Case 3- Illness Flashcards
Nephritic syndrome
Nephritis causes inflammation which increases the permeability of the filtration membrane. More water, proteins, and blood can leak across so can cause haematuria, proeteinuria and hypertension. Red blood cell casts are present
Nephrotic syndrome
Increases permeability so large amounts of proteins can go across the barrier. In response the liver produces more lipoproteins. Causes proteinuria, hypoalbulminemia and oedema. Diagnosed with dipstick
Hyponatraemia
Too low sodium in the blood <135mM. Causes low plasma osmolarity
Hypernatremia
Too high levels of sodium in the blood >145mM. Causes high plasma osmolarity
Major causes of Hyponatraemia- Hypoaldosteronism
Due to lack of aldosterone which causes Na reabsorption. Causes include Addison’s disease and adrenal insufficiency
Major causes of Hyponatraemia- thiazide diuretics
Inhibit a coupled NaCl cotransporter leading to a decrease in Na reabsorption
Other causes of Hyponatraemia
1) Vomiting/diarrhoea/sweating- disturbance in salt balance
2) Excess water intake
3) When formula milk is made with more water then recommended when access to formula is restricted i.e. in poverty
Causes of Hypernatraemia- salt balance
Too much salt in diet, too much saline in the IV. Hyperaldosteronism (too much aldosterone promoting the absorption of sodium). Hyperaldosteronism can be due to a tumour in the adrenal gland
Causes of Hypernatraemia- water balance
When there is decreased water intake. Could be because the patient is unconscious, a lack of access to water and vomiting. When there is increases insensible loss of water in exercise. Can be sensible losses such as vomiting/diarrhoea and no ADH due to diabetes insipidus
Syndrome of inappropriate ADH secretion- SIADH
Excessive ADH secretion leads to a high urine osmolality which increases total body water. This leads to hyponatremia, hypo-osmotic blood plasma and hypervolemia. The kidney recognises the increase in blood volume so reduces its production of Renin. This causes a decrease in Angiotensin 2 which decreases Mineralocorticoid production which decreases sodium absorption in the blood. Meaning there is more sodium in urine so Hyponatremia gets worse. Can be causes by stress, head trauma, tumours and some drugs (opiods, anti-depressants and nitocine)
Diabetes insipidus
Non-functional ADH system which results in excessive loss of water. Can cause Polyuria (urinating more), polydipsia (wanting to drink more), hypernatremia and hypotension.
The 2 types of diabetes insipidus
Neurogenic DI- failure of ADH secretion, can be due to lesions or tumours in the hypothalamus or pituitary, so no signals are sent out. To treat this you provide synthetic ADH.
Nephrogenic DI- the failure of the principal cells to respond to ADH, caused by V2 receptor mutation which binds to ADH setting up the camp signalling cascade. Treat with a restricted Na+ diet.
Thiazide diuretics- renal
Most commonly prescribed diuretic. Inhibit the Na+/Cl- cotransporter in the early DCT on the apical surface. Promotes sodium excretion by blocking reabsorption. This increases the osmolarity of the filtrate, more water remains in the filtrate and is excreted. Example of thiazides= chortalidone and indapamide.
Loop diuretics
Works on the thick ascending limb of the loop of Henle. They antagonise the Na+/K+/2Cl- cotransporter and inhibit its action. Promotes sodium excretion by blocking its reabsorption. This increases the osmolarity of the filtrate so more water remains to be excreted. Example- Furosemide and bumetanide.
Potassium sparing diuretics
Work on principal cells found in the late distal convoluted tubule and in the collecting duct. They fall into two main classes: aldosterone antagonists such as Spironolactone. And we also have ENaC antagonists such as Amiloride.
Aldosterone antagonists
Prevents aldosterone from binding to the mineralocorticoid receptors. Sodium is unable to be reabsorbed, so more sodium and water is excreted as water follows sodium. Potassium channels are also not created so stops K+ from being transported to the filtrate and excreted, so K+ is spared.
