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
CAUTI’s
UTI’s caused by catheters. You get pooling of urine in the bladder and side of the catheter as bacteria is not flushed out. Bacteria can also colonise the inside of a catheter and block it. Bacteria can drop of the catheter causing infections in other parts of the urinary tract. You would remove and replace the catheter.
Vesicouretic reflux (VR) causing UTI’s
This is when there is an abnormality in the ureter. There are five different grades, the higher the grade the more abnormal it is. At grade 5 you have a distended ureter with little flow out of it, and get urine pooling in it. This leads you more susceptible to infection. Urine is a good growth factor for bacteria.
Tests which can be done to diagnose UTI’s
- A dipstick analysis on urine can be done to confirm this, it can be done in a GP surgery, shows what’s present in the urine. A urine microscopy can be performed, leukocytes indicate presence of infection.
- A urine culture will be performed to grow the bacteria in the urine in order to identify them, also look at their antibiotic sensitivity. A urine culture should always be performed in men with a history suggestive of UTI regardless of the results of the dipstick test.
- An ultrasound evaluation of the upper urinary tract
How is a UTI diagnosed in women
Normally empirically based on their history
UTI- in what groups should urine be cultured before starting antibiotic treatment?
- Men
- Pregnant woman
- Children under three years old
- In patients with suspected upper urinary tract infection (flank pain)
- Complicated or recurrent infection
- If resistant organisms are suspected
- If urine dipstick testing gives a single positive result for leucocyte esterase or nitrite
- If clinical symptoms are not consistent with dipstick testing results.
Treatment for lower UTI
Trimethoprim (avoid during pregnancy) and nitrofurantoin, this is based on empirical history. If you know the organism and its resistance to antibiotics this will influence what you do
Treatment for Pyelonephritis (kidney infection)
Treated with Cefalexin. Can change with microbiology results
Frequency of UTI’s
UTI’s are far more common in woman, can occur in woman where there is no underlying problem. Uncommon in men and children, when they do occur it is likely there is an underlying abnormality in the urinary tract. Increases in both sexes with age.
Frequency of UTI’s in infants
1-2% per year
Frequency of UTI’S in preschool children
More common in preschool girls (4.5%). When it occurs in boys (0.5%) its usually associated with serious congenital abnormalities.
Frequency of UTI’S in schoolchildren
Girls 1.2%, boys 0.03%
Frequency of UTI’S in adults
Between 1-3% in young non-pregnant woman. 10-20% of females experience a UTI at some point in their life. Less then 0.1% in men until later years when it rises.
Frequency of UTI’S in over 65’s
At least 20% in men and 20% in woman. High rate of spontaneous cure and re-infection.
Urine appearance in renal and urinary tract diseases
Urine can be frothy, cloudy or red
What is a UTI
An infection in any part of the urinary system
Symptoms of a UTI
Change in urination frequency, Dysuria (painful urination), passing only a small amount of urine frequently, Haematuria (blood in the urine), pyuria (foul smelling and or cloudy urine). You also have urgency which means that you constantly feel like you should urinate but not passing any urine. Urinary inconstance, you have leakage. Can have flank pain
More severe symptoms can be rigors where you shiver and feel feverish. May have pyrexia (high temperature) as well as nausea and vomiting. For elderly people they may have an acute confusional state
Bacteriuria
Bacteria present in the urine. Asymptomatic bacteriuria is without symptoms
Significant bacteriuria
The number of bacteria in voided urine that exceeded the number usually due to contamination from the anterior urethra (>10^5 bacteria/ml).
