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SOM 304: KIDNEY AND URINARY TRACT > WEEK 1: Control of water and electrolytes > Flashcards

WEEK 1: Control of water and electrolytes Flashcards

1
Q

What is the internal pool?

A

Internal pool – the quantity of any particular substance in the ECF.

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2
Q

State 2 aspects that affect the internal pool.

A

If quantity is to remain stable within the body
Input must be balanced with output.

  1. Ingestion: Metabolic Production
  2. Excretion: Metabolic consumption
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3
Q

State 2 ways of input into the internal pool.

A
  1. Input form external environment (inhalation, absorption through body surface, artificial injection and ingestion
  2. Body metabolic production
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4
Q

State 2 ways of output from the internal pool.

A
  1. Excretion to external environment (Kidney, lungs, digestive tract and body surface.)
  2. Body metabolic consumption
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5
Q

Describe the following:
Positive balance:
Negative balance:
Stable balance:

A

Positive balance: input > output
Negative balance: output > input
Stable balance: input = output

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6
Q

Between input and out, which is poorly controlled?

A

Input
-Input of substances into plasma is poorly controlled or not controlled
-Eating habits are variable
Output
-Compensatory adjustments usually occur on output side by urinary excretion

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7
Q

Water (synonymous with ‘fluid’)
*Most abundant substance in body

*Amount varies in different kinds of tissues

*Content remains fairly constant within an individual

In human physiology, what is the reference point of weight is an apparently healthy man?

A

In human physiology, the reference point is a 70kg apparently healthy man.

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8
Q

What is the % TBW for males?

What is the TBW for females? Why?

Describe the trend of TBW with age. Does it increase or decreases? Why?

A

60% of the total body weight is water (about 40L)

About 50% in females (35L), They generally have high body fat.

% water declines with age.

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9
Q

Classification of body fluids REVISION TABLE ON NOTES!!!

A
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10
Q

State the minor ECF components.

A

(i) Lymph
(ii) Transcellular fluid
-Cerebrospinal fluid
-Intraocular fluid
-Synovial fluid
-Pericardial, intrapleural, and peritoneal fluids
-Digestive juices

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11
Q

Ionic Composition of the Major Body-Fluid Compartments (Revision) CHECK THE NOTES

A
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12
Q

State the barriers separating the body fluid compartments.

Describe the distribution of ions between the ICF and ECF.

What is Interstitial fluid?

A

(i) Plasma membrane: ICF and ECF

ICF (more K+, Proteins, Phosphates)
ECF (more Na+, Cl- & HCO3-)

(ii) Capillary walls: Plasma and ISF

NB! ISF is essentially plasma minus proteins

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13
Q

What is extracellular fluid?

A

ECF - an intermediary between cells and external environment.

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14
Q

State Two factors are regulated to maintain fluid balance in the body.

A

Two factors are regulated to maintain fluid balance in the body.
ECF volume

(ii) ECF osmolarity

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15
Q

What is the difference between osmolarity and osmolality?

A

Osmolarity= mOsmol/L
Osmolality= mOsmol/ kg

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16
Q

ECF volume must be closely regulated to help maintain blood pressure.

What is very important in long-term regulation of ECF volume?

How does ECF volume maintain blood pressure?

A

Maintaining salt balance is very important in long-term regulation of ECF volume.

NB- Osmo… has to do with water! Plasma volume very influential in BP regulation. BP regulation influenced by salt control.

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17
Q

ECF osmolarity must be closely regulated to prevent swelling or shrinking of cells.

What is very important in regulating ECF osmolarity?

A

Maintaining water balance is very important in regulating ECF osmolarity.

18
Q

State the 2 main processes in the kidney to keep salt constant in ECF.

A

(i) Glomerular filtration rate (GFR)
(ii)Tubular reabsorption of sodium

19
Q

State the daily amount of salt input?

How is it input into the body?

A

10.5g/day

Ingestion

20
Q

State the daily amount of salt output in the body?

How is it output from the body?

A

10.5g/day
*Obligatory loss in sweat and faeces. 0.5g
*Controlled excretion in urine. 10g

21
Q

Describe the Effect of Na+ on blood pressure.

A

Increase in sodium results in increase in BP and vice-versa.

22
Q

Name the salt conserving hormone.

Name the water conserving hormone.

In which parts of the nephron do these hormones predominantly act?

A

NB! Aldosterone – salt conserving hormone

Vasopressin (aka ADH)- water conserving hormone

The distal convoluted tubule acting on the principal cells.

