H2CO3 HCO3 + H
| pH = 6.1 + log ([HCO3]/[CO2])
140
What type of acid is CO2 and what does this mean?
Volatile
| Can be eliminated from the body as a gas - 12-13000 mmol/day exhaled
141
What acids are fixed and cannot be exhaled (converted to CO2) and what implications does this have?
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
What organs are responsible for CO2 and HCO3 regulation?
CO2 - lungs
| HCO3 - kidneys
143
How do the kidneys regulate acid-base balance?
Reabsorb filtered HCO3
| Secrete fixed acid - titrate buffer (PO4) in urine, secrete NH4 into urine
144
How much HCO3 is filtered daily?
>4000 mmol/day
| All of it
145
Where is HCO3 reabsorbed in the kidneys and what does failure of this cause?
PCT (and thick ascending limb and DCT)
| Metabolic acidosis
146
What is the daily amount of fixed acid?
70 mmol/day
147
What mechanism of fixed acid excretion is regulatable?
Secretion of NH4
| PO4 is relatively fixed
148
How is fixed acid excreted by the kidneys?
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
Where does NH4 originate from in order to buffer H+?
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
How much H+ is excreted via titration of phosphate and excretion of ammonium daily?
Phosphate - 40 mmol/day
| Ammonium - 50-100 mmol/day (can be increased)
151
What is glutamine metabolism stimulated by?
Acidosis stimulated transport and oxidation of glutamine
152
What is the difference between efficiency of renal and respiratory compensation?
Renal compensation may be complete but there is a limit to how hard patients are able to breath which can limit compensation
153
What is acidosis and acidaemia?
Acidosis - abnormal HCO3
Acidaemia - decreased pH (increased H+)
More patients will be acidotic
154
What would happen to H+, pCO2 and HCO3 in metabolic acidosis?
H+ - increased or normal
pCO2 - decreased (compensation)
HCO3 - decreased
155
What would happen to H+, pCO2 and HCO3 in respiratory acidosis?
H+ - increased or normal
pCO2 - increased
HCO3 - increased (compensation)
156
What would happen to H+, pCO2 and HCO3 in metabolic alkalosis?
H+ - decreased or normal
pCO2 - increased (compensation)
HCO3 - increased
157
What would happen to H+, pCO2 and HCO3 in respiratory alkalosis?
H+ - decreased or normal
pCO2 - decreased
HCO3 - decreased (compensation)
158
How is an acid-base disorder diagnosed?
Initial clinical assessment - history, examination, investigation
Acid-base diagnosis - blood-gas and other results
Clinical diagnosis - collate information
159
What are the causes of metabolic acidosis?
Addition of extra acid (metabolism, ingestion)
Failure of acid excretion (renal tubular acidosis)
Loss of HCO3 (stool or urine)
160
What is the primary abnormality and compensatory mechanism in metabolic acidosis?
Abnormality - decreased HCO3
| Compensation - fall in pCO2 (increased respiration)
161
What are the systemic effects of metabolic acidosis?
CV - arrhythmia, decreased contractility, vasodilation
Respiratory - increased ventilation (Kussmaul's breathing)
Metabolic - protein wasting, bone resorption
Other - neutrophilia
162
What is the anion gap and what is its normal value?
The difference between measured cations (Na+ and K+) and anions (Cl- and HCO3-) in blood
***(Na) - (Cl + HCO3)***
6-12 mmol/L
163
What information does the anion gap give?
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
What adjustments need to be made to the anion gap if albumin is decreased?
Decreased anion gap by 2.5 for every 10 g/l fall in albumin
165
How would you check if the respiratory compensation of a patient with metabolic acidosis is adequate?
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
How does acidosis due to chronic renal failure progress?
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
How does lactic acidosis occur?
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
What is the primary abnormality and compensatory response in metabolic alkalosis?
Abnormality - decreased H+ and increased HCO3
| Compensation - increased pCO2 (hyperventilation)
169
What are the main causes of metabolic alkalosis?
Inability to excrete HCO3
Volume depletion - gastric acid loss (vomiting), diuretics
Volume repletion - mineralocorticoids, hyperaldosteronism, Cushing's, profound K depletion
170
Why does HCO3 excretion fail to occur in maintained metabolic alkalosis?
HCO3 is reabsorbed in the kidneys with Na, especially when there is a Cl deficiency
171
Outline the mechanisms of volume, chloride and potassium depletion in metabolic alkalosis
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
What is the treatment for metabolic alkalosis?
Fluid resuscitation - 0.9% NaCl
| Treat cause
173
Describe respiratory acidosis
Hypoventilation
Increased pCO2 with compensatory HCO3 retention
H+ buffered intracellularly with later renal compensation
174
Describe respiratory alkalosis
Hyperventilation
| Decreased pCO2 with compensatory HCO3 excretion
175
What happens to Ca in acute alkalosis?
Increased binding of Ca to albumin causes a fall in free ionised Ca, leading to tetany
176
How is concentration of H+ found from pH using a calculator?
```
pH = -log[H+]
[H+] = 10^-pH
```
177
What is the most important vehicle for H+ excretion?
NH4+ as it is regulatable and produced by glutamine metabolism
178
What conditions can be investigated using dipstick urinalysis?
Kidney function
UTIs
Diabetes mellitus
Liver disease
179
What needs to be checked before doing a urinalysis?
Patient details
Expiry date on container
Visual inspection of sample
180
How long should a dipstick be submerged in urine during urinalysis?
2 seconds
181
What might leukocytes in a urine sample mean?
Infection
Inflammation
Tumour
182
What might nitrites in a urine sample mean?
UTI (nitrates usually present)
183
What might urobilinogen in a urine sample mean?
Haemolytic anaemia (usually in stool)
184
What might blood in a urine sample mean?
Infection
Stone
Trauma
Glomerulopathy
185
What might specific gravity in a urine sample mean?
Diabetes insipidus (concentration measurement)
186
What might ketones in a urine sample mean?
Ketoacidosis
| Diabetes mellitus
187
What might glucose in a urine sample mean?
Diabetes mellitus
188
What might protein in a urine sample mean?
Albumin >300 mg/L
189
Would a normal urinalysis rule out renal pathology?
No
| Further tests and renal imaging required
