This document provides information on fluid and electrolyte therapy. It discusses indications for IV fluid therapy including severe dehydration. It describes the two components of fluid therapy as maintenance therapy to replace normal losses and replacement therapy to correct existing deficits. The document gives guidelines for calculating maintenance fluid requirements based on body weight and additional fluid needs for conditions like fever. It also provides guidance on calculating and correcting water and electrolyte deficits. The document discusses various fluid solutions and considerations for fluid management in different clinical scenarios like dehydration, hyponatremia, hypernatremia, and hypokalemia.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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2. I.V fluid therapy:-
•
Indications:-
1-severe dehydration
2-mild to moderate dehydration if there is:-
*diarrhea >100 cc/hr
*abdominal distension due to paralytic ilius or
gastric distention.
*comatose patient.
*repeated vomiting.
*patient refused oral route.
3. Fluid therapy
There are two components to fluid therapy:
•
Maintenance therapy
•
Replacement therapy
4. Maintenance therapy:-
•
replaces the ongoing losses of water and electrolytes under
normal physiologic conditions via urine, sweat, respiration,
and stool.
•
Measured according to body weight;
Body weight(kg) Volume per day Hourly rate
0-10 100ml/kg 4 ml/kg/hr
11-20 1000 ml+50 ml/kg for
each 1kg >10 kg
40 ml/hr +2
ml/kg/hr*(wt-10)
>20 1500 ml +20 ml/kg for
each 1 kg >20kg
60 ml/hr+1 ml /kg/hr
*(wt-20)
5. Maintenance requirements of
electrolyte:
•
2-3 mEq/kg/day of sodium
•
1-2 mEq/kg/day of potassium.
•
Maintenance fluids
5% dextrose (D5),1/2,1/4 and 1/5 glucose saline
•
Children weighing less than about 20 to 25 kg do
best with the solution containing quarter NS
because of their high water needs per kilogram.
•
larger children and adults may receive the solution
with half NS.
6.
7.
8.
9. •
The glucose in maintenance fluids provides
approximately 20% of the normal caloric needs of
the patient.
•
This percentage is enough
1. to prevent the development of starvation
ketoacidosis and
2. diminishes the protein degradation that would
occur if the patient received no calories.
•
avoiding the administration of hypotonic fluids,
which may cause hemolysis
10. •
a child on maintenance IV fluids loses 0.5% to
1% of real weight each day because .
Maintenance fluids do not provide adequate
calories, protein, fat, minerals, or vitamins.
•
The maximum total fluid per day is normally
2400 mL.
•
The maximum fluid rate is normally 100
mL/hr.
14. Heat stress:-
•
Fever leads to a predictable increase in
insensible losses, causing a 10% to 15%
increase in maintenance water needs for each
1°C increase in temperature greater than
38°C.
e.g:-12 kg ,39c
=1100+(1100*10%)
=1100+110
=1210 ml
16. Replacement therapy
•
corrects any existing water and electrolyte
deficits.
•
These deficits can result from gastrointestinal,
urinary, or skin losses, bleeding, and third-
space sequestration.
17. Calculation of deficit:
•
Water deficit(L)=degree of dehydration*B.wt
•
Na deficit=water D in litter*80 mEq/L
•
K deficit=water D*30mEq/L
e.g:-12 kg ,10% dehydrated?
Water D=10% *12=1.2L
Na D=1.2 *80 =96 mEq/L
K D=1.2*30 =36 mEq/L
18. Adjusting Fluid Therapy for
Gastrointestinal Losses
Average Composition Approach to Replacement
Diarrhea Replacement of Ongoing Stool
Losses
Sodium: 55 mEq/L Solution: 5% dextrose in ¼ normal
saline + 15 mEq/L bicarbonate + 25
mEq/L potassium chloride
Potassium: 25 mEq/L Replace stool mL/mL every 1-6 hr
Bicarbonate: 15 mEq/L
Gastric Fluid Replacement of Ongoing gastric
Losses
Sodium: 60 mEq/L Solution: 5% dextrose in half normal
saline + 10 mEq/L potassium
chloride
Potassium: 10 mEq/L Replace output mL/mL every 1-6 hr
Chloride: 90 mEq/L
19. •
mild moderate Severe
Infant 5% 10% 15%
Infant/young
children
Thirsty; alert;
restless
Thirsty; restless or
lethargic but
irritable or drowsy
Drowsy, cold,
sweaty, cyanotic
extremities; may be
comatose
Older children Thirsty; alert;
restless
Thirsty; alert
(usually)
Usually conscious
(but at reduced
level),
apprehensive; cold,
sweaty, cyanotic
extremities;
wrinkled skin on
fingers and toes;
muscle cramps
dehydration
20. Signs &
Symptoms
Severe Moderate Mild
Tachycardia Present Present Absent
Palpable pulses Decreased Present (weak) Present
Blood pressure Hypotension Orthostatic
hypotension
Normal
Cutaneous
perfusion
Reduced &
mottled
Normal Normal
Skin turgor Reduced Slight reduction Normal
Fontanel Sunken Slightly
depressed
Normal
Mucous
membrane
Very dry Dry Moist
Tears Absent Present or
absent
Present
Respirations Deep & rapid Deep, may be
rapid
Normal
Urine output Anuria & severe
oliguria
Oliguria Normal
21.
