Week 5 - CKD Flashcards

1
Q

How is H+ gained in tubular system?

A
  • From CO2 in tissue
  • Metabolism of protein and organic molecules
  • Loss of bicarbonate in diarrhoea
  • Loss of bicarbonate in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is H+ gained in the tubular system?

A
  • H+ + HCO3- –> H2O + CO2
  • Utilisation of H+ in metabolism or organic anions
  • Loss of H+ in vomitus
  • Loss of H+ in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 ways pH is maintained?

A
  • Buffers
  • Ventilation
  • Renal H+ and HCO3- regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do kidney regulate H+?

What happens during alkalaemia and acidaemia?

A
  • H+ excretion or reabsorption
  • Regulation of plasma HCO3-

Alkalaemia = low H+ = kidneys inhibit H+ excretion, increase HCO3- excretion in urine

Acidaemia = high H+ = kidneys increase H+ excretion in urine, add new HCO3- to blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens in the tubules to allow no net gain of HCO3-?

A

HCO3- = reabsorbed in proximal tubule

1 HCO3- absorbed = 1 HCO3- filtered

HCO3- also reabsorbed in thick ascending limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the process of ammonium trapping?

A
  • NH4+ produced and secreted by proximal epithelium
  • NH4+ reabsorbed at thick ascending limb, into medullary interstitium
  • Exists as NH4+ and NH3
  • NH3 diffuses into lumen of collecting duct
  • NH3 + H+ –> NH4+ –> excreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens when HCO3- is added to the blood?

A
    • H+ secretion
    • urine NH4+ concentration
    • urine H2PO4- concentration (because + HPO4 required as immediate buffer for increase in H+ secretion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What effect does aldosterone have on pH?

A

Stimulates H+ secretion

+ HCO3-

Aldosterone excess = leads to metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do kidneys compensate for respiratory acidosis and alkalosis?

A

Acidosis = new HCO3- in blood = +NH4+ and H2PO4- in urine = acidic urine

Alkalosis = + HCO3- excretion, - H+ excretion = alkaline urine = + HPO4, - H2PO4-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the renal compensation for metabolic acidosis?

A

Kidneys = act with lungs if not source of problem

Hyperventilation

  • Lungs shed H+ and put new HCO3- in blood
  • Causes acidic urine
    • H2PO4- and NH4+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the renal compensatino for metabolic alkalosis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the renal actions of osmotic diuretics?

When are they used?

A
  • Freely filtered at Bowman’s capsule
  • Increase osmolality of tubular fluid in proximal convoluted tubule and loop of Henle

Use = cerebral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the renal actions of loop diuretics?

When are they used?

A
  • FUROSEMIDE
  • +++ powerful diuretic –> peeing buckets
  • Block Na+/2Cl-/K+ symporter in thick ascending limb
  • Prevent creation of hypertonic interstitium so reduce ability of loop to concentrate urine
    • Na+ delivery to distal convoluted tubules - loss of K+
  • Decrease Na+ entry into macula densa = renin release
  • Loss of transepithelial potential - reduced catino absorption

Use = chronic heart failure and renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the renal actions of thiazides?

When are they used?

A
  • Powerful
  • Act on distal convoluted tubule
  • Inhibit active Na+ reabsorption and accompanying Cl-
    • solute in tubular fluid = decreased H2O reabsorption gradient
  • So + H2O in tubular fluid
  • Reduce circulating volume

Use = hypertension and mild/moderate heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the renal actions of aldosterone receptor antagonists?

A
  • Prevent Na+ pump insertion and Na+ channel insertion
  • Used in primary and secondary hyperaldosteronism
  • Low dose used in CHF to block aldosterone actions on heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the renal actions of amiloride?

A
  • Sodium channel blocker
  • Block luminal Na+ channels in late distal convoluted tubule and collecting ducts
  • Na+ not retained at K+ expense
17
Q

What are the consequences of diuretics?

A
  • Hypokalaemia - K+ loss secondary to loop diuretics and thiazides
    • Leads to cardiac arrhythmias and potentiates action of digoxin
    • Due to RAAS activation
  • Alkalosis - H+ loss due to Na+ delivery to distal convoluted tubule
18
Q

What causes hyponatremia and hypernatremia?

A

Hypo = Na+ < 135 mmol/L

  • H2O retention secondary to excretion defect

Hyper = Na+ > 145 mmol/L

  • H2O loss and impaired thirst
  • Na+ retention
19
Q

What is the role of K+ in renal?

A
  • K+ affects membrane potential
  • Intracellular K+ affects protein and glycogen synthesis
    • K+ = redcued sensitivity to ADH
20
Q

What physiological factors affects K+ transcellular distribution?

A
  • Na+/K+ ATPase
  • Insulin = + K+ intake into cells to activation fo Na+/K+ ATPase
  • Catecholamines = + K+ uptake = + Na+/K+ ATPase activation
  • Plasma K+ concentration
  • Exercise = + K+
21
Q

What are the consequences of Hypokalaemia and Hyperkalaemia?

A

Hypo:

    • Muscle weakness / paralysis
    • Cardiac arrhythmias
    • Rhabdomyolosis
    • Renal dysfunction

Hyper:

    • Muscle weakness / paralysis
  • Cardiac arrhythmias
22
Q

What are the treatments for hypo and hyperkalaemia?

A

Hypo = KCl and HCO3- oral or IV

Hyper = Antagonism of membrane actions, + K+ entry into cells with insulin + glucose and removal of excess K+ with diuretics or dialysis

23
Q

What are the properties of somatic pain?

A
  • Pain arising from skin
    • modalities
  • Sensitive, well-localised, sharp pain
  • Many sensory receptors
24
Q

What are the properties of visceral pain?

A
  • Fewer sensory endings in viscera
  • Iften in smooth muscle
  • Poorly localised
  • Dull, heavy pain
  • May be referred
  • Pain not from harm, just overstretching or contraction
25
Q

What are the properties of visceral autonomic afferent fibres?

A
  • No peripheral synapse
  • Join spinal nerve and enter CNS along dorsal nerve root
  • Cell body in dorsal root ganglion
  • T1-L2 = sympathetic motor outflow
  • S2-4 = sacral parasympathetic outflow
26
Q

Where do you feel pain with problems with the following organs?

A
27
Q

What happens during enterohepatic recirculation?

A
  • Drug excreted in bile
  • Drug travels to GI tract
  • Drug reabsorbed
  • Drug travels to liver
  • Process repeats
28
Q

What drugs should you avoid when breastfeeding?

A
  • Anticancer drugs
  • Amiodarone
  • Lithium
  • Iodine containing radiocontrast media
  • Tetracyclines
29
Q

What are the 3 processes of renal handling of drugs?

A

Glomerular filtration

Active secretion

Passive reabsorption

30
Q

What happens during glomerular filtration?

A
  • Unbound drug and metabolites freely filtered
  • Protein-bound drug not filtered
31
Q

What are the 2 main drugs to remember that are actively secreted?

What is a key drug interaction to remember?

A

Uric acid

Methotrexate

Thiazides

NSAIDs block excretion of methotrexate

32
Q

What happens during passive reabsorption?

A
  • Tubule acts as lipid barrier
  • Reabsorption depends on pH, pKa and lipid solubility
  • Acid drugs are alkaline when ionised and vice versa
  • Can be used in overdose
33
Q

What determines oncotic pressure?

What is nephrotic syndrome?

A

Albumin

Caused by low albumin - low oncotic pressure - + interstitial fluid from + hydrostatic pressure

34
Q
A