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Case 8: GIT diarrhoea > Electrolyte & Water losses (Physiology & Chem Path) > Flashcards

Electrolyte & Water losses (Physiology & Chem Path) Flashcards

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1
Q

How is the intestinal fluid balance maintained

A

Due to absorption at the villi & secretion at the crypts of water & electrolyte in the small intestine

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2
Q

What is osmosis

A

Solvent particles move across membrane form diluted to concentrated solution
Low to high

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3
Q

What is diffusion

A

Particles moving from high concentration to lower concentration
High to low concentration

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4
Q

Why is it important for absorption of fluids to be greater than secretion of fluids

A

To maintain nutrients in solution & dilute hypertonic intestinal content

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5
Q

What happens with diarrhoea or constipation

A

There is a disturbance in the balance of absorption & secretion
Diarrhoea: reduced absorption or increase secretion

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6
Q

On what does the absorption & secretion rate depend on

A

Osmotic gradient

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7
Q

What is the two ways in which the osmotic gradient is maintained & explain

A
  1. Change in luminal osmotic pressure:
    Ingestion of food that is hypertonic, food is digested & becomes hypertonic & draw water
    Absorption occurs & solution becomes hypotonic & water is drawn back into cell
  2. Movement of electrolytes:
    Na, K & Cl is mainly responsible for ionic & osmotic balance
    Movement occurs due to active or passive transport
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8
Q

What is the main component of ECF

A

Na & Cl

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9
Q

What is the main component of ICF

A

K

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10
Q

What is the 2 importance things of maintaining osmotic gradient

A
  1. Absorption of CHO & protein
  2. Water balance
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11
Q

Explain the movement of Na

A

Na is transferred to ECF that raises the osmolality
Na is absorbed into cell & facilitates glucose entry
Water moves into cell due to increased osmolality & as Na moves into extracellular space water moves along
Na is actively reabsorbed into the cell & Cl is transported out of cell (diffusion) leading to electrical chemical gradient

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12
Q

Explain chloride secretion

A

The crypts of small intestine actively secrete electrolytes leading to water secretion
Cl enters crypts due to co-transport w/ Na & K
Activation of Adenylyl cyclase, cAMP & CFTR transports Cl into lumen
Cl attracts Na to forms NaCl & water is drawn into the lumen via osmosis

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13
Q

What happens to the chloride secretion during diarrhoea

A

Abnormal activation of CFTR leading to Cl channel stuck in open position & Cl moves continuously into the Lume that increases osmolality & water follows

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14
Q

What is the chloride transport system in the ileum & colon

A

Cl is absorbed by active transport in exchange for water, bicarbonate & Na to neutralise acidic products of bacteria

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15
Q

What is the definition of diarrhoea

A

Passing 3 or more watery stools per day

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16
Q

What is the 3 types of diarrhoea

A
  1. Acute watery diarrhoea: several hours pr days
  2. Acute bloody diarrhoea: dysentery
  3. Persistent diarrhoea: more than 14 days
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17
Q

What is the 5 mechanism of diarrhoea

A
  1. Secretory
  2. Osmotic
  3. Inflammatory or infection
  4. Structural, functional & motility
  5. Medication, genetic, food allergy/intolerance
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18
Q

What is inflammatory & infectious diarrhoea

A

Due to damage to intestinal mucosa that release blood, mucous & plasma protein into intestines & increase fluid content in feces

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19
Q

What is secondary lactase deficiency

A

Damage to brush border & temporary deficiency of lactase after diarrhoea episodes & will restore when lactose is avoided for a few days

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20
Q

What is structural/functional/motility diarrhoea

A

Increase propulsive colon activity or decrease surface area that leads to rapid transit & decrease water absorption

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21
Q

What is genetic, medication of food allergy/intolerance diarrhoea

A

Genetic: CF, inborn errors of metabolism, inborn enzyme deficiency
Food allergy: inflammation diarrhoea
Food intolerance: osmotic diarrhoea