22. Fluid Management of Dehydration
Restore intravascular volume
Normal saline: 20 mL/kg over 20 min (repeat until intravascular volume restored)
Calculate 24-hr water needs
Calculate maintenance water, calculate deficit water
Calculate 24-hr electrolyte needs
Calculate maintenance Na & K, calculate deficit Na & K
Select an appropriate fluid (based on total water & electrolyte needs)
Administer half the calculated fluid during the first 8 hrs, first subtracting any boluses from this
amount
Administer the remainder over the next 16 hrs
Replace ongoing losses as they occur
23. Example:-12 kg baby presented with severe
dehydration.
•
M=10*100+2*50
=1100 ml
•
D=degree of dehydration*B.wt
D=150*12=1800
•
1st
8 hr=1/2M+1/2D
=550+900
=1450ml
1st
hr10-30 ml/kg
=20*12=240ml
Next 7 hr=1450-240
=1210ml
•
Next 16 hr
=1/2M+1/2D
=1450 ml
•
Rate=44 ml/hr
24. Hyponatremia: Na<130 mEq/L
•
Hyponatremia usually associated with
hyposomolality.
•
Types of hyponatremia
1. Pseudohyponatremia(lab artifact)
2. Hyperosmolality(hyperglycemia,mannitol)
3. Hypovolemic(extrarenal,renal)
4. Euvolemic(SIADH, hypothyroidism, water
intoxication)
5. Hypervolemic(CHF,cirrhosis,nephrotic syndrome,
RF,hypoalbominemia)
25. Clinical manifestations:-
•
Lethergy, apathy, disorientation, muscle cramps,
anorexia, and agitation
•
Reduced mental status, decreased deep tendon
reflexes, hypothermia, seizures, pseudobulbar
palsies.
•
More severe symptoms associated with acute
decrease of Na level below 120 mEq/L
•
Chronic decrease to 110 mEq/L may be
asymptomatic.
26. Treatment:
1-acute or symptomatic hyponatremia:
Initial therapy should be calculated to raise Na level to 120
mEq/l
Subsequent correction to 130 mEq/l can be carried out over the
next 24-36 hr
Avoid rapid correction over 130 mEq/l because this will lead to
central pontine myelinolysis
Na level should not be raised or lowered more rapidly than 12
mEq/24 hr
Hypertonic saline 3% can be used
Each milliliter of 3% sodium chloride per kilogram increases
the serum sodium by approximately 1 mEq/L.
27. •
Fluid restriction and NaCl (NS)
required Na mEq=(desired Na-current Na)*0.6*wt
•
in symptomatic hyponatremia without edema diuretics can be
used.
volume of diuresis needed to correct hyponatremia may be
calculated by the following equation:
TBW=0.6*wt(kg)
excess water=TBW-current Na/desired Na*TBW
28. Hyponatremic dehydration
•
occurs in children who have diarrhea and
consume a hypotonic fluid (water or diluted
formula).
•
Volume depletion stimulates secretion of
ADH, preventing the water excretion.
•
some patients develop symptoms,
predominantly neurologic.
29. Treatment of hyponatremic
dehydration•
Need water and Na replacement
•
Required mEq=(desired Na-current
Na)*0.6*wt(kg)
e.g:-12 kg ,severely dehydrated ,Na level 110
mEq/l ?
Fluid requirement=1800 ml
mEq=(120-110)*0.6*12
=72 mEq
•
Given over 24-36 hr
30. •
Clinical manifestations:
Most children with hypernatremia are dehydrated and have the
typical signs and symptoms of dehydration.
•
Blood pressure and urine output are maintained, and
hypernatremic infants are less symptomatic initially and
potentially become more dehydrated before seeking medical
attention.
•
the pinched abdominal skin of a dehydrated, hypernatremic
infant has a "doughy" feel.
Hpernatremia:- Na>150 mEq/l
31. –
Hypernatremia, even without dehydration, causes
CNS symptoms that tend to parallel the degree of sodium
elevation and the acuity of the increase.
–
Patients are irritable, restless, weak, and lethargic.
–
Some infants have a high-pitched cry and hyperpnea.
–
Alert patients are very thirsty, although nausea may
be present.
–
Hypernatremia causes fever, although many patients
have an underlying process that contributes to the fever.
–
Hypernatremia is associated with hyperglycemia and
mild hypocalcemia; the mechanisms are unknown
32.
