General pathophysiology - water & electrolyte balance Flashcards
1
Q
Antidiuretic hormone (ADH) - signals the kidneys to
A
recover water from urine.
2
Q
Aldosterone – a mineralocorticoid hormone produced by the adrenal
cortex; increases
A
the reabsorption of Na+ and water from renal tubules into the blood.
3
Q
Renin – release is triggered by the juxtaglomerular apparatus; renin is
converted into angiotensin which in turn stimulates the release of
A
aldosterone
(causes sodium to be absorbed and potassium to be excreted into the lumen by principal cells)
4
Q
Water exchange depends on: (4)
A
- Vascular permeability
- Capillary surface area
- Hemodynamic factors
- Osmotic factors
5
Q
Decrease in vascular permeability is associated with
A
– calcium
– glucocorticoid hormones
6
Q
What is responsible for the osmotic pressure of body fluids
A
Ionised salts
NaCl accounts for 90 % of the osmotic pressure of blood and extracellular fluid.
Osmotic activity is also associated with glucose, urea, proteins, and other substances.
7
Q
the sum of cations equals the sum
of anions in body fluid meaning the fluids are
A
electroneutral
8
Q
ICF and interstitial fluid differ considerably in the ionic content – what ions are found in much higher concentrations intracecllularly?
A
K+ and Mg2+ are higher inside cells
Na+ and Cl- are low compared to the interstitial fluid
9
Q
The proper distribution of cations is maintained by
A
an active transport mechanism that requires energy.
10
Q
the sodium-potassium pump pumps sodium and potassium ions in which direction?
A
Na+ passes freely into the cell through the cellular membrane; the sodium-potassium pump pumps sodium ions out of the cell (powered by ATP).
while Na+ is taken out from the cell, K+ is pumped into the cell by the
sodium-potassium pump
As more Na+ is taken out than K+ pumped in, the inside of the membrane is negatively charged
11
Q
Osmoregulation is the process of
A
maintenance of water and salt balance (osmotic balance) across membranes within the body’s fluid compartments.
12
Q
Major constituents (ions) responsible for osmotic pressure in plasma and in IC compartment?
A
Plasma –> Na+ (cation), Cl- and HCO3- (accompanying anions)
Intracellular compartment – K+
13
Q
Renal water excretion is controlled by
A
the
hypothalamic-pituitary-adrenal system:
- Sensation of thirst
- ADH secretion
- Urinary concentrating ability
14
Q
ADH is released by the
A
posterior lobe of the pituitary gland aka the neurohypophysis
15
Q
ADH affects what cells in the kidneys?
A
ADH affects the receptors located in the principal cells of the distal convoluted tubule and the collecting duct.
Stimulation of the receptors induces production of cyclic adenosine monophosphate that activates protein molecules (aquaporins) which increase the permeability of cellular membranes to water.
16
Q
What is the major cation in the extracellular fluid (ECF) compartment?
concentration in ECF and ICF?
A
Sodium ion is the major cation in the extracellular fluid (ECF) compartment
ECF sodium concentration is 144 mmol/L while that of the
intracellular fluid (ICF) is only 10 mmol/L.
17
Q
What regulates the volume
of the ECF?
A
The total Na+ in the body regulates the volume of the ECF.
A decrease in sodium concentration from normal values will result in ECF deficiency while increase in Na+ levels will lead to ECF volume expansion.
18
Q
Renal excretion of sodium depends on? (5)
A
- The effective arterial blood volume (EABV)
- The functions of RAAS
- The functions of the sympathetic nervous system
- The atrial natriuretic factor/hormone/peptide
- Intrarenal mechanisms
19
Q
What is EABV?
A
The effective arterial blood volume is the part of the intravascular volume that is in the arterial system.
It affects renal sodium excretion and is not a measurable quantity.
There is no distinct relationship with ECF volume.
Decrease in EABV stimulates reabsorption of Na+ in renal tubules, whereas ECF volume expansion does not trigger increase in Na+ excretion.
20
Q
The renin-secreting cells, which compose the juxtaglomerular apparatus, release renin in
response to?
