Renal colic Flashcards

(39 cards)

1
Q

What are the 3 main types of renal stone formed from?

A

Calcium oxalate (usually with some Ca phosphate) (65%).
Calcium phosphate alone (15%).
Struvite (10-15%).

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2
Q

What is the main condition that leads to stone formation?

A

Hyperparathyroidism. 90% of calcium is reabsorbed through the kidney. If calcium levels are high (controlled by parathyroid hormone), the chances of stone formation are higher.

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3
Q

Why do GI conditions such as Crohns lead to increased risk of stone formation?

A

Malabsorption such as increased absorption of oxalate causes hyperoxaluria, leading to the formation of oxalate stones.

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4
Q

Why do UTIs increase the risk of stone formation?

A

bacterial infections can make the conditions for stone formation more favourable by increasing the pHand depositing metabolites. This can cause (most frequently) struvite stones - stag horn/caluculi stones.

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5
Q

What are the risk factor of stone formation?

A
age 30-50.
male
hot climates (middle east).
previous stone(s).
family history of stones.
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6
Q

why is there an increased risk of developing a stone during pregnancy?

A

physiological hydronephrosis. Increased CO, leading to increased GFR. Rapid metabolic changes (making conditions more favourable).

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7
Q

How many patients with renal colic will have heamaturia?

A

85%

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8
Q

Symptoms of renal lithiasis?

A
\+++++colicky pain from loin to groin.
Cannot get comfortable.
haematuria.
acute renal failure.
Sepsis.
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9
Q

Examination findings of pt with renal lithiasis

A

Paucity.

Tender loin/lower quadrants.

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10
Q

Investigations for renal obstruction.

A
Dip test (blood/pH/leukocytes).
Urine for microscopy and culture.
Blood tests (U&E/inflamm markers/FBC/Ca)
Abdomen X-ray.
CT (gold standard).
IV Urogram.
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11
Q

Initial drugs given for management of pt with stones

A

NSAID.
poss Desmopressin
poss alpha blockers

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12
Q

What positive effect do NSAIDs have for renal stones?

A

analgesia, and inhibits GFR by reducing prostaglandins which normally dilate arterioles in glomerulus.

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13
Q

What does desmopressin do?

A

inhibits urine output

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14
Q

why may alpha blockers be used to manage renal lithiasis

A

they inhibit the contraction of the internal sphincter of the bladder and therefore encourage the passing of water.

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15
Q

If there is no sign of obstruction on a CT, and there is no pain. What is the next step?

A

Send home with a review in 4/52.

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16
Q

If there is an obstruction on CT, but no signs of infection, what is the next step?

A

Admit - will the stone pass?

17
Q

If there is an obstructed infected kidney, what is the next step.

A

Admit. Penicillin and gentamicin.

Urgent nephrostomy/stent.

18
Q

What is ESWL?

A

Extra Corporeal Shockwave Lithoscopy.

Vert effective.

19
Q

When would PCN be used?

A

Per Cutaneous Nephrolithotomy.

Used to remove pelvic/staghorn stones.

20
Q

When would uteroscopy be used?

A

When the blockage is distal to the kidney.

21
Q

What is the next step with a well patient after the sone has been removed?

A

Analyse the stone and urine to see what type it is and suggest pathology. Refer to clinic if there is an increased chance of reoccurrence.

22
Q

What investigation could be done to show the anatomical and functional health of the kidneys after a stone has been removed.

A

Radioisotope renography. Injections of (e.g.) MAG3 or DTPA are given, which are then excreted. Excretion is quantifiable.

23
Q

Where is a kidney stone most likely to obstruct?

A

Pelvi-uteric junction.
ureter at the common iliac crossing.
vesicle-ureteric junction (entrance to bladder).

24
Q

How much of the cardiac output goes to the kidneys?

A

25% (1.5l/min)

25
normal GFR
100ml/min. Most is reabsorbed.
26
What is eGFR based on?
Serum creatinine. Age. Sex. Ethnicity.
27
What hormaones control GFR?
ADH. Aldosterone. Renin.
28
what does aNVH and sNVH stand for?
asymptomatic and symptomatic Non Visible Haematuria.
29
Which patients with haematuria should be referred?
All with VH and sNVH. Over 40 with aNVH. Under 40 with aNVH plus abnormal eGFR/BP.
30
next step with any VH?
urgent suspect cancer. (24% of VH is bladder cancer).
31
What happens in renal failure wrt K? How is it treated?
unable to clear K - hyperkalaemia - metabolic acidosis - K into serum - cardiac issues. Dextrose and insulin encourages K back into cells.
32
What is reflux nephropathy?
failure of valve at vesicle-ureteric junction to form in utero. Reflux of urine into kidney in utero - failure of kidney to develop properly. Kidney failure presents at about 17 years old. More in females.
33
What causes the detrusor to contract for micturition?
PELVIC NERVE, ACh on M3 receptor
34
What causes relaxation of the detrusor to allow the bladder to fill?
HYPOGASTRIC NERVE , NA on beta 3 receptor
35
What causes the internal urethral sphincter to contract?
HYPOGASTRIC NERVE, NA on alpha1 receptor
36
What causes the external urethral sphincter to contract?
SOMATIC PUDENDAL NERVE, ACh in NICOTINIC receptor.
37
What allows the bladder to fill?
Hypogastric nerve (SNS) stimulated - NA onto B3 receptor to relax detrusor, and NA onto alpha1 receptor to contract internal sphincter.
38
What causes bladder to empty?
Hypogastric nerve relaxes (internal sphincter relaxes). PELVIC NERVE stimulated - ACh onto M3 receptor to contract detrusor.
39
What conscious control do you have over micturition?
PUDENDAL NERVE is somatic. When stimulated it releases ACh onto nicotinic receptor to contract the external sphincter and prevent micturition.