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22
Q

What is secretory diarrhoea

A

Caused by infection like rota virus or E.Coli & continues even if fasting

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23
Q

What is the 2 mechanism of secretory diarrhoea

A

1.Activation of adenylyl cyclase: activating CFTR & continued excretion of Cl leads to increased fluid secretion
2. Inhibition of Na transport: impaired or inadequate absorption from villi leading to reduced absorption of fluids

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24
Q

What is osmotic diarrhoea

A

Caused by osmotic imbalance & stops when fasting
It is caused by substances that increase osmolality & draw water from cell (laxatives, antibiotics, radiation, chemotherapy, secondary lactase deficiency or unabsorbed solutes like fructose)

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25
Q

What is the biggest consequences of diarrhoea

A

Dehydration

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26
Q

What is the 3 types of dehydration

A
  1. Isotonic
  2. Hypertonic
  3. Hypotonic
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27
Q

State isotonic diarrhoea definition, biochemical features & clinical manifestations

A

Definition:
Loss of Na & water in same proportion normally found in ECF
Biochemical features:
Normal s-Na & osmolality but hypovolumic
Clinical manifestations:
Thirst, lack of tears, sunken fontanelle/eyes, tachycardia, oliguria, dry mucous membrane, reduce skin turgor

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28
Q

State hypertonic dehydration definition, biochemical features & clinical manifestations

A

Definition:
Loss of water in excess of free Na
Caused by hypertonic solution, insufficient water intake or excessive sweating
Biochemical features:
Increase s-Na & osmolality
Clinical manifestations:
Severe thirst, irritability & seizures

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29
Q

State hypotonic dehydration definition, biochemical features & clinical manifestations

A

Definition:
Loss of Na in excess of free water
Caused by increased water intake, hypotonic solution (marathon runner or excess IV fluids)
Biochemical features:
Low s-Na & osmolality
Clinical manifestations:
Lethargy & seizure can be present

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30
Q

What is the base deficit acidosis

A

Hypovolaemia from dehydration leads to poor renal perfusion & poor reabsorption of bicarbonate
Therefor large amount of intestinal bicarbonate is lost in diarrhoea leading to based edifice & acidosis
Hypovolaemic shock adds to acidosis through lactate production of under perfumed tissue

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31
Q

What is the 4 biochemical markers of base deficit acidosis

A

Low s- bicarbonate
Low arterial pH
Kussmaul’s breathing
Increased vomiting

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32
Q

Beside bicarbonate what is also lost

A

Potassium

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33
Q

What is the 3 signs of K depletion

A

Generalised muscle weakness
Cardiac arrhythmia
Paralytic ileum

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34
Q

What is the 3 treatments of diarrhoea

A
  1. ORS
  2. Other fluids
  3. Zinc
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35
Q

What is the composition of ORS & reason for giving

A

1l of boiled cooled water, 8 levelled tsp of sugar, 1/2 level tsp of salt
SGLT-1 transporter is not influenced by toxin & should still be used for reabsorption of Na & water to prevent dehydration

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36
Q

What other fluids can be given to treat dehydration

A

Breast milk, formula & salted legumes soups

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37
Q

What fluids can not be given treating dehydration

A

Plain IV, oral glucose/dextrose, commercial soups, undiluted soft drink or cool drinks

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38
Q

What is the role of zinc

A

Reduce stool volume, duration & re-occurrence

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39
Q

What is the dosage of zinc

A

>6months: 20mg/day
<6months: 10mg/day
For 10-14 days

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40
Q

What is the 3 effects of diarrhoea on nutritional status

A
  1. Reduced dietary intake: vomiting, LOA or withholding foods
  2. Increased nutritional requirements: fever, illness, repair to gut mucosa
  3. Decreased nutrient absorption: mage to villi, deficiency in brush border enzymes, loss of bile salts or rapid gut transit
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41
Q