A
a decrease in afferent arteriolar perfusion pressure. Thus are
sensitive to changes in blood flow and blood pressure
21
Q
How do the functions of the SNS affect renal sodium excretion?
A
Increased tone of the sympathetic nervous system affects blood supply to the kidneys and the activity of the renin-angiotensin-aldosterone system, but is also directly associated with proximal tubule reabsorption of Na+ (dopamine inhibits sodium reabsorption).
22
Q
How does ANF or ANH affect renal sodium excretion?
A
decreases sodium reabsorption
The atrial natriuretic factor or hormone, is a peptide hormone produced in mammalian cardiac atria.
ANF acts on the kidneys increasing the glomerular filtration rate and decreasing sodium reabsorption in the distal convoluted tubule.
ANF is secreted by the heart atria in response to atrial stretch.
23
Q
What types of intrarenal mechanisms affect renal sodium excretion? (3)
A
- Oncotic and hydrostatic pressure in postglomerular capillaries
- liquid composition in tubular lumina and the interstitial compartment
- hormones, etc.
24
Q
dehydration is
A
Loss of water from the body = ECF volume deficit
25
Isotonic dehydration is
isotonic loss of both water and sodium from the ECF compartment;
hypovolemia with no osmotic water shift from the ICF to the ECF compartment.
26
Causes and clinical signs of Isotonic dehydration
Causes:
* severe vomiting and diarrhoea; renal disorder; diuretics; removal of ascites, etc.
Clinical signs:
* thirst, fatigue, weakness, nausea, tachycardia, tendency to collapse.
* Sudden dehydration may lead to a hypovolemic shock.
27
Hypotonic dehydration is
Hypotonic dehydration is characterized by low sodium and osmolality and loss of water volume.
Decrease in the osmotic pressure in the ECF compartment will result in anosmotic gradient, and water is relocated into ICF compartment (fluid and electrolyte deficits are treated with water replacement only).
28
Causes and clinical signs of hypotonic dehydration.
characterized by low sodium and osmolality.
Causes:
* Diarrhoea, vomiting, etc.
Clinical signs:
* Beside the symptoms associated with isotonic dehydration, cerebral symptoms such as vomiting,
convulsions, and disorders of consciousness due to cerebral edema
29
Hypertonic dehydration is
pure water loss or dehydration associated with hypernatremia resulting in an increase in the osmotic pressure in the ECF compartment.
results in cellular crenation
30
Causes and clinical sings of hypertonic dehydration.
pure water loss, dehydration in conjunction with hypernatremia
Causes:
- Inadequate water intake
- Excessive water loss – sweating, hyperventilation, lack of ADH, vomiting, diarrhoea.
Clinical signs:
- Symptoms of cellular dehydration – thirst, decreased skin turgor, dry mucous membranes, increase in body temperature, anxiety, disorders of consciousness.
- Oliguria (low urine output) due to extrarenal loss of water, and excretion of concentrated urine.
- Polyuria in case of diabetes insipidus; decrease in the urine specific gravity and osmolality.
- Decrease in the intravascular fluid volume – hypotonia, tachycardia, decreased venous filling.
31
What is isotonic hyperhydration?
An isotonic increase in the water volume and salt concentration in ECF with no change in ICF volume.
32
Causes and clinical signs of isotonic hyperhydration.
Causes:
* Reduction in renal excretion of sodium (influx of isotonic fluid into the ECF compartment alone cannot trigger such changes).
Clinical signs:
* Weight gain (prior to visible swelling)
* Swelling syndrome (cardiac and renal disorders, cirrhosis of the liver)
33
What is hypotonic hyperhydration?
Excessive pure water intake resulting in hypervolemia and lowered plasma osmolarity.
Water intoxication with influx of water into the ICF compartment (brain swelling) because of the lowered osmotic gradient in plasma.
34
Causes and clinical signs of hypotonic hyperhydration.
excessive water with lowered osmolarity in plasma
Causes:
- Excessive liquid consumption, parenteral administration of salt-free solutions may cause water intoxication when there is a disturbance in water excretion (postoperative kidney and liver diseases).
