Tubular absoprtion

Common types of transporters in the renal tubules

PCT basolateral - Na/K exchanger
luminal - Na/H exchanger
Cl/HCO3 exchanger
thick ascending loop
basolateral - Na/K exchanger, K/Cl co-transporter
luminal - Na/K/2CL co-transporter (blocked by loop diurectics)
DCT
basolateral - Na/K exchanger (aldosterone depedent up-regulation)
luminal - Na/cl co-transporter (blocked by thiazides)
GOO
Cause: Peptic ulcer, CA, caustic ingestion, bezoar, pseudocyst, gallstone, extrinsic tumour
Hypokalaemic, hypochloraemic metabolic alkalosis with parodoxical aciduria
2 main problems with GOO
1. Loss of H, Cl from stomach
2. volume loss and Na loss from stomach
Resulting in:
Loss of Cl
1. kidney preserve electrical neutrality by conserving HCO3 due to lack of Cl
2. lack of Cl for co-transporter of Na absorption
3. Chloride shift (Hamburger shift) worsening the alkalosis
Loss of volume/Na:
Resultant - hyperaldosteronism, preservation of Na
kidney primarily preserve Na over H and K
Lack of Cl for co-transporter, hence need to use exchanger
proximal tubule - kidney preserve Na in preference to H
Uses Na/H exchanger at proximal tubule
Uses Na/K exchanger at distal tubule (aldosterone sensitive)

Alkalosis

Due to aciduria and direct loss of hydrogen ions from the vomitus
Treatment - NaCl drip
replaces the Cl - allows HCO3 to be absorbed, allows H/K to be conserved
replaces the Na and H20 hence volume - removes aldosterone stimulation
If hypokalaemic - try to withhold K replacement till urine output present
Other complications to think about:
Obstruction, fluid, electrolytes, aspiration, diaphragmatic splinting
Hyponatraemia
Rule out pseudohyponatraemia first
Hypovolemia

Euvolemia

Hypervoloemia

Renal

Polydipsia
SIADH
Hypothyroidism
Adrenal insufficiency

cirrhosis, renal failure +

nephrosis, CCF
iatrogenic

Diuretics
Aldosterone deficiency
Renal tubular dysfunction
GI
vomiting, diarrhoea
3rd space
Addisonian crisis

Hypertonic saline - 1mmol/kg

3% saline ~ 0.5mmol/ml ~ 513/L
Expected change in Na = (513 - serum sodium) / (TBW +1)
TBW = 0.6(M) or 0.5(W) x weight
eg expected change in sodium for 70kg man with 3%saline = (513 - 110)/ ((0.6 x 70)+1)
= 9.37mmol/L
Attempt to raise sodium by 0.5mmol/hr (to give ~12 mmol/day)
= 0.5/9.37 = 0.053L/hr = 53ml/hr

Post-obstructive diuresis
Pathophysiology
1. Excess water/Na retention
2. Retention of urea and other non-reabsorbable solutes
3. Decreased tubular absorption due to altered expression of transporters
4. Increased tubular flow rate with resultant less time for absorption of water and Na

Acid base
CO2 diffuses freely btw interstitium, capillaries, cells
Intracelluar - Carbonic anhydrase -found in most cells but high concentration in RBC, kidney,
lungs
CO2 + H20 >>>>>>> H2CO3
Carbonic anhydrase is found in RBC, kidneys ? lung, brain
H2CO3 then spontaneously dissociates into Hydrogen and bicarbonate ions
Chloride shift (Hamburger shift) - bicarbonate exchanged with chloride across cell membrane
Hydrogen trapped in RBC but bicarbonate exchanged with chloride by Band 3 exchanger
CO2 transport in blood - 5% dissolved, 10% bound to Hb, proteins, majority as bicarbonate ions
O2 transport - 1.5% dissolved, rest by Hb
Use 40mmHg as ideal CO2, 24 as ideal bicarbonate
Expected PaO2 for any given FiO2 =
FiO2 - 10 (KPA) or
FiO2 x 5 (mmHg)