How do you differentiate between secretory & osmotic diarrhoea

A

Secretory diarrhoea: does not stop when fasting & has an osmolar gap <100 due to solutes being secreted w/ secretions
Osmotic diarrhoea: does stop when fasting & has an osmolar gap >100 due to unaccounted solutes

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42
Q

What is lactose deficiency

A

Lactase deficiency causing osmotic diarrhoea

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43
Q

What is the 2 treatments of lactose intolerance

A

Avoiding diary or taking lactase orally daily

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44
Q

What is 4 ways in which lactose intolerance can be diagnosed

A
  1. Exclude lactose from diet
  2. Ingesting lactose & monitor blood glucose levels
  3. Hydrogen breath test
  4. Stool reducing substance test & TLC
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45
Q

What is steatorrhoea

A

Presence of abnormal amount of fat in stool

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46
Q

What is the appearance of steatorrhea

A

Greasy, floats & difficult to flush

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47
Q

What is the clinical manifestation of steatorrhoea

A

Weight loss & deficiency of fat soluble vitamins

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48
Q

What is the 5 causes of steatorrhoea

A
  1. Infection
  2. Coeliac disease (damage mucosa & ability to absorb)
  3. Infiltrations of GIT (TB & lymphoma)
  4. Lack of bile salts
  5. Deficiency of pancreatic lipase
49
Q

What is 3 ways to diagnose steatorrhoea

A

1.Histologically test for fat globules
2. Steatocrit: mixing stool w/ water & centrifuging to measure proportion of fat
3. Radioactive 14C TG breath test

50
Q

What is an example of primary hyperaldosteronism

A

Conns Adenoma

51
Q

What does primary hyperaldosteronism cause & why

A

Hypertension due to Na & water retention w/ hypoK & metabolic acidosis (increased exchange of Na for H/K)

52
Q

Is oedema present in primary hyperaldosteronism

A

No due to ANP & BNP limiting fluid retention & renin suppressed

53
Q

Why does secondary hyperaldosteronism occur

A

Due to increased renin secretion w/o ECF volume depletion

54
Q

What is 2 instances where secondary hyperaldosteronism occur

A

Renal artery stenosis
Low oncotic pressure states

55
Q

What is 3 low oncotic pressure states

A

Nephrosis
Cirrhosis
Protein losing encephalopathy

56
Q

Is oedema present w/ secondary hyperaldosteronism & why

A

Yes, peripheral oedema due to fluid shift from ICF to ECF causing hyponatraemia

57
Q

What other complication other than oedema result from secondary hyperaldosteronism & why

A

Congestive cardiac failure due to high hydrostatic pressure

58
Q

If there is a Na overload why is there still hypoNa

A

ADH causing water retention

59
Q

What is SIADH

A

Syndrome of inappropriate ADH
Common cause of hypoNa due to water retained is shared between ECF & ICF

60
Q

What is the Na status in the urine of SIADH

A

High Na concentration & urine concentrated

61
Q

What severe complication can be caused by SIADH

A

Brain oedema

62
Q

What is the 2 treatments of SIADH

A
  1. Restrict water intake
  2. Severe hypoNa saline & mannitol
63
Q

What is the function of mannitol in treatment of SIADH

A

Pull water out of cell & prevent brain oedema

64
Q

What happens if hypoNa is corrected to quickly

A

Central pontine myelinosis/damage nerve cells

65
Q

What is 5 causes of SIADH

A
  1. Direct stimulation of hypothalamus
  2. Pulmonary pathology where volume receptors send incorrect signals
  3. Ectopic ADH production
  4. Pain
  5. Drugs like NSAIDS, morphine & narcotics
66
Q

What is a consequence of acute diarrhoea

A

Metabolic acidosis w/ normal anion gap due to loss of bicarbonate

67
Q

What is the consequences of chronic diarrhoea

A

Metabolic alkalosis due to K depletion & increase H loss due to transporter in kidney

68
Q

What happens w/ chronic diarrhoea in a biochemistry point of view

A

Rapid but prolonged transit resulting in some time for Na/K/H exchange decreasing the severity of dehydration

