Renal 2 Flashcards
What are the Urine & Blood findings in pyloric stenosis
Metabolic Alkalosis
Hypochloraemia, Hypokalaemia
Urine
pH High
Low urine Cl-
High urine K+ and sodium
Most common cause of fanconi syndrome
Cystinosis
Rx - cysteamine
What is Liddle’s Syndrome
Mutation in ENAC channel (gain of function)
Increased activity of ENac channel in CD which causes over reabsorption of Na and H20 , excretion potassium and hydrogen, and hence HTN, hypokalemia, metabolic acidosis
Aka pseudohyperaldosteronism
Where does the kidney Lie
retroperitoneal T12-L3
How much of the cardiac output does the kidney take
22%
Mechanism of action ADH
Synthesised by hypothalamus, released by posterior pituitary in response to Angiotensin II, hyperosmolality and hypotension
works to increase H20 permeability in cortical collection duct & DCT
binds to the V2 receptor which increases cAMP formation and stimulates the movement of aquaporins into luminal membrane for H20 reabsorption
What Does ANP do into Kidney
is triggered by hypertension (Atrial stretch)
Works to dilate afferent and constrict efferent arteriole which increases GFR and natriuresis
inhibits renin and aldosterone secretion
which inhibits sodium reabsorption and inhibits the action of ADH on kidney
Action of Endothelin & Prostaglandin on Kidney
Prostagandins:
- dilates afferent arteriole in response to low perfusion (which increases renal blood flow)
Endothelin
-vasconstrcitors
modulate vasomotor tone, cell proliferation and hormone production
- release are stimulated by angiotensin II (AII), antidiuretic hormone (ADH), thrombin, cytokines, reactive oxygen species, and shearing forces acting on the vascular endothelium.
- ET-1 release is inhibited by prostacyclin and atrial natriuretic peptide as well as by nitric oxide.
Actions
ET-1 has a number of other actions besides vasoconstriction and cardiac stimulation that can indirectly affect cardiovascular function. ET-1 stimulates aldosterone secretion, decreases renal blood flow and glomerular filtration rate, and releases atrial natriuretic peptide (ANP).
PTH affects on Kidney
Triggered release by hypocalcaemia
acts on DCT and LoH to increase Ca2+ reabsorption
inhibits PO4 reabsorption by proximal tubule and stimulates Mg reabsorption
acts on PCT to increase PO4 excretion and on ascending LoH to increase Ca2+ reabsorption
Functions of Glomerulus