Relapse- UTI
When you have a UTI with the same bacteria from your last UTI. So will be bacteriuria with the same infecting bacterium
Reinfection- UTI
When a bacterium different to the original infecting bacterium infects you
Urethritis
Infection of urethra
Cystitis
Infection of the bladder
Pyelonephritis
Infection of the kidney
Symptoms of kidney infection (acute pyelonephritis)
Upper back and flank pain, high fever, shaking and chills, nausea, vomiting
Symptoms of bladder infection (cystitis)
Pelvic pressure, urge incontinence, lower abdomen discomfort, frequent urination, painful urination (dysuria) and blood in the urine
Symptoms or urethra infection (urethritis)
Burning with urination
Urinary dipstick tests
A stick covered in small square patches that have various assays and enzymes on them, you dip it into a sample of urine. The bottle will have a reference picture printed on it which you compare the dipstick to, first thing you do when you suspect a renal cause
What does a urinary dipstick test for
Blood, proteins, nitrates, Leukocyte esterase, Glucose, bilirubin, Urobilogen, specific gravity, pH ketones. The top 5 are more routinely looked at by clinicians but the bottom 5 can be useful. Leukocyte esterase detects white blood cells
Urinary tract stones
When solutes become super saturated in urine they can precipitate and crystalise, forming a stone. This can happen because of increased solute or decreased solvent i.e. dehydration. Vary in size from mm to cm and can be anywhere along the urinary tract. Some migrate along the urinary tract others stay in place, the migration can cause symptoms.
Urinary tract stones- calcium oxalate
Formed by a calcium cation binding with an oxalate anion to create calcium oxalate. Most common form of calculi, present in 60% of cases. Most likely to form in acidic conditions. They are radio opaque, meaning they show up on an x-ray as a white dot.
Urinary tract stones- calcium phosphate
Formed by calcium binding with phosphate and hydrogen. Account for 15% of cases, more likely to form in alkaline conditions. Also radio-opaque
Urinary tract stones- struvite
Bacteria using urease to break down urea to create ammonia which favours precipitation of Magnesium and phosphate in the urine to create Struvite. 15% of cases. Commonly called Staghorn calculi and can fill the whole of the renal pelvis or multiple clayces. Associated with infection. Radio-opaque. Made of Magnesium, Ammonium and Phosphate
Urinary tract stones- uric acid
The urate anion binds to the sodium cation to form monosodium urate. Accounts for 10% of stones. Radiolucent i.e. they don’t show up on an x-ray
Urinary tract stones- cystine
An amino acid, about 5% of stones. Associated with cystinuria (autosomal recessive disease inheritance) with high levels of cysteine in the urine. Radio-opaque
Urinary tract stones- risk factors
- Structural abnormalities affecting flow of urine e.g horseshoe kidneys
- Loop diuretics e.g. furosemide
- Relative dehydration
- Diet high in purines (e.g. red meat, oily fish) increases risk of uric acid stones
- Hypercalcaemia- for calcium containing stones
- Increased levels of oxalate in the urine can be due to genetic defects which cause increased oxalate excretion or high dietary intake (beer, rhubarb, kiwis)
- Metabolic disorders e.g. cystinuria
- Can be caused by necrosis following AKI
- History of renal calculi or recurrence.
Renal stones- symptoms
Many small calculi are asymptomatic and pass without the patient realising. Patients will often be sweating with pallor, nausea, vomiting and some dysuria. Often haematuria (can be non-visible). Renal stones if obstructive can be associated with infection. Stones high up in the kidney will cause flank pain that may not radiate anywhere else, a dull pain. Stones that are moving down the ureter to the bladder will cause pain that radiates from the loin to the groin due to spasm and dilation of the ureter, called renal colic. The pain is not always intermittent but can be constant. There may be short periods of relief but a persisting dull ache. As calculi move further down the pain can radiate to the labia or scrotum.
Urinary stones- Examination and findings
You check their vital signs then a general inspection, what’s the appearance of the patient, sweating, pallor, obvious pain. You then examine the abdomen, there should be nothing to see externally and the abdomen should be soft. Depending on the location of the stone examination findings may vary but tenderness can be present over the flanks (over the kidneys) and radiate round and down to the groin. Next urinalysis should be done to check for haematuria. Look for systemic signs of the patient being unwell. Looking for signs of infection which may be associated with an obstructing stone or staghorn calculus.