69
Q

What is lost w/ hyperemesis

A

Gastric fluid rich in H, Cl & K

70
Q

What 4 things does the loss of gastric fluid in hyperemesis cause

A
  1. Metabolic alkalosis
  2. Hypochloraemia
  3. Hypokalaemia
  4. Dehydration
71
Q

What is paradoxical aciduria

A

Na is absorbed in exchange for H/K in the kidney but hypoK results in secretion of H
Sodium chloride rather than sodium bicarbonate is exchange at the proximal tubule but if chloride is depleted result in bicarbonate absorption making urine more acidic
Hypovolaemia causes hyperaldosteronism- more H is being excreted in urine

72
Q

What is the IV treatment of hyperemesis

A

NaCl/KCl

73
Q

Why is NaCl/KCl used for treatment

A

Added volume to mixture helps with dehydration & reduce aldosterone, decreasing Na absorption in proximal tubule allowing for H & K loss distally
Cl will replace bicarbonate in kidney & Na reabsobred
Excess bicarbonate excreted & help w/ alkalosis

74
Q

Where is potassium lost that can lead to depletion

A

Faceal loss

75
Q

Who is at greatest risk w/ potassium depletion

A

Infants
People w/ prior K depletion

76
Q

What is the link between metabolic acidosis & K depletion

A

Metabolic acidosis can mask depletion as K in ICF is exchanged for H in ECF as compensatory mechanism of acidosis
This can cause rebound hypoK when treating acidosis w/o treating hypoK

77
Q

What 2 factors influence water movement

A
  1. Hydrostatic pressure gradient
  2. Colloid osmotic pressure gradient
78
Q

What is hydrostatic pressure gradient & water’s net movement

A

Pressure fluid exerts on cells
Water will push away from areas of high hydrostatic pressure to area of low hydrostatic pressure
(At the arteriolar end of blood vessel push water out of vessel into interstitial fluid)

79
Q

What is colloid osmotic pressure gradient & water’s net movement

A

Force of solute in a solution
Water moves from low to high colloid osmotic pressure & plasma has high colloid osmotic pressure & water gets pulled back that was lost at arteriolar end

80
Q

What is tonicity

A

Measurement of the osmotic pressure gradient between 2 fluid compartments

81
Q

What happens in a hypotonic ECF solution to the cell

A

Cell swells

82
Q

What happens in a hypertonic ECF solution to the cell

A

Cell shrinks

83
Q

What is the 2 most common causes of transcellular fluid shift

A

Na & glucose

84
Q

What happens when the brain swells

A

Brain can herniate & pressure can cause blood vessels to collapse

85
Q

What happens when the brain shrinks

A

Brain can have a subdural bleed & central pontine myelinosis if rapidly corrected

86
Q

Against what changes does the BBB protect

A

Changes in glucose but not Na

87
Q

How does the brain adapt to changes in Na

A

Increase or decrease idiogenic osmoles

88
Q

Where is the osmostat & the function

A

Hypothalamus
Controls thirst & release ADH

89
Q

How is the osmostat stimulated

A

Substances that pull fluid from osmocytes & cause them to shrink & shrinking action activates them

90
Q

What is 4 examples of osmostat substances

A

Na shrinks during hypotonic fluid loss
Glucose thirst in diabetes
Mannitol for cerebral oedema
Angiotensin 2 thirst during hypovolaemia

91
Q

What is 3 substances that promote K secretion

A

Aldosterone
Insulin
Catecholamines

92
Q

What is the action of aldosterone in K secretion

A

Na dependent & K stimulated aldosterone directly to be secreted

93
Q

What is the action of insulin in K secretion

A

Drive K into cell because when glucose enters cell it is phosphorylated & K follows negative PO43- into cell

94
Q

What is the action of catecholamines on K secretion

A

Drives K into cells as it causes glucogenolysis which generate phosphorylated glucose intermediates