Metabolic acidosis
expected compensated PCO2 = (1.5 [HCO3-]) + 8 2
Respiratory acidosis
Acute
H2CO3 + Hb- HHb + HCO3As shown above, each buffering reaction produces HCO3-, which leads to an increase in
plasma [HCO3-]
Expected 1 meq/L rise in HCO3 = every 10 mmHg rise in the PCO2.
Chronic
Increased excretion of titratable acid and ammonium, resulting in the addition of new
HCO3- to the extracellular fluid, complete after 3-5 days
Expected 3.5 meq/L rise in plasma HCO3- concentration for every 10 mmHg increase in
the PCO2.
Metabolic Alkalosis
Expected 0.7 mmHg rise in pCO2 for every 1.0 meq/L increment in the plasma [HCO3-]
Respiratory alkalosis
Acute

Result of cell buffering

Expected 2meq/L fall in HCO3- for every 10 mmHg decrease in the PCO2
Chronic
Renal compensation
4 meq/L reduction in plasma [HCO3-] for every 10 mmHg reduction in PCO2.

Peripheral
chemoreceptor

Aortic body - Mainly PaO2, CO2

Carotid body - Mainly PaO2, CO2, pH, temp

Central
chemoreceptor

Ventrolateral medulla - Mainly pH but hydrogen cannot diffuse across, only

CO2 can, then converted to carbonic acid by carbonic anhydrase

Regulator

Respi centre in medulla

Effector

Diaphragm, intercoastal muscles - depth and rate

TURP Complications
Early
1. haemorrhage
2. bladder perforation
3. hypothermia
4. TURP syndrome
1. osmolality/Plasma Na
- cerebral oedema, raised ICP, LOC, nausea, vomiting, confusion, seizure, fluid shift with
resultant hypotension
2. Intravascular volume
- APO, cardiac failure, bradycardia
3. Glycine toxicity
-inhibitory neurotransmitter of GABA
- oxidative deamination to glyoxylic acid and ammonia (unclear role of ammonia)
- ammonia urea cycle to form urea requiring arginine ?deficiency
- restlessness, headache, tachypnoea, a burning sensation in the face or
hands or visual disturbance
Risk factors:
Long surgery, high irrigation pressures, large amt of prostate cut out with bleeding,

hypotensive pt
Prevention:
Short surgery, good technique, limit cutting of prostate to limit open venous plexus,
maintain BP to increase capillary hydrostatic pressure, height of fluid ~60cm, spinal
anaes to monitor neuro, no administration of hypotonic IV fluids, using vasopressors
rather than IV fluids to bring up BP after spinal
Treatment:
Stop surgery, stop IV fluids
Airway, O2
Vasopressors
Control seizures, benzo, KIV Mg
Bloods - Hb, Na, osmolality, ABG, ecg
Insert monitoring lines
Transfer HDU/ICU
If APO - lasix/mannitol (less shift of Na)
If Na not too bad - can just get away with fluid restriction
Check osmolaltiy and Na frequently
If Na <120 or severe symptoms - hypertonic saline
Calculate total body water as 0.6body weight (kg),
e.g. for a 70 kg man, TBW = 42 litre
2 x TBW is the number of millilitres of NaCl 3% which will raise serum [Na] by
1 mmo/ litre, e.g. 2x 42 = 84 ml of NaCl 3% over 1 h will raise serum sodium
by 1 mmol/litre - aim for resolutionf of symtpoms

5. bacteraemia, sepsis
Late
Retrograde ejaculation
failure to TOC

Respiratory acidosis
Respi depression
OSA
COPD

Anatomical
Chest wall deformity
Flail chest
Diaphragmatic splinting
Drugs
- Opiods, pinpoint pupils
- BDZ
- Barbiturates
Neurological:
MG
Diaphragm paralysis
Motor neuron disease
Head injury
Eletrolytes/alcohol/metabolic >> unconsciousness