23
Q

What is water deficit in ECF called?

Often associated with dehydration

A

Water deficit in ECF
hypertonic: Has low water
Often associated with dehydration

24
Q

What is Excess water in ECF called?
What is it usually associated with overhydration?

A

Excess water in ECF
hypotonic: Have a lot of water
Usually associated with overhydration

25
Q

What is the normal Na+ concentration in the body?

A

135-145 mmol/L

26
Q

What is the key thing needed in order to maintain stable water balance?

A

In order to maintain stable water balance, water input must equal water output.

27
Q

State the total water input per day.

How is this water input?

A

2600ml/day

Fluid intake: 1250
Water in food: 1000
Metabolically produced water: 350

28
Q

State the total water output per day.

How is this water output?

A

2600ml/day

Urine: 1500
Insensible loss (from lungs and non-sweating skin)
Sweat: 100
feces: 100

29
Q

Hypertonicity is a consequence of changes in ECF osmolality.

Statethe causes of hypertonicity.
State the signs and symptoms of hypertonicity?

A

Hypertonicity
Cell shrinkage

Causes
*Insufficient water intake
*Excessive water loss
*Diabetes insipidus (lack of ADH)

Symptoms and effects
1. Shrinking of brain neurons: Confusion, irritability, delirium, convulsions, coma

  1. Circulatory disturbances: Reduction in plasma volume, lowering of blood pressure, circulatory shock.
  2. Dry skin, sunken eyeballs, dry tongue
30
Q

Hypotonicity is a consequence of changes in ECF osmolality.

State the causes of hypotonicity?

State the signs and symptoms of hypotonicity?

A

Hypotonicity
Cells tend to swell.

Causes

*Patients with renal failure who cannot excrete a dilute urine become hypotonic when they consume more water than solutes

*Can occur in healthy people when water is rapidly ingested, and kidney’s do not respond quickly enough (endurance athletes!!!)

*When excess water is retained in body due to inappropriate (↑) secretion of vasopressin (SIADH)

Symptoms and effects

*Swelling of brain cells: Confusion, irritability, lethargy, headache, dizziness, vomiting, drowsiness, convulsions, coma, death

*Weakness (due to swelling of muscle cells)

Circulatory disturbances (hypertension and edema)

*Water intoxication

31
Q

Vasopressin (AKA ADH) release and thirst

What produces vasopressin?

Where is it stored?

What commands its release?

Where are Hypothalamic osmoreceptors located?

Describe the effect of osmolality on vasopressin secretion and thirst.

A

Produced by hypothalamus.

Stored in posterior pituitary gland.

Released on command from hypothalamus.
Also, location of thirst center

Hypothalamic osmoreceptors
Located near vasopressin-secreting cells and thirst center.

↑Osmolarity → ↑ vasopressin secretion and thirst stimulated.
↓Osmolarity → vasopressin secretion decreased, and thirst suppressed.

32
Q

Describe the activities that happens at cellular level to control osmolality due to vasopressin. (ADH)

A

Stimulus for Vasopressin Release:

Vasopressin release is stimulated by various factors, primarily changes in blood osmolality and blood volume.
When blood osmolality increases (indicating higher solute concentration) or blood volume decreases (indicating dehydration), osmoreceptors in the hypothalamus detect these changes and stimulate the release of vasopressin from the posterior pituitary gland.
Vasopressin Binding to V2 Receptors:

Released vasopressin binds to V2 receptors on the basolateral membrane of principal cells in the renal tubules.
Activation of cAMP Pathway:

The binding of vasopressin to V2 receptors activates the adenylate cyclase enzyme, leading to an increase in cyclic adenosine monophosphate (cAMP) within the principal cells.
Aquaporin-2 (AQP2) Insertion:

The elevated cAMP levels trigger the insertion of water channels called aquaporin-2 (AQP2) into the apical membrane of principal cells in the collecting ducts.
AQP2 allows water to move from the tubular lumen through the cells and into the interstitial fluid surrounding the tubules.
Water Reabsorption:

As water moves through the AQP2 channels, it is reabsorbed from the tubular lumen into the interstitial fluid.
This water reabsorption concentrates the urine, reducing its volume and preventing excessive water loss from the body.
Concentration of Urine:

The concentrated urine, which results from the increased reabsorption of water, helps to conserve water in the body and maintain appropriate fluid balance.

33
Q

Name the receptors that water uses to enter into the interstitial fluid which are found in the basolateral membrane of the principal cells.