Brain hemorrhage is the most devastating
consequence of hypernatremia. As the
extracellular osmolality increases, water
moves out of brain cells, resulting in a
decrease in brain volume. This decrease in
volume can result in tearing of intracerebral
veins and bridging blood vessels as the brain
moves away from the skull and the meninges.
Patients may have subarachnoid, subdural,
and parenchymal hemorrhage.
Seizures and coma are possible squeal of the
hemorrhage, although seizures are more
common during treatment.
33. Treatment:
•
Hypernatremia should be corrected slowly
over 24-36 hr.
•
Lowering Na level not > 12 mEq/L/day
because rapid correction lead to cerebral
edema.
•
normal TBW=0.6*normal wt(kg)
current TBW=TBW*normal Na/current Na
water deficit=normal TBW-current TBW
34. Hypernatremic dehydration
•
is usually a consequence of an inability to
taken fluid, owing to a lack of access, a poor
thirst mechanism (neurologic impairment),
intractable emesis, or anorexia.
•
Children with hypernatremic dehydration
often appear less ill than children with a
similar degree of isotonic dehydration.
•
Children with hypernatremic dehydration are
often lethargic and irritable when touched.
35.
36. Hypokalemia: K < 3.0 mEq/L
•
Clinical manifestations:
ileus, muscle weakness, polyuria, polydipsia,
areflexic paralysis.
•
ECG changes include:
i. ST depression
ii. T wave reduction
iii. Presence of U wave
37.
38. Factors that influence the therapy of hypokalemia
include:
the potassium level
clinical symptoms,
renal function,
presence of transcellular shifts of
potassium(DKA,metabolic acidosis)
ongoing losses
patient's ability to tolerate oral potassium
41. Hyperkalemia: K >5.5 mEq/l
•
Clinical manifestations
paresthesia ,weakness ,flaccid paralysis ,cardiac
arrhythmia.
•
ECG changes
1 . (5.5-7 mEq/l)peaked or tented T-wave.
2 . (7-8 mEq/l)prolonged PR, ST depression,
initial widening of the QRS complex.
3 . ( >8mEq/l)flat P wave, wide QRS.
4 . no treatment lead to asystole or ventricular
42.
43. Treatment
Rapidly decrease the risk of life-threatening arrhythmias
- Shift potassium intracellularly
Sodium bicarbonate administration (IV)
Insulin + glucose (IV) Glucose ( 0.5 g/kg insulin 0.1 U/kg IV over 30
minutes)
β-Agonist
- Cardiac membrane stabilization
IV calcium gluconate 1 mL/kg of 10% solution IV over 3-5 minutes
Remove potassium from the body
Loop diuretic (IV or PO)
Sodium polystyrene (PO or rectal)
Dialysis
44. AGENT MECHANISM DOSE PRECAUTIONS/COMP
LICATIONS
Kayexalate Exchange K+
across
colonic mucosa
1-2 g/kg oraly or PR Hypernatremia,
constipation
Glucose and insulin Cell uptake Glucose 0.5 g/kg
insulin 0.1 U/kg IV
over 30 minutes
Hypoglycemia,
hypophosphatemia
Sodium bicarbonate Cell uptake 0.5 meq/Kg IV over
10-15 minutes
Hypernatremia,
alkalosis,
hypocalcemia, tetany
Calcium gluconate Stabilizes membrane
irritability
1 mL/kg of 10%
solution IV over 3-5
minutes
Bradycardia,
hypercalcemia
47. treatment:-
•
Severe tetany treated with I.V calcium
gluconate 2ml/kg of 10% solution, given
slowly over 10 min while cardiac status is
monitored for bradycardia.
•
Keep serum calcium in the lower half of the
normal range to avoid episodes of
hypercalcemia
51. Treatment:-
•
Aggressive therapy with normal saline
because the child is usually dehydrated
•
Loop diuretics enhance Ca excretion,started
after rehydration.
•
Furosemide (Lasix) (0.5-1mg/kg, Max Dose
10mg/kg/day)
•
Monitor serum sodium, potassium,
bicarbonate and magnesium.
52.
53. Metabolic acidosis:-
•
defined as pH < 7.35, PCO2< 35 mm Hg, and
serum bicarbonate < 20 meq/L
•
the most common acid-base abnormality
encountered in children. Causes of Metabolic
Acidosis
Normal anion gap
•
Diarrhea
•
Renal tubular acidosis
•
Urinary tract diversions
•
Increased anion gap
54. Anion gap:
•
Useful to diffrentiate between bicarbonate
loss from net acid gain.
•
Normal range 10-14 mEq/L.
•
In acidosis:
Undetermind anion above normal range is
considered to be net acid gain.
Normal anion gap indicate bicarbonate loss by
gastrointestinal or renal system.
•
Anion gap=SNa - (SCl + SHC03)