How do aldosterone antagonists spare K+
It is able to “spare” K+ because the Na+/K+ ATPase is not created so the potassium cannot be moved from the interstitium into the principal cells. As there is less sodium it is less likely Na+ and K+ will be exchanged using this pump. The net charge of the filtrate becomes more positive so there is no concentration gradient for K+ to move from the principal cells to the tubular fluid.
ENac antagonists
Prevent the formation of ENaC channels in the principal cells of the late DCT and collecting duct. Preventing the reabsorption of sodium from the filtrate promoting its excretion. “Spares” K+ in the same way as Aldosterone antagonists.
Hypokalaemia
When the Potassium levels are below 4mM. Cells become more negative and less sensitive to depolarisation. Can lead to muscle weakness and paralyses (calcium channels dont open and no nerve impulses). As well as abnormal neural conduction leading to confusion and coma. There will also be decreased cardiac excitability.
Hyperkalaemia
When extracellular K+ levels are above 5mM.They are more excitable meaning they depolarise more; this can lead to cardiac arrhythmias and increased risk of cardiac arrest. Also causes abnormal neuronal conduction.
Causes of Hypokalaemia
When they are unable to obtain or digest food, when their diet is deficient in K+. Can be lost in increased sweating, vomiting and diarrhoea. Patients on loop diuretics or increased Aldosterone levels will stimulate K+ loss. Alkalosis or administration of insulin where K+ moves from the extracellular to intracellular
Effects of Hypokalaemia
1) Neuromuscular manifestations- muscle weakness, fatigue, cramps and tenderness. This can lead to Paraesthesia and paralysis.
2) Renal manifestations- polyuria, urine with low osmolality and polydipsia.
3) Gastrointestinal manifestations- anorexia, nausea and vomiting as well as constipation, abdominal distention and paralytic ileus.
4) Cardiovascular manifestations- arrhythmias and increased sensitivity to digitalis toxicity. Can also cause metabolic alkalosis
Causes of Hyperkalaemia
Increased dietary intake, people with poor renal function may not be able to compensate for this. Decreased renal function, treatment with potassium sparing diuretics or decreased Aldosterone levels (Addison’s disease). Can also be due to a transcellular shift where K+ moves from the intracellular to the extracellular. This can be due to metabolic acidosis, can be a response to extreme exercise or seizures or tissue injury (burns or crushing). When you get a tissue injury, cells will be damaged and break up releasing the intracellular K+ causing an increase in plasma K+. Insulin is administered to reabsorb the K+
Effects of Hyperkalaemia
1) Gastrointestinal manifestations- anorexia, nausea, vomiting, diarrhoea
2) Cardiovascular manifestations- ventricular fibrillation and cardiac arrest
4) Neuromuscular manifestations- paraesthesia, muscle cramps, weakness and tiredness.
Can also cause metabolic acidosis
Risk factors of a UTI
Female, increased age, recent antibiotic use (destruction of normal bacteria flora), recent sexual activity, new sexual partner, use of spermicide, diabetes, presence of catheter (CAUTI- catheter associated urinary tract infection). Institutionalisation, for example, being in a care home or hospital for a long time. Pregnancy as well
Uncomplicated UTI
Woman can develop a UTI when they are healthy and have no abnormalities. When the infection is in a structurally and neurologically normal urinary tract
Why are women more likely to get UTI’s
They have a small urethra and their vagina is near the anus
Complicated UTI
A UTI when there are abnormalities in the urinary tract. Can be caused by diabetes, kidney stones, blockages and developmental abnormalities.
What must happen for a UTI to be caused
Bacteria must get into the urinary tract, adhere to the epithelial surface, multiply and elicit an inflammatory response
The ascending route in UTI’s
Where bacteria colonise and ascent the UT by bowel flora, this is more common in females the males, goes from the bottom of the UT to the bladder
The Haematogenous route for UTI’s
When blood borne bacteria cause infections in the urinary tract, mainly the renal parenchyma
Bacteria which cause UTI’S
Similar in males and females. UPEC (gram negative rod) is the leading cause. Many of the bacteria are normal flora that become opportunistic when they enter the UT, can include fungi