A

Aquaporin 3 and 4

34
Q

Where does vasopressin work in the nephron?

A

The main target cells for vasopressin are the principal cells in the renal tubules, particularly the distal convoluted tubules (DCT) and collecting ducts.

35
Q

Describe the vasopressin release and thirst via the following:

  1. Left atrial volume receptors
  2. Angiotensin II
A
  1. Left atrial volume receptors

*Monitor pressure of blood flowing through (reflects ECF volume)

*Upon detection of major reduction in arterial pressure, receptors stimulate vasopressin secretion and thirst

*Upon detection of elevated arterial pressure, vasopressin secretion and thirst are both inhibited

  1. Angiotensin II
    Stimulates vasopressin secretion and thirst when the RAAS is activated to conserve Na+
36
Q

Describe the physiology of the RAAS system.

A

The Renin-Angiotensin-Aldosterone System (RAAS) is a complex hormonal cascade that plays a crucial role in regulating blood pressure, fluid and electrolyte balance, and overall cardiovascular homeostasis. The RAAS system involves a series of steps and interactions between various organs, hormones, and enzymes. Here’s a simplified overview of the physiology of the RAAS:

  1. Renin Secretion:
    The process begins in the kidneys, specifically in the juxtaglomerular apparatus, where specialized cells called juxtaglomerular cells release an enzyme called renin.

Renin is released in response to various stimuli, including low blood pressure, decreased blood volume, or low sodium levels.

  1. Angiotensinogen Conversion:
    Renin acts on a precursor protein in the blood called angiotensinogen, which is produced by the liver.
    Renin cleaves angiotensinogen to produce angiotensin I.
  2. Angiotensin I to Angiotensin II Conversion:
    Angiotensin I is relatively inactive. To become active, it needs to be converted to angiotensin II.
    Angiotensin-converting enzyme (ACE), primarily found in the lungs, converts angiotensin I into angiotensin II.
  3. Angiotensin II Actions:

*Angiotensin II is a potent vasoconstrictor, causing blood vessels to narrow, which increases blood pressure.

*It stimulates the release of aldosterone from the adrenal glands.

  1. Aldosterone Release:
    Aldosterone acts on the kidneys, specifically on the distal tubules and collecting ducts.
    It promotes the reabsorption of sodium and water and the excretion of potassium. This reabsorption increases blood volume and, consequently, blood pressure.
  2. Antidiuretic Hormone (ADH) Release:
    Angiotensin II also stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary.
    ADH increases water reabsorption in the kidneys, further contributing to an increase in blood volume.

Negative Feedback:
The increased blood pressure and volume lead to a negative feedback loop, inhibiting the release of renin and slowing down the RAAS system.

The RAAS system, therefore, plays a crucial role in maintaining blood pressure, fluid balance, and electrolyte homeostasis. Dysregulation of this system can contribute to conditions such as hypertension, heart failure, and kidney disorders.

Medications that target the RAAS, such as ACE inhibitors and angiotensin II receptor blockers, are commonly used in the management of cardiovascular diseases.

37
Q

Describe how the brain controls High osmolality.

A

Hypothalamic osmoreceptors act on the hypothalamic neurons which promote thirst. There is the increased water intake which reduces the Plasma osmolality to normal.

38
Q

Describe how the kidney controls low osmolality.

A

Low ECF volume results in low arterial pressure which triggers the Left atrial volume receptors in the heart which will stimulate hypothalamic neurons to stimulate vasopressin secretion.

There is then increased permeability for water in the distal and collecting tubules resulting in increased water reabsorption.

Urine Output is decreased.

The plasma volume increases.

39
Q

State the 3 Regulatory Factors Not Linked to Vasopressin and Thirst.

A
  1. Dryness of mouth stimulates thirst but not vasopressin.
  2. Oral metering
    Some animals will rapidly drink only enough H2O to satisfy its H2O deficit.
    Mechanism is less effective in humans.
  3. Fluid intake often influenced by habit and sociological factors.
40
Q

State the following general characteristics of normal urine.

pH
Specific gravity
Osmolarity
Water content
Volume
Color
Odor
Bacteria content

A

pH: 4.5-8 (mean =6)
Specific gravity: 1.003-1.030
Osmolarity: 855-1335 mOsmol/L
Water content: 93-97%
Volume: 700-200ml/day
Color: Clear yellow
Odor: Varies with composition
Bacteria content: Sterile

SOM 304: KIDNEY AND URINARY TRACT (15 decks)

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