Acid – Base Balances and Common Electrolyte Disorders
Session 21: Acid – Base Balances and Common Electrolyte Disorders
Total Session Time: 120 minutes
Prerequisites
Learning Tasks
By the end of this session students are expected to be able to:
Resources Needed:
Computer
SESSION OVERVIEW
|Step |Time |Activity/ |Content |
| | |Method | |
|1 |05 minutes |Presentation |Introduction, Learning Tasks |
|2 |25 minutes |Presentation | Acid, Base and Acid Base Balance |
| | |Brainstorming | |
|3 |15 minutes |Presentation |Acidosis and Alkalosis |
|4 |50 minutes |Presentation |Common Electrolyte Disorders |
| | |Small Group | |
|5 |15 minutes |Presentation |Oedema and Ascites |
|6 |05 minutes |Presentation |Key Points |
| 7 |05 minutes |Presentation |Evaluation |
SESSION CONTENTS
STEP 1: Presentation of Session Title and Learning Tasks (5 minutes)
READ or ASK students to read the learning tasks and clarify
ASK students if they have any questions before continuing
STEP 2: Acid Base Balance (25 minutes)
|Activity: Brainstorming (5 minutes) |
| |
|Ask students to brainstorm on the following questions: |
| |
|What is acidity? |
|What is alkalinity? |
|What is pH? |
| |
|ALLOW few students to respond |
| |
|WRITE their responses on the flip chart/ board |
| |
|CLARIFY and SUMMARISE by using the content below |
(H+) of any substance in aqueous solution or the body fluids.
ions (OH-) or the salinity of any substance in aqueous solution or the
body fluids.
body fluids
the more the acid the substance is.
The Body pH
bases produced by the body cells.
is safely eliminated from the body, better known as the buffer system.
convoluted tubules secret hydrogen ions. In the filtrate hydrogen ions
combine with buffers
o Bicarbonate forming carbonic acid
o Ammonia forming ammonium ions
o Hydrogen phosphate forming dihydrogen phosphate
carbon dioxide is reabsorbed, maintaining the buffering capacity of
the blood.
sulphate.
excess hydrogen ions (H+).
amount of carbon dioxide lost (increased or decreased respiration).
eventually dissociates to bicarbonates and hydrogen ions thus lowering
the body pH.
increase the blood acidy and vice versa.
lost through urine.
STEP 3: Acidosis and Alkalosis (15 minutes)
fluctuations, but these reserves are limited and in extreme cases, can
become exhausted
buffers are consumed, the condition of acidosis exists
alkali uses up all the acid reserve and the state of alkalosis ensues
the central nervous and cardiovascular systems. In practice acidotic
states are more common than alkalotic ones, because the body tends to
produce more acid than alkali
CO2 as efficiently as normal, or if the body is producing excess acid
as in diabetic ketoacidosis or in renal diseases when kidneys are not
excreting H+ as normal
diarrhoea, and rarely through hyperventilation (excess CO2 loss)
STEP 4: Electrolyte Disorders (50 minutes)
|Activity: Small Group Discussion ( 30 minutes) |
| |
|DIVIDE students into small manageable groups |
| |
|ASK students to discuss on the following question |
| |
|What are the common electrolyte disorders? |
| |
|ALLOW students to discuss for 15 minutes |
| |
|ALLOW few groups to present and the rest to add points not mentioned |
| |
|CLARIFY and SUMMARIZE by using the contents below |
•
An electrolyte disorder is an imbalance of certain ionized salts( which
include bicarbonate, calcium, chloride, magnesium, phosphate, potassium
, and sodium) in the blood
Sodium
normal.
•
Hypernatremia can be caused by inadequate water intake, excessive fluid
loss kidneydisease, severe burns, and prolonged vomiting or diarrhea),
or sodium retention (caused by excessive sodium intake oraldosteronism
).