- Decreased removal of liquid from ECF compartment e.g. excessive ADH.
Clinical signs:
- Cerebral failure – nausea, vomiting, bradycardia, coma
- Concentrated urine (excess ADH)
- Excessive sodium removal despite hyponatremia – increase in ECF volume inhibits reabsorption of sodium in proximal renal tubules.
(When arterial pressure increases, the nephron reduces sodium and water reabsorption thus increasing sodium and water excretion, to return ECFV and blood pressure to normal; the so called “pressure natriuresis” phenomenon.)
35
What is hypertonic hyperhydration.
Hypervolemia and hyperosmolarity* that occur due to excessive influx of sodium ion and water into ECF compartment.
Increase in blood osmotic pressure causes fluid shift from the ICF compartment to ECF compartment.
36
difference bewteen osmolality and osmolarity
* osmolality is a measure of the osmoles (Osm) of solute
per kilogram of solvent
(osmol/kg or Osm/kg)
* osmolarity is defined as the number of osmoles of solute per liter (L) of solution (osmol/L or Osm/L).
37
Causes and clinical signs of hypertonic hyperhydration.
excessive accumulation of salts and water, an osmolarity increase in the ECF
Causes:
o Parenteral administration of hypertonic fluids
o Sea water ingestion
Clinical signs:
o Severe brain disorders
o Signs of dehydration due to cellular exsiccosis (= insufficient fluid intake) as ICF moves into the ECF compartment because of the osmotic gradient. The cells experience crenation.
38
The plasma Na+ concentration reflects the ratio of the
amounts of Na+ and water present, not the absolute amount of Na+ in the body.
39
The plasma Na+ concentration is the major contributor to the osmolarity of the plasma, and its level determines the
volume of the ECF compartment.
40
Hyponatremia
sodium deficit in plasma
decrease in the ECF osmotic pressure - water is attracted to the ICF; symptoms refer to cerebral edema
41
Hypernatremia
excess sodium in plasma
increase in the ECF osmotic pressure – water moves from ICF to ECF; dehydration/crenation of cells will occur.
Symptoms:
disturbances of the central nervous system.
42
Normal range of Na+ dog mmol/l
141 – 153
Hyponatremia < 140
Hypernatremia > 155
43
Normal range of Na+ cat mmol/l
147 – 156
Hyponatremia < 147
44
Normal range of Na+ mmol/l
horse
cow
pig
horse 132 – 146
cow 132 – 152
pig 139 - 152
45
Hydrops
abnormal fluid (transudate) accumulation in serous cavities
46
Edema
excessive accumulation of fluid (transudate) within the
interstitial spaces in different organs due to disturbances in water and electrolyte metabolism.
Local(ised) edema
Diffuse (generalised) edema
47
Ascites
abnormal accumulation fluid in the abdominal (peritoneal)
cavity (common cause of ascites is cirrhosis of the liver).
48
Hydrocephalus
accumulation of cerebrospinal fluid in the cerebral ventricles
49
Anasarca
a severe and generalized form of edema, with subcutaneous tissue swelling throughout the body
50
myxedema
Edema induced by endocrine factors / Accumulation of transudate in the subcutaneous connective tissue.
For example, hypothyroidism results in the increase in chloride levels in tissues which leads to increased oncotic pressure.
"Myxedema is a term generally used to denote severe hypothyroidism. Myxedema is also used to describe the dermatologic changes that occur in hypothyroidism and occasionally hyperthyroidism."
51
describe Cardiac edema
Venous edema due to the failure of the left ventricle.
Swellings occur in the regions of the body where the hydrostatic pressure is the highest – limbs, lower body, but also body cavities.
51
describe renal edema
characterized by hypoproteinemia caused by renal failure
Caused by nephrosis (= is any of various forms of nephropathy; protein leakage into the urine leads to hypoproteinemia.
Decrease in the blood oncotic pressure will occur and results in a decrease in reabsorbtion and increase in filtration.
52
describe Cachectic or starvation-induced edema
Diffuse edema;
mechanisms involved in edema formation are complex, associated with hypoproteinemia and metabolic disorders of tissues.
