Renal system Flashcards

1
Q

S2, S3, and S4

A

Sensory afferents travel from the bladder (cholinergic parasympathetic), cause contraction of the bladder and relaxation of the internal sphincter.

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2
Q

Nephrons

A

About a million nephrons in each kidney.
Each nephron consists of - bowmans capsule (in the cotex), a proximal convuluted tubule (PCT- in the cortex), loop of henle (in the medulla), and a distal convoluted tubule (DCT - in the cortex, forms the collecting ducts which empty into the pelvis).
The loop of henle has an ascending limb and a descending limb.

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3
Q

Blood supply

A

The blood supply comes from the abdominal aorta and enters the kidney via the renal artery. This divides to form arterioles, one arteriole enters each bowmans capsule. The glomerulous is a small capillary bed inside the bowmans capsule. Normally capillary endothelial cells are tight but in the kidney they arevfenestrated and act as a seive alongside potocytes.
There is no leaving venule from the glomerulous, instead another arteriole (efferent arteriole). A second capillary bed (peritubular capillaries) is wrapped around the PCT. Both of these converge into a venule and small veins, eventually the renal vein which becomes the vena cava.

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4
Q

PCT structure

A

Lined with highly specialised columnar cells which has mircovilli on their luminal surface and basal infoldings on the basal surface. Very tichtly joined hy zona occludens at the apical membrane, full of mitochondria.

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5
Q

Bowmans capsule

A

Enetering BP is 45mmHg.
Filtration occurs due to high hydrostatic pressure (no absorption).
Filtration rate of 125ml/min in each kidney.
This is ultrafiltrate, containing everything from plasma except plasma protein,140mM sodium, 5mM glucose.
Urine flow is 1ml/min therefore reabsoption of 124ml/minute in the kidney.

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6
Q

What happens in the PCT?

A

On the basolateral membrane there is a sodium potassium pump, this extrudes sodium and is not limited by external potassium as potassium recycles throughpotassium channels. This causes a net accumulation of sodium in the intercellular cleft. Chloride ions are also expelled into the intercellular cleft causing electroneutrality.
H2O travels through cells into intercellular cleft through aquaporins forming 150mM sodium chloride solution. This process is kept going by the peritubular capillaries that sweep away the solution (adequate blood flow is necessary). This process is known as the standing gradient mechanism.
Lowninternal sodium is countered by a sodium transporter that pumps sodium and glucose into cells. This is driven by the sodium gradient. The glucose is transported into the peritubular capillaries by a glucose transporter, no sodium involved. The same occurs for amino acids.

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7
Q

Micturition

A

Peristaltic waves propel urine along ureters into the bladder.
This is necessary as ureters enter the base of the bladder obliquely so reflux is prevented by the compressed entrance.
Fullness of the bladder is first detected at 100ml, desire to micturate at 400ml, pain at 700ml (L1-4 afferents).
Some reabsorption of fluid and electrolyte occurs across the wall of the bladder which is lined by transitional epithelium.
Nervi erigentes (pelvic splanchnic nerves) - causes detrusor muscle of bladder wall to contract and internal sphincter to relax.

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8
Q

ADH

A

Polyurea if lesions are present on the Supraoptic nucleas or supraopticolypophysical tract.
Normal function is still possible if medial eminence is intact.
ADH is transported by axoplasmic flow into nerve terminals from which it is released into capillary bed.
Carried attached to neurophysin.
Released in response to hypertonic blood and decreased plasma volume.

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9
Q

Aldosterone

A

Synthesieed and released from the zona glomerulosa of the adrenal cortex.
Deficiency (addisons syndrome) leads to natriuresis and circulatory collapse.
Excess (Cushing’s) leads to kaliuresis, sodium retention and hypertension.
3 mechanisms of control -
1. ACTH negative feedback
2. Renin-angiotensin system
3. Increased potassium plasma concentration leading to release of aldosterone.

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10
Q

Control of renin

A

Inhibited by increased intracellular calcium.
Increased release on reduction of diameter in afferent artioles, activation of the sympathetic nervous system or reduced dietary sodium intake.

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11
Q

Atrial natriuretic hormone - ANH

A

Released from myocytes of the atria in response to increased plasma volume, also released from the supraoptic nucleas.
Actions -
Inhibits sodium reabsoption in the PCT
Increases renal blood flow
Inhibits ADH release and action.
Inhibits aldosterone release - both directly and indirectly (by the inhibition of renin release).

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12
Q

Urodilatin

A

Renal counterpart of ANH
Released j. Response to increased blood pressure and blood volume.
Inhibits sodium absorption from the meduallary collecting duct.
Acts locally within the kidney, does not appear in systemic circulation.

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13
Q

Calcitonin

A

Activates same pool of cAMP as ADH.

Increases water permeability of collecting duct.

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14
Q

Parathyroid hormone

A

Increases calcium reabsorption in ascending limb, DCT and cortical collecting duct.
Decreases phosphate reabsorption in the PCT.

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15
Q

Glucocorticoids

A

Increases acidity of lumen of PCT by stimulation of sodium hydrogen exchanger.

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16
Q

Thyroid hormones

A

Modulates PCT sodium/Potassium ATPase.

Increases number of ATPases present in the basolateral membrane.