Urinary stones- diagnoses
Imaging is used to confirm diagnoses. You can use an x-ray as most stones contain calcium so are radio opaque. Better to use CTKUB (CT kidney-ureter-bladder) which is more sensitive than IVU (intravenous urogram) and can identify non-radio opaque calculi. USS (ultrasound scan) can be used and is preferable in groups where exposure to radiation should be avoided i.e. pregnant women. Can be useful in situations where the patient is acutely unwell e.g. sepsis from obstructed stone and preference would be to initiate management rather than wait for CT scan results. It will be tender on palpation
Urinary stones- management
People who should be hospitalised= fever (infection), solitary functioning kidney, persistent pain, anuria (no urine), cant take adequate fluids (vomiting), pregnancy and people over 60
Urinary stones- medication
- Analgesia (usually NSAIDs to PR/IM diclofenac if vomiting or PO. Opiates will relieve less pain in this group and increase nausea further
- Anti-emetics and rehydration (IV fluid)
- Antibiotics if infection is present.
Urinary stone size
Split into three groups, <5mm, 5-10mm, 10-20mm and >20mm
Urinary stones- conservative management
Stones that are small (<5mm) should pass spontaneously within a few weeks. If stones can be captured, by sieving the urine they can be sent to the laboratory for testing.
indication for active removal of renal stones
Obstruction caused by stones, infection, symptomatic stones (pain or haematuria), stones >15mm, combability, social situation of the patient.
Urinary stones- medical expulsive therapy
Alpha blockers (e.g. tamsulosin) and calcium channel blockers (e.g. nifedipine) can be used to reduce ureteric spasm with the aim to help stones pass. This is only given to patients with stones 5-10mm that are distal and could pass spontaneously given assistance.
Urinary stones- extracorporeal shockwave lithotripsy (ESWL)
Uses high energy shock waves to break the stones down into smaller crystals so they can pass. Success can vary. Routine antibiotic prophylaxis is not required. Complication include fragments reforming and the fragments causing renal colic. Can also cause UTI and infection, tissue damage within the kidney (increased shockwave rates and energy and cardiovascular dysrhythmias. In the kidney used for for stones between 0-2cm, in the ureter it can be used for stones under 10mm
Urinary stones- uteroscopy (URS)
Performed under general anaesthesia. You insert a ureteroscope into the ureter via the external meatus to directly extract the stone. The retrograde approach, the scope will travel up the ureter from the bladder towards the kidney. The antegrade approach would be percutaneous (through the skin) and travel down the ureter to find the stone. This is used less often and would be for larger stones, stones lodged in the distal collecting duct of the kidney or when the retrograde approach has failed. Not used when you cant remove the stone completely, instead use SWL during ureteroscopy. Stents can be inserted to decompress the ureter (e.g. with an obstructing stone). Used in the ureter when stones are under 10mm and over 10mm if you have a fever or nausea/vomiting
Urinary stones- percutaneous nephrolithotomy (PNL)
Involves key-hole access through the flank to the kidney itself. An antegrade approach. Done under anaesthetics for larger stones. Involves a high risk of bleeding so anticoagulants must be stopped. Contradicted in pregnancy, untreated UTIs, where there is potential malignancy in the kidney or ureter near the access sites. Intracorporeal shockwave lithotripsy can be used in this procedure to fragment stones. Nephrostomies (draining system connected to an artificial exterior collection vesicle, similar to stroma) can also be placed. Possible complications include bleeding, infection, and organ injury. Used in the kidney when the stones is >2cm
Renal stones- surgery/laparoscopic
Not used a lot anymore. Surgery is offered in cases where shock wave litripsy, retrograde or antegrade ureteroscopy and percutaneous nephrolithotomy have failed or are unlikely to be successful.
Complications of Urolithiasis (kidney stones)
- Recurrence- someone with lots of risk factors is at higher risk of recurrence. Cystinuria increases recurrence
- Failure of stone to pass- The bigger the stone the less chance they will pass spontaneously.
- Obstruction- can completely obstruct the ureter. The build up of pressure of urine behind the stone can lead to the formation of hydronephrosis, if not decompressed this can lead to permanent kidney damage. Hydronephrosis is dilation of the renal pelvis and/or calyces due to increased pressure in the ureter and kidneys. Anuria suggests there is complete blockage, as no urine can get passed the stone, they should be hospitalised.
- Infection- Can develop around an obstructed stone, can either be localised or systemic. If a patient develops systemic infection secondary then it’s sepsis