52
Pulmonary edema associated with
left-sided heart failure or damage to pulmonary blood vessels (stenosis?).
53
Reference ranges of plasma potassium levels (mmol/L):
dog
cat
horse
cattle
pig
* Dog 3.7 – 5.8
* Cat 3.8 – 4.5
* Horse 2.4 – 4.7
* Cattle 3.9 – 5.8
* Pig 4.9 – 7.1
54
3 points about renal excretion of K+
1.Glomerular filtration
2.The bulk of filtered K+ is reabsorbed in the proximal tubule and loop of Henle.
3. K+ secretion by the distal convoluted tubule, mediated by aldosterone.
K+ secretion is linked to Na+ reabsorption.
55
How do mineralcorticoids (e.g. aldosterone) affect K+?
enhance K+ secretion in distal tubules;
but in tissues they facilitate potassium entry into cells
56
How does insulin affect K+?
Insulin promotes cellular potassium uptake
Acute hyperkalemia stimulates
insulin release.
57
How do catecholamines affect K+?
They stimulate potassium uptake by cells.
58
Status of K+ during alkalosis
Alkalosis is usually accompanied by hypokalemia.
Alkalosis stimulates tubular secretion of K+.
Leads to the shifting of K+ from ECF to ICF.
NB! Hypokalemia is both a cause and a frequent consequence of metabolic
alkalosis.
58
Status of K+ during acidosis
Acidosis is usually accompanied by hyperkalemia.
Acidosis inhibits tubular secretion of K+.
NB! For each 0.1 unit decrease in pH, there is an increase of 1 mmol/L in plasma K+.
A variety of mechanisms account for the hyperkalemia in acidosis (for example hyperkalemia associated with diabetic ketoacidosis or
hypercalcemia associated with lactic acidosis, etc.).
It is also possible to see low K+ and acidosis with failing kidneys that excrete potassium instead of conserving it.
59
Hypokalemia and diagnostic tests: it must be determined
* whether K+ deficiency is real, i.e. due to renal or enteral loss
* whether there is exchange of K+ between ICF compartmnet (high potassium levels) and ECF compartment (low potassium levels)
* whether there are changes in the acid-base balance and osmolality
60
1. Renal loss of K+ can be due to (2)
a) Due to mineralocorticoids
- Primary hyperaldosteronism – adrenal gland tumours or hyperplasia
- Secondary hyperaldosteronism – decrease in the effective blood volume due to heart failure that stimulates the release of renin from juxtaglomerular cells.
(Renin is secreted from juxtaglomerular kidney cells, regulates blood pressure by increasing sodium reabsorption, water reabsorption and vascular tone.)
b) Non-hormonal factors such as pharmaceutical diuretics
60
Causes of hypokalemia (4)
1. Renal loss of K+
2. Loss of K+ from the GI tract
3. K+ shifts out of the ECF and into the cells
4. Shortage in feed/decreased intake
61
2. Loss of K+ from the gastrointestinal tract can be due to
a) Vomiting
– The concentration of K+ in the gastric juice is low; leads to hypochloremic metabolic alkalosis and hypovolemia.
Associated with renal loss of K+ (hypovolemia and hypochloremia) and alkalosis.
b) Diarrhea
- Increase in the secretion of K+ in the terminal part of the GI tract.
62
Contributing factors/Causes of hyperkalemia: (3)
1. Excessive administration/ high dietary intake of K+
2. Decreased renal excretion of K+
- Acute renal failure with decreasing diuresis – decreased distal tubule urine flow results in decreased secretion of K+
3. Shift of K+ into the ECF compartment
- Metabolic acidosis, massive tissue damage
NB Pseudohyperkalemia – hemolysis during the blood draw
63
paresthesia
refers to a burning or prickling sensation that is usually felt in the hands, arms, legs, or feet, but can also occur in other parts of the body.
The sensation, which happens without warning, is usually painless and described as tingling or numbness, skin crawling, or itching.