Treatment ABC
NIV, invasive ventilation
drugs A. Bronchodilators
B. Naxolone - pure competitive antagonist of opioid miu receptors, short half life
0.4 - 2mg IV aliquots, repeated every 2-3min till reversal of effect - unless addiction then give much less to prevent withdrawal
If needed for long - IV infusion (give of total dose given in 1st hour)
Monitor in High-D, continuous pulse ox
C. Flumazenil 0.2 mg IV inj over 15-30 sec
then 0.3 mg over 15-30 sec 1 min later
then 0.5 mg IV over 15-30 sec to max cumulative dose of 3 mg/hr
Rarely pt may require titration up to total dose 5 mg; if no response after 5 min, sedation
unlikely to be 2ndary to benzodiazepines, slow infusion of lowest dose required decr to
adverse events

Blood products

Product

Contents

Storage and Lifespan

Whole blood

70 ml citrate preservative solution is added

to 420 ml blood. After 3 days, the platelets
will not function and after 3 weeks the
levels of 2,3-diphosphoglycerate (2,3-DPG)
diminish. There are normal concentrations
of albumin and clotting factors, except
factors V and VIII, which are reduced to
20% of normal.

Storage temp 1-6C

Has a shelf-life of 35 days.

PRBC

Each 250 ml bag has a haematocrit of 0.6.

There are no platelets, and 2,3-DPG levels
remain normal for up to 14 days.

Storage temp 1-6C

35 days with SAGM (saline,
adenine, glucose, mannitol)
42 days with A-CPD
(adenine, citrate, phosphate,
dextrose)

FFP

This is produced from plasma from a single

donation. Each 150 ml bag contains all
clotting factors, albumin and gammaglobulin. The usual starting dose is 10-15
ml/kg (equivalent to four packs of FFP for a
70kg person), which raises the coagulation
levels 12-15%.

Storage temp: below -20C

Shelf life 12 months

precipitated from FFP when slowly thawed.

Contains high levels of factor VIII,
fibrinogen and von Willebrand factor.
Cryoprecipitate is prepared from a single
donation. Each unit contains a volume of
20-40 ml. The concentration of fibrinogen is
>140mg/unit and factor VIIIc >70 IU/unit.
ABO compatible units should be used, and
treatment considered if the plasma
fibrinogen is <0.8 g/litre. Ten units of
cryoprecipitate should increase fibrinogen
level by 1 g/litre.

Storage temp: below -20C

Shelf life 12 months

1 unit contains ~55 plt

Pooled units contained ~200 -240 plts

Store room temp 20 to 24

degrees in an agitator
Given within 60 min
Shelf life 5 days

Cryoprecipitate

Platelet

Clotting factor
concentrate
Prothrombin
complex
concentrate

Factors II, VII, IX, X

Use in conjunction with factor VII complex
concentrate/FFP due to low levels of factor

Must be used immediately

after thawing
Must be ABO compatible.
30 minutes to thaw out

Must be used immediately

after thawing
Must be ABO compatible.
30 minutes to thaw out

Also known as
Factor IX
complex
concentrate

VII

Albumin

Jehovahs witnesses
2.5.1 Treatment generally regarded as unacceptable by Jehovahs Witnesses:
Transfusion of whole blood, packed red cells, white cells, plasma (FFP), and platelets
Preoperative autologous blood collection and storage for later reinfusion (pre-deposit)
2.5.2 Matters that Jehovahs Witnesses recognise as being of personal choice: Each Witness
decides whether he/she wishes to accept the following as a matter of individual choice. It is
therefore important to discuss with each patient whether or not these are acceptable.
Blood salvage (intra and post-operative), haemodilution, haemodialysis, and cardiac bypass
Blood fractions of plasma or cellular components (eg albumin, immunoglobulins, clotting
factors)
Whilst haemoglobin based oxygen carrying solutions are not yet licensed in the UK, they may
soon be available and may be acceptable to some Jehovahs Witness patients.
Transplantation, including solid organ, bone, tissue etc
Epidural blood patch (see below)

Young adults of sound mind aged 1618 years have a statutory right
in England and Wales to consent to procedures on their own account
and there is no legal requirement to obtain additional consent from a
parent or guardian. The patients consent takes precedence over parental
objections. Parents may give lawful consent to a young adult unable to
consent in their own right, because of decreased consciousness.
In Scotland, young persons aged 16 or over have an exclusive right to
determine their own medical treatment. The parent has no right to consent
or interfere; similarly, recourse to the Courts would not be available.