Kidney Function: Producing Dilute Urine

How much waste are we obliged to eliminate in urine per day?

What is the maximum urinary osmolarity possible?

How much urine are we obliged to produce per day if we need to eliminate 600mosmol but can only produce urine concentrated up to 1400mosm/l?

What is oliguria?

What is polyuria?

Why do we consider urine dilute when it has a concentration of less than 300mosmol/litre?

What is the name given to the volume of plasma cleared of osmotically active particles per unit time?

What is the correct equation for osmolar clearance if... V = urine flow rate Uosm = urine osmolarity Posm = plasma osmolarity

What is the correct equation for free water clerance if... V = urine flow rate Uosm = urine osmolarity Posm = plasma osmolarity

If free water clearance is greater than 0, the urine will be hypo-osmotic or [blank_start]dilute[blank_end]. If free water clearance is 0, the urine will be [blank_start]iso[blank_end]-osmotic with respect to [blank_start]plasma[blank_end]. If free water clearance is less than 0, the urine will be [blank_start]hyper[blank_end]-osmotic or concentrated.

Where are the osmoreceptors found in the brain?

Fill in the blanks below to describe the release of ADH. 1. When plasma osmolality is [blank_start]high[blank_end], receptors in the o[blank_start]rganum vasculosum lamina[blank_end], m[blank_start]edian preoptic nucleus[blank_end] and s[blank_start]ubfomical organ[blank_end] signal to neurosecretory cells in the [blank_start]paraventricular[blank_end] and [blank_start]supraoptic[blank_end] nuclei in the [blank_start]hypothalamus[blank_end]. 2. The nuclei synthesise a [blank_start]precursor[blank_end] of ADH 3. The [blank_start]precursor[blank_end] is passed into axons of neurons where it is cleaved into a [blank_start]9[blank_end] amino acid ADH molecule in the [blank_start]posterior pituitary[blank_end] 4. ADH is released into the blood of the [blank_start]internal carotid[blank_end] artery to be targeted to the [blank_start]collecting duct[blank_end]

ADH has a long half life in the blood.

Alcohol inhibits ADH secretion.

Nicotine, nausea, pain and stress stimulate ADH secretion.

Which factor is ADH secretion most sensitive to?

What symptoms characterise diabetes insipidus?

What is neurogenic diabetes insipidus?

What name is given to diabetes insipidus caused by mutated V2 receptors or aquaporin channels OR acquired by infection or drug use?

What condition is typical of diabetes mellitus whereby the presence of small molecules in the renal tubule prevents water reabsorption causing production of large quantities of dilute urine?

Potassium has a concentration of [blank_start]5[blank_end]mM in the extracellular fluid and [blank_start]150[blank_end]mM in the intracellular fluid.

In the proximal tubule, the Na+/K+ [blank_start]pump[blank_end] moves potassium ions [blank_start]into[blank_end] the epithelial cell. This concentration gradient draws potassium into the epithelial cell from the [blank_start]lumen[blank_end] and out into the [blank_start]interstitial[blank_end] fluid via [blank_start]channel[blank_end] proteins. Potassium can also diffuse between cells via [blank_start]tight junctions[blank_end].

How does potassium enter the epithelial cells of the thick ascending limb of the loop of Henle?

How does potassium enter the epithelial cells of the distal tubule?

In the collecting duct, potassium is reabsorbed by [blank_start]type A[blank_end] intercalated cells in exchange for [blank_start]H+[blank_end] ions. This is outweighed by [blank_start]secretion[blank_end] by the [blank_start]prinicipal[blank_end] cells. In the principal cells, potassium moves out of the epithelium via [blank_start]renal outer medullar K+ channels[blank_end] (ROMKs). It also moves out through [blank_start]calcium[blank_end]-activated big-[blank_start]conductance[blank_end] K+ channels when tubular flow rates are [blank_start]high[blank_end]. The K+/[blank_start]Cl-[blank_end] transporter also removes potassium from the cell.

If more sodium enters the principal cells in the collecting duct epithelium, what happens to the secretion of potassium?

What hormone stimulations the K+ channels, Na+ channels and Na+/K+ ATPases of the collecting duct to increase secretion?

Which favours secretion more?

What is hypokalaemia?

Hypokalaemia can occur due to increased internal losses. For example, in the kidney, [blank_start]high[blank_end] tubular flow rates favour [blank_start]high[blank_end] rates of potassium [blank_start]secretion[blank_end]. Hyperaldosteronism [blank_start]increases[blank_end] the activity of the potassium channels, favouring potassium [blank_start]secretion[blank_end]. Alkalosis is also associated with hypokalaemia because potassium is secreted due to changed in [blank_start]electrochemical gradients[blank_end]. In the GI tract, vomiting and [blank_start]diarrhea[blank_end] can cause excess potassium loss. Potassium can be lost from the skin due to burns or intense [blank_start]sweating[blank_end].

How does insulin affect potassium uptake in cells?

Why does potassium intake into cells increase due to metabolic alkalosis?

What is severe hypokalaemia?

In hypokalaemia, membrane potentials become more [blank_start]negative[blank_end]. Therefore, a larger intake of [blank_start]sodium[blank_end] is required to exceed the [blank_start]threshold[blank_end] and fire an [blank_start]action potential[blank_end]. Therefore, action potentials are less likely to fire and the [blank_start]refractory[blank_end] period is [blank_start]longer[blank_end] so muscles become weak and paralysed.

What is hyperkalaemia?

Reduced release of what hormone can cause hyperkalaemia?

Hyperkalaemia can be caused by redistribution of potassium out of cells. Check the two specific examples of this.

In hyperkalaemia, the resting membrane potential becomes more [blank_start]positive[blank_end]. This means less [blank_start]sodium[blank_end] is required to exceed the [blank_start]threshold[blank_end] and fire an [blank_start]action potential[blank_end]. Action potentials are [blank_start]more[blank_end] likely to fire, causing hyperreflexia and [blank_start]cramping[blank_end] of the muscles.

What can we administer intravenously to treat hyperkalaemia to decrease the action potential threshold in the heart?

Which drug could we administer during hyperkalaemia to shift K+ into cells?

Of the treatments listed below, which are appropriate for treating hypokalaemia?

What is severe hyperkalaemia?