64
K+ status for this electrocardiogram
normokalemia
65
K+ status for this electrocardiogram
In hypokalemia the ST interval will be depressed, T wave will be shallow and U wave will be prominent.
66
K+ status for this electrocardiogram
In hyperkalemia, PR interval will be prolonged, QRS complex will be wide and T wave overly peaked.
67
Plasma total magnesium concentration is
0.75 – 1.50 mmol/L
68
What ?% of plasma Mg++ is protein bound.
30%
Distribution of Mg++:
ECF compartment – 1%;
ICF compartment – 99%.
About 50 – 60 % of total body magnesium is located within bone tissue.
69
Mg++ is an intracellular cation; the physiological role/functions of magnesium in the body: (3)
1.Structural function (bones)
2.Muscle contraction/relaxation; neurotransmitter release; action
potential conduction in nodal tissue (calcium antagonist)
3.Enzyme function (cofactor, in particular for ATPases)
70
Factors affecting Mg++ metabolism: (3)
1. parathyroid hormone and vitamin D (calcitriol)
2. Renal control
3. Aldosterone
71
How do parathyroid hormone and vitamin D regulate magnesium homeostasis
- PTH enhances renal tubular reabsorption
- stimulate intestinal Mg++ absorption; feeding high levels
of Mg++ inhibits absorption. (feedback loop)
calcitriol completed in the kidneys,
parathyroid hormone (PTH) is secreted by the parathyroid glands, and calcitonin is secreted by the thyroid glands.
72
How does renal function/control regulate magnesium homeostasis?
- Unbound Mg++ filtrates/passes freely through the glomerular membranes, but only 3 – 5 % reaches final
urine.
Renal excretion and intestinal absorption are
interdependent – renal tubules regulate reabsorption.
both magnesium and calcium can activate the calcium-sensing receptor on the basolateral membrane and modulate paracellular magnesium transport
73
How does aldosterone regulate magnesium homeostasis?
- Inhibits reabsorption of Mg++ by renal tubules.
Increase in the ECF volume, hypercalcemia, and increased daily intake of NaCl have a similar effect.
74
3 causes of hypomagnesemia
1.Continually low dietary intake of magnesium.
e.g. Grass tetany - occurs in ruminants grazing rapidly growing grasses that are low in Mg++ during the early grazing season.
2. Mg++ malabsorption
e.g. Diarrhoea caused by small intestine diseases.
3. Renal Mg++ wasting
*Increase in renal wasting is due to acidosis associated with ketosis.
Clinical manifestation (similar to hypocalcemia)
*Tetania, tremor
*Tonic-clonic seizures
*Tachycardia, arrhythmias
*Often accompanied by hypocalcemia and hypokalemia
75
2 causes of hypermagnesemia:
and clinical signs
1.Renal failure
2.Hypothyroidism
Clinical manifestation:
Neuromuscular irritability (curare-like action = muscular paralysis)
*>2.5 mmol/L
Vomiting
Lethargy
Muscle weakness
Constipation
*↑↑> 2.5 mmol/L
Respiratory paralysis;
cardiac arrest
76
Blood plasma calcium concentration is --?-- in mammals.
2.0 – 2.5 mmol/L
77
About ? % of total plasma calcium is ionised,
? % protein-bound and
? % is in the form of phosphate or citrate, and the rest present as a calcium complex of unknown nature.
About 45 % of total plasma calcium is ionised, 45 % protein-bound, 2 % is
in the form of phosphate or citrate, and the rest present as a calcium complex of unknown nature.
Consequently, plasma calcium levels cannot be used to indicate calcium intake/status.
78
Biological functions of calcium: (4)
1. Regulates muscle contraction and neural transmission.
2. Activates ATPase that is essential for muscle contraction.
3. Acts as a catalyst in many of the coagulation pathways in the blood.
4. Affects metabolic processes in the cell, and membrane permeability.
79
Regulation of calcium metabolism via absorption.
Calcium is absorbed in the mammalian small intestine by a transcellular active
transport process.
Absorption depends on dietary intake, physiological
requirements, age, Ca:P ratio, vitamin D status.