•
Low sodiumlevels may also be triggered by inadequate dietary intake of s
odium, excessive perspiration, water intoxication, and impairment of ad
renal gland or kidney function.
Potassium
•
Hyperkalemia may be caused by ketoacidosis (diabetic coma), myocardial
infarction (heartattack), severe burns, kidney failure, fasting, bulimi
a nervosa, gastrointestinal bleeding, adrenal insufficiency, oraddison'
s disease.
o Severe dehydration
o Aldosteronism
o Cushing's syndrome
o Kidney disease
o Long term diuretic therapy
o Certain penicillins
o Laxative abuse
o Congestive heart failure
o Adrenal gland impairments
Calcium
o Thyroid disorder,
o Multiple myeloma,
o Metastatic cancer,
o Multiple bone fractures,
o Milk alkali syndrome,
o Paget's disease.
o Thyroid disorders
o Kidney failure
o Severe burns
o Sepsis
o Vitamin d deficiency,
o Medications such as heparin and glucogan
Magnesium
•
It may occur with endstage renal disease,addison's disease, or an overdo
se of magnesium salts
occur due to
inadequate dietary intake of magnesium, often caused by chronic alcohol
ism or malnutrition.
•
Other causes include malabsorption syndromes, pancreatitis,aldosteronis
m, burns, hyperathyroidism, digestive system disorders, and diuretic us
e
Chloride
severe dehydration, kidney failure, hemodialysis, traumatic brain injur
y,and aldosterone
•
Hypochloremia usually occurs as a result of sodium and potassium depleti
on
(i.e.hyponatremia,hypokalemia)severe depletion of serum chloride levels caus
es metabolic alkalosis.
Phosphorus
•
Skeletal fractures or disease, kidney failure, hypoparathyroidism, hemod
ialysis, diabetic ketoacidosis, acromegaly, systemic infection, and int
aused by hypomagnesemia and hypokalemia.
ketoacidosis, kidney disease, hyperparathyroidism,hypothyroidism, cushi
ng's syndrome, malnutrition, hemodialysis, vitamin d
deficiency, and prolonged diuretic therapy
STEP 5: Oedema and Ascites (15 minutes)
Oedema
cavities.
depending on the site where it accumulates.
o Increased hydrostatic pressure,
o Reduced plasma oncotic pressure,
o Lymphatic obstruction and
o Water and sodium retention
childhood protein-energy malnutrition characterized by oedema,
irritability, anorexia, ulcerating dermatoses, and an enlarged liver
with fatty infiltrates.
o Peripheral oedema – in the feet (pedal oedema), ankles, legs, hands and
arms.
o Cerebral oedema – in and around the brain (cerebral oedema).
[pic]
Source: Standring, S., 2008
Figure 21.1 a: Oedema
Ascites (peritoneal cavity
fluid)
kidney disorders
[pic]
Source: Standring, S., 2008 Figure 21.1 b: Ascites
STEP 6: Key Points (5 minutes)
buffers are consumed the condition of acidosis exists but when the pH
rises above 7.45, the increased alkali uses up all the acid reserve and
the state of alkalosis
hyponatremia, hypokalaemia, hypercalcemia, hypocalcaemia, oedema, ascites
accumulation of fluid in the peritoneal cavity
STEP 7: Evaluation (5 minutes)
References
Anne, W. & Grant, A. (2006). Ross and Wilson Anatomy and Physiology in
Health and
Illness, (10th ed.). UK: Churchill Livingstone.
Kumar, V., Abbas, A.K., Fausto, N. & Mitchell, R. (2007). Robins Basic
Pathology (8th
ed.). Philadelphia: Saunders Elsevier.
Tortora, G.J & Derrickson, B (2009) Principles of Anatomy and Physiology
12th Edition,
USA, John Wiley & Sons Inc, USA
Walter, J.B. & Tabot, I.C. (1996). General Pathology (7th ed.). Edinburg:
Churchill
Livingstone.
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