2. water and salt balance Flashcards

1
Q

How is the TBW distributed by volume?

assume healthy 70 kg man

A

28L/11L/3L

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2
Q

describe distribution of water in the main fluid compartments

A

total body water = 60% of body weight
intracellular fluid= 65% of TBW
extracellular fluid = 35% ( interstitial =28%, plasma fluid (7%)

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3
Q

what is the most prevalent cation within the cell?

A

potassium

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4
Q

what is insensible fluid loss

A

not easily measured e.g. sweating, water lost from respiration

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5
Q

what is sensible fluid loss

A

easily measured e.g. urine output, vomit, fluid from surgical drains

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6
Q

describe the relationship between albumin and oedema

A

a low albumin causes a decrease in oncotic pressure and water diffuses from the blood into the interstitial fluid

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7
Q

what is the site of synthesis of ADH?

A

hypothalamus

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8
Q

what is the site of synthesis of aldosterone?

A

adrenal cortex

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9
Q

what is the principle site of renin production?

A

Juxtaglomerular cells

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10
Q

what does renin do?

A

proteolytic enzyme which activates angiotensinogen to produce angiotensin I

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11
Q

describe what happens when someone drinks excess fluid

A

osmolarity falls > ADH secretion stops > increased urine volume

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12
Q

where is sodium concentrated

A

mainly concentrated in extracellular fluid , Na ions main contributor to ECF volume and osmolality

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13
Q

osmolality

A

the concentration of a solution expressed as the total number of solute particles per kilogram

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14
Q

oncotic pressure

A

the osmotic pressure generated by large molecules (especially proteins) in solution, in a blood vessel’s plasma (blood/liquid) that displaces water molecules, thus creating a relative water molecule deficit with water molecules moving back into the circulatory system within the lower venous pressure end of capillaries. – e.g. albumin

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15
Q

osmosis

A

movement of a solvent (such as water) through a semipermeable membrane (as of a living cell) into a solution of higher solute concentration that tends to equalize the concentrations of solute on the two sides of the membrane.
determined by differences in hydrostatic pressure and differences in osmotic pressure

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16
Q

pitting oedema

A

in which external pressure leaves a persistent depression in the tissues. it occurs because the pressure pushes the excess fluid out of the intercellular spaces in the tissue
When the level of protein in the blood is low, water may leave the blood vessels and collect in the tissue

17
Q

what are the key routes of water loss from the body?

A
  • Urine
  • Sweating
  • Breathing
  • Vomiting – Mr Palmer
  • Faeces
18
Q

water and sodium homeostasis - hypothalamus and osmoreceptors

A

hypothalamus- able to notice changes in the water potential off the blood that passes through the brain. This is process is carried out by the osmoreceptors cells in the hypothalamus. As a response to the change in water potential
Hypothalamus sends signal to salivary gland which decreases water in saliva

19
Q

water and sodium homeostasis - posterior pituitary gland and arginine vasopressin

A

.Antidiuretic hormone (ADH or arginine vasopressin) ADH is released from the posterior pituitary. Vasopressin is transported down the axons of these cell bodies to the posterior lobe of the pituitary, where it is stored until it is released into the circulating blood as the result of action potentials passing down the axons Released in response to osmoreceptors in the hypothalamus detecting hypertonicity; Hypertonicity also stimulates thirst sensation; Increase in plasma osmolality (and increased plasma Sodium concentration) Increased ADH secretion; Water retention.

20
Q

role of kidneys in water conservation

A

ADH travels in the blood to your kidneys and affects the tubules so more water is reabsorbed into your blood. As a result you make a smaller volume of more concentrated urine. Loop of Henle creates gradient

21
Q

the role of the kidneys in sodium homeostasis (Renin-angiotensin-aldosterone system 0

A
  1. The first stage of the RAAS is the release of the enzyme renin. Renin released from granular cells of the renal juxtaglomerular apparatus (JGA) in response to one of three factors: Reduced sodium delivery to the distal convoluted tubule detected by macula densa cells, Reduced perfusion pressure in the kidney detected by baroreceptors in the afferent arteriole. Sympathetic stimulation of the JGA via β1 adrenoreceptors. The release of renin is inhibited by atrial natriuretic peptide (ANP), which is released by stretched atria in response to increases in blood pressure.
  2. Production of Angiotensin II
    Angiotensinogen is a precursor protein produced in the liver and cleaved by renin to form angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE). This conversion occurs mainly in the lungs where ACE is produced by vascular endothelial cells, although ACE is also generated in smaller quantities within the renal endothelium.
  3. Binding of Angiotensin II
    Angiotensin II exerts its action by binding to various receptors throughout the body. It binds to one of two G-protein coupled receptors, the AT1 and AT2 receptors. Most actions occur via the AT1 receptor Angiotensin II acts on the kidneys to produce a variety of effects, including afferent and efferent arteriole constriction and increased Na+ reabsorption in the proximal convoluted tubule.
  4. Finally, angiotensin II acts on the adrenal cortex to stimulate the release of aldosterone. Aldosterone is a mineralocorticoid, a steroid hormone released from the zona glomerulosa of the adrenal cortex. Aldosterone acts on the principal cells of the collecting ducts in the nephron. It increases the expression of apical epithelial Na+ channels (ENaC) to reabsorb urinary sodium. Furthermore, the activity of the basolateral Na+/K+/ATPase is increased. This causes the additional sodium reabsorbed through ENaC to be pumped into the blood by the sodium/potassium pump. In exchange, potassium is moved from the blood into the principal cell of the nephron. This potassium then exits the cell into the renal tubule to be excreted into the urine. As a result, increased levels of aldosterone cause reduced levels of potassium in the blood.
22
Q

thirst

A

Thirst is a sensation created by the hypothalamus, the thirst centre of the human body. Thirst is an important component of blood volume regulation, which is slowly regulated by homeostasis. Hypothalamus-Mediated Thirst. The thirst mechanism is activated in response to changes in water volume in the blood but is even more sensitive to changes in blood osmolality. Blood osmolality is primarily driven by the concentration of sodium cations.

23
Q

hyponatraemia

A

the very low osmolality of sodium (Na+). when severe, can lead headache, dizziness, disorientation and confusion. Ultimately it can lead to coma and death.

24
Q

response to dehydration

A
  • osmolality goes up
  • You get a desire to drink - thirst.
  • ADH released
  • ADH changes the way the kidneys react to blood flowing through them.
  • The kidneys are continuously filtering the blood and can alter how much water is allowed to go into the urine and how much is reabsorbed back into the body.
  • stops you making as much urine and so you don’t pass as much urine. The urine you do pass will be darker in colour, as it is more concentrated.
  • If you don’t pass as much urine, you don’t lose as much water.
  • If you don’t lose as much water and you have a drink because you are thirsty, there is more water in your body.
  • If there is more water in your body, your osmolality goes down.