Absorbed calcium enters the readily exchangeable pool (calcium in bones is present in two pools: pool of stable calcium and pool of readily exchangeable calcium).
80
Regulation of calcium metabolism via excretion.
Calcium is excreted into the gastrointestinal tract through saliva, bile, and pancreatic
and intestinal secretions, and by the kidneys.
In carnivores, calcium is mostly
excreted in urine;
in ruminants through the gastrointestinal tract.
81
4 factors regulating Ca++ metabolism:
* Parathyroidhormone
* Calcitonin
* Vitamin D
* Phosphorus metabolism
82
How does calcitonin regulate Ca+ metabolism
C-cells of the
thyroid gland produce calcitonin
Calcitonin decreases calcium levels by inhibiting osteoclast action,
and by preventing your kidneys from reabsorbing calcium.
And inhibits intestinal calcium absorption.
83
How does vit D regulate Ca++ metabolism
Vitamin D functions by stimulating intestinal calcium and phosphorus absorption,
by stimulating bone calcium mobilization, and
by increasing renal reabsorption of calcium in the distal tubule.
These functions on bone and possibly kidney, but not intestine, require the parathyroid hormone.
84
How does phosphorus regulate Ca++ metabolism
The dietary Ca:P ratio affects resorption of these macronutrients.
The amount of phosphate in the blood affects the level of calcium in the blood. Calcium and phosphate in the body react in opposite ways: as blood calcium levels rise, phosphate levels fall.
Optimum Ca:P ratio is between 1.5:1 and 2.5:1.
85
What mineral excess can cause parakeratosis in pigs?
hypercalcemia
Parakeratosis refers to incomplete maturation of epidermal keratinocytes, resulting in abnormal retention of nuclei in the stratum corneum. It occurs in many diseases of the skin, particularly in psoriasis.
86
ostitis fibrosa and hypocalcemia
ostitis fibrosa = osteomalacia (softening of the bones)
*High-phosphorus and low-calcium diet may lead to the hyperfunction of the
parathyroid glands resulting in the overproduction of parathyroid hormone, and
increase in the excretion of phosphates by the kidneys.
Concurrent mobilisation
of mineral substances from the bones will cause an increase in plasma calcium content. Demineralisation of bones will occur.
87
paresis puerperalis and hypocalcemia
Parturient paresis / milk fever
Mostly in cows, but also in small ruminants and pigs.
Large quantities of Ca++ and P are excreted with milk that results in improper Ca:Mg
ratio whereas calcium concentration drops to ˂1.75 mmol/L.
Excess dietary calcium causes alimentary hypercalcemia during late pregnancy that inhibits parathormone and stimulates secretion of calcitonin; excess calcium is
deposited in bones.
Hormonal regulation of calcium metabolism is slow, the
levels of PTH in blood are low during parturition and calcium
mobilization from bone into the serum pool is insufficient.
Onset of lactation will
result in further decrease in plasma calcium concentration.
88
The plasma inorganic phosphorus concentration is ?.
Around ? – ? % of body’s phosphorus is located in bones.
1.30 – 3.20 mmol/L.
Around 75 – 80 % of body’s phosphorus is located in bones; phosphorus is
also found in organic compounds such as lipids, lecithin, sphingomyelin.
Plasma phosphorus concentration reflects the effect of long-term phosphorus
deficiency.
89
Phosphorus levels are the highest in what part of plants?
in the generative rather than vegetative plant parts.
Though the phosphorus concentration of root vegetable greens/tops is higher than that of grass.
90
Phosphorus resorption occurs in the
proximal part of the small intestine against a concentration
gradient.
Young animals absorb nearly 100% of the phosphorus present in milk;
the absorption of phosphorus from (plant-based) feeds is around 50%.
In ruminants, phytic acid (major storage form of plant P) is broken down by rumen microorganisms into absorbable components.
91
Monogastric animals excrete phosphorus in ?,
ruminants mainly in ?,
and pigs in ?.
Monogastric animals excrete phosphorus in urine, ruminants mainly in faeces,
and pigs in both faeces and urine.
Substantial quantities of phosphorus (35 – 40 g/day) are secreted in saliva.
92
Phosphorus deficiency causes what: (3)
1.Results in the reduction in feed intake accompanied by decrease in plasma inorganic phosphorus
2.Rickets (affects young animals)
3.Mobilisation of phosphorus from bones that leads to osteomalacia (affects adults)
93
Phosphorus excess/overdose causes what: (2 interconnected)
*Affects magnesium and manganese metabolism and stimulates parathyroid glands.
thus
*Parathyroid hormone induces bone demineralisation.
94
Fe is an essential component of several enzymes.
About ? – ? %
of iron is a component of hemoglobin and myoglobin.
About 75 – 80 % of iron is a component of hemoglobin and myoglobin.
95
Iron absorption occurs in the?
small intestine.
96
Iron is stored in the ?
Name 2 ironstorage proteins.
liver;
storage proteins – ferritin and hemosiderin contain Fe3+ (ferric iron)
(> 20 – 30 %)
97
Uptake of iron:
Adult animals obtain very small quantities of iron from feeds;
most of the iron is excreted in feces. Iron supplementation does not improve iron uptake.
Iron released from decomposed erythrocytes is recycled for the synthesis of hemoglobin.
98
Iron deficiency anemia can be described as ?
microcytic hypochromic anemia.
Usually affects neonatal piglets.
Due to reduced synthesis of Hb (˂ 80 g/L) tissues are deprived of oxygen; cardiac symptoms – tachycardia.
Disturbed oxygen
transportation to tissues hinders oxidative processes that results in growth retardation and impaired resilience.
99
Iron poisoning is usually associated with
administration of iron
preparations to piglets. The upper tolerance level for iron is
decreased in pigs that are deficient in vitamin E.
* Surplus iron is stored in liver and bone marrow; it causes
decrease in plasma calcium and phosphorus levels.
100
What is desoxycorticosterone?
is a mineralocorticoid hormone
used asreplacement therapy for dogs with primary hypoadrenocorticism (Addison's disease).
101
PTH increases renal
phosphorus excretion by
decreasing proximal tubule absorption.
102
In the intestinal mucosal cells, ferrous iron (Fe2+) is oxidized to the ferric (Fe3+) form
and is incorporated into?
apoferritin (a protein).
Ferritin that is not combined with iron is called apoferritin.
The important biological function of apoferritin is its ability to bind and store iron, by combining with a ferric hydroxide–phosphate compound to form ferritin.
Ferritin is a universal intracellular protein that stores iron and releases it in a controlled fashion.
Iron is released in the form of Fe2+ (ferrous).
103
After being transported into plasma, iron is oxidised back to
the Fe3+ (ferric) form and
incorporated into transferrin.
Transferrins are glycoproteins found in vertebrates which bind to and consequently mediate the transport of iron through blood plasma.
104
what are the "measured" cations and how big a portion of all cations do they take up?
In a healthy individual, sodium and potassium (also called “measured” cations) account for about 95% of total cations.
105
what are the "measured" anions and how big a portion of all anions do they take up?
chloride and bicarbonate (also called “measured” anions) account for about 85% of the total anions
106
which ones are more abundant - unmeasured anions or cations?
Since “unmeasured” anions are more abundant than unmeasured cations and are more important in terms of disease than the cations, the anion gap is essentially a marker of the amount of “unmeasured” anions in circulation.
107
largest contributor to the anion gap in health
albumin negatively charged at physiologic pH is the largest contributor to the anion gap in health
because “unmeasured” anions are found in higher concentrations than “unmeasured” cations, they have a far greater impact on the anion gap.
Note that the term “unmeasured” is really a misnomer, as many of these anions and cations are actually or can be measured, however they are not included in the anion gap equation (and are “unmeasured” for this purpose).
108
in a normal anion gap metabolic acidosis, you may typically find which ions altered?
decreased bicarbonate (anion) resulting also in increased chloride (anion) to maintain electroneutrality
109
in an increased anion gap metabolic acidosis, you may typically find which ions altered?
increased unmeasured anions meaning increased organic acids (such as lactic acid or keto acids)
