Session 1: Homeostasis and Biological Signalling Molecules

Question 1

1. Average Restring respiratory rate? What rate is it a red flag symptom?
2. Average Resting HR? What rate is it a red flag?

Answer 1

1. 2-20

>=25

2.60 to 100 beats a minute

(athlete down to 40)

>130

Question 2

1. What is hypothermia?
2. Symptoms?
3. Causes?
4. Body temp is normally regulated within what range?
5. Traditional gold standard measurement used to estimate core temperature

Answer 2

1. core temperature below 35.0 °C
2. Mild - shivering & mental confusion

Moderate hypothermia - shivering stops and confusion increases.

Severe hypothermia - paradoxical undressing, in which a person removes his or her clothing, as well as an increased risk of the heart stopping

3. Extreme cold

Reduced body heat production or inc heat loss - elderly, anorexic, alcohol induced, low blood sugar

4. 36.5–37.5 °C (97.7–99.5 °F)
5. Rectal

Question 3

1. Causes
2. What is hyperthermia

Answer 3

1. Heat stroke, adverse reaction to drugs (CNS) (common))

thyrotoxicosis & an adrenal gland tumor, called pheochromocytoma (rare)

Many psychotropic medications, such as selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants, can cause hyperthermia. Serotonin syndrome is a rare adverse reaction to overdose of these medications or the use of several simultaneously

2. temperature greater than 37.5–38.3 °C
3. Early - inc sweating, rapid breathing & a fast, weak pulse

Mild - nausea, vomiting, headaches, and low blood pressure

Severe -intoxicated behavior, tachycardia, tachypnea, blood vessels to contract reflexively, resulting in a pale or bluish skin color in advanced case, seizures ( children), MOF

Question 4

State the intracellular and extracellular conc on K+, Na+, Cl- & Ca2+

Question 5

1. What is the normal ECF & ICF value for [K+]
2. What is hyperkalemia
3. Causes
4. Signs/symptoms
5. Diagnostic
6. Treatment

Answer 5

1. ECF: Serum potassium 3.5 and 5.0 mmol/L

ICF

2. Blood potassium > 5.5 mmol/L, electrocardiogram
3. • kidney failure
     - hypoaldosteronism -> no induction of ROMK
     - rhabdomyolysis -> crush injury
     - medications: spironolactone, NSAIDs, ACE inhibitors
     - metabolic acidosis
4. malaise, palpitations, and muscle weaknes

hyperventilation (metabolic acidosis)

cardiac arrythmias

5. ECG -> elevated t waves

severe-> larger QRS interval

6. Medications: Calcium gluconate, dextrosewith insulin, salbutamol, sodium bicarbonate

Low potassium diet

Hemodialysis

Question 6

1. What is the normal ECF & ICF value for [K+]
2. What is hypokalemia
3. Causes
4. Signs/symptoms
5. Diagnostic
6. Treatment

Answer 6

1.

2. [K+] levels below 3.5 mmol/L
3. • Reduced dietary intake • Increased entry into cells
   – Metabolic alkalosis
   – ↑ β-adrenergic activity (e.g. NA with stress) • Increased GI loss
   – Vomiting / NG drainage
   – Diarrhoea • Increased urine loss
   – ↑ aldosterone
   • Volume depletion • Primary hyperaldosteronism • Secondary hyperaldosteronism (↓ EABV)
   – ↑ urine flow (Loop diuretic Thiazide diuretic)
   – Renal tubular acidosis
   – Magnesium deficiency
4. • Weakness

• Polyuria (dec K+ causes ADH resistance)
• Constipation (smooth muscle dysfunction)
• Arrhythmias

5. An ECG in a person with a potassium level of 1.1 meq/l showing the classical changes of ST segment depression, inverted T waves, large U waves, and a slightly prolonged PR interval
6. Mild - changes in the diet, potassium supplements PO/IV

Magnesium replacement may also be required

Question 7

Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium. These include renal artery stenosis and tumors (generally nonmalignant) of the adrenal glands, e.g., Conn’s syndrome (primary hyperaldosteronism). Cushing’s syndrome can also lead to hypokalemia due to excess cortisol binding the Na+/K+ pump and acting like aldosterone. Hypertension and hypokalemia can also be seen with a deficiency of the 11-beta-hydroxysteroid dehydrogenase type 2 enzyme which allows cortisols to stimulate aldosterone receptors. This deficiency—known as apparent mineralocorticoid excess syndrome—can either be congenital or caused by consumption of glycyrrhizin, which is contained in extract of licorice, sometimes found in herbal supplements, candies, and chewing tobacco.

Question 8

An increase in the pH of the blood (alkalosis) can cause temporary hypokalemia by causing a shift of potassium out of the plasma and interstitial fluids into the urine via a number of interrelated mechanisms. 1) Type B intercalated cells in the collecting duct reabsorb H+and secrete HCO3. Protons are reabsorbed via both H+-K+ATPases and H+ ATP-ases on the apical/luminal surface of the cell. By definition, the H+-K+ATPase reabsorbs one potassium ion into the cell for every proton it secretes into the lumen of the collecting duct of a nephron. In addition, when H+ is expelled from the cell (by H+ATP-ase), cations—in this case potassium—are taken up by the cell in order to maintain electroneutrality (but not through direct exchange as with the H+-K+ATPase).[7] In order to correct the pH during alkalosis, these cells will use these mechanisms to reabsorb great amounts of H+, which will concomitantly increase their intracellular concentrations of potassium. This concentration gradient drives potassium to be secreted across the apical surface of the cell into the tubular lumen through potassium channels (this facilitated diffusion occurs in both Type B intercalated cells and Principal cells in the collecting duct). 2) Metabolic alkalosis is often present in states of volume depletion, such as vomiting, so potassium is also lost via aldosterone-mediated mechanisms. 3) During metabolic alkalosis, the acute rise of plasma HCO3− concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate.[8]

Question 9

Rare hereditary defects of renal salt transporters, such as Bartter syndrome or Gitelman syndrome, can cause hypokalemia, in a manner similar to that of diuretics. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartter’s or Gitelman’s.

Question 10

Distribution away from extracellular fluidEdit

In addition to alkalosis, other factors can cause transient shifting of potassium into cells, presumably by stimulation of the Na+/K+pump.[9] These hormones and medications include insulin, epinephrine, and other beta agonists (e.g. salbutamol or salmeterol), and xanthines (e.g. theophylline).[10]

Rare hereditary defects of muscular ion channels and transporters that cause hypokalemic periodic paralysis can precipitate occasional attacks of severe hypokalemia and muscle weakness. These defects cause a heightened sensitivity to the normal changes in potassium produced by catecholamines and/or insulin and/or thyroid hormone, which lead to movement of potassium from the extracellular fluid into the muscle cells.

Question 11

Symptoms of hyper- and hypokalaemia relate to effect on membrane potential
• Low serum K+ leads to bigger K+ gradient between intracellular and
extracellular compartment
– depolarisation leads to increased excitability – risk of arrhythmia • High serum K+ leads to smaller K+ gradient
– decreased membrane excitability – risk of cardiac arrhythmias
• Risk of symptoms depends on both degree and rapidity of change

Question 12

Explain what this state ‘Mineralocorticoids and distal delivery of Na+ normally have a reciprocal relationship’ means

Answer 12