95
Q

What 2 ions compete for the same intracellular binding spot

A

H & K

96
Q

What is the concentration of K in acidosis

A

HyperK (a lot of K remain in cell)

97
Q

What is the concentration of K in alkalosis

A

HypoK (a lot of K leaves cell)

98
Q

What does hypoK cause & why

A

Alkalosis due to distal tubular excretion as lack of K & H is exchanged for Na

99
Q

What is the effect of high K in ECF on contractility

A

More excitable due to K leaving cell slowing because of lower osmotic gradient

100
Q

What is the effect of low K in ECF on contractility

A

Less excitable
K leak out of cell due to osmotic gradient

101
Q

What is 3 symptoms of hyperK

A
  1. Cardiac arrhythmia (asystolic & ventricular fibrillation)
  2. Muscle weakness & respiratory failure
  3. N, V & D
102
Q

What is 8 causes of hypoK

A
  1. Increased kidney excretion
  2. Drugs like B2 adrenergic agonist, thiazide or loop diuretic
  3. Metabolic alkalosis
  4. Increased GIT secretion
  5. Increased sweating
  6. Administration of insulin/epinephrine
  7. Decreased intake during ketogenic diet, fasting or starvation
  8. Refeeding syndrome
103
Q

What is the treatment of hypoK

A

KCl

104
Q

What is the 2 ways to diagnose hypoK

A
  1. Urine K to differentiate between renal & GIT losses
  2. Flat/inverted T wave & prominent U wave
105
Q

In what 2 instance does increase kidney excretion cause hypoK

A

Primary hyperaldosteronism due to adenoma
Secondary hyperaldosteronism due to renal artery stenosis

106
Q

Why does thiazide or loop diuretic cause hypoK

A

Increase Na enter distal tubule in exchange for K

107
Q

Why does increase GIT secretion cause hypoK

A

Vomiting & diarrhoea due to direct fluid loss & indirect metabolic alkalosis

108
Q

Why does refeeding syndrome cause hypoK

A

Already in hypoK & if add food it causes insulin to be released & decrease K

109
Q

What is the 3 diagnosis for hyperK

A
  1. Peaked T wave
  2. Loss of P wave
  3. Widen QRS complex
110
Q

What is the 4 causes of hyperK

A
  1. Increase intake
  2. Drugs like B2 adrenergic antagonist or drugs blocking aldosterone
  3. Acute renal failure
  4. Increased cell lysis
  5. Hyperosmolarity
  6. Lack of insulin
  7. Acidosis
  8. Adrenal insufficiency
111
Q

What is the 4 treatments of hyperK in a medical emergency

A
  1. Insulin & glucose: push K into cell
  2. Salbutamol: push K into cell
  3. NaHCO3 infusion: alkalosis will push K into cell & increase in H will allow more K into cell
  4. IV calcium gluconate: antagonises the effect of K on cardiac excitability
112
Q

What is the 3 treatments of hyperK once patient stabilised

A
  1. NaCl infusion w/ diuretic to increase NaCl delivery to distal tubules & more K exchange
  2. Haemodialysis
  3. Polystyrene sulfonate resin PO binds oral K
113
Q

Why does massive cell lysis cause hyperK

A

Release K into ECF like in crush injury, tumour lysis syndrome & haemolysis

114
Q

Why does hyperosmolarity syndrome cause hyperK

A

Osmotic gradient pulls water out of cells increasing ICF concentration of K being pushed out of cell

115
Q

Why does lack of insulin cause hyperK

A

Na/K pump action is decreased

116
Q

Why does acidosis cause hyperK

A

Increased H outcompetes K to enter cell

117
Q

Why does acute renal failure cause hyperK

A

Results in no K excretion

118
Q

Why does drug blocking aldosterone cause hyperK

A

Prevent K excretion by blocking Na retention

119
Q

Why does adrenal insufficiency cause hyperK

A

Less aldosterone w/ metabolic acidosis & low Na

Case 8: GIT diarrhoea (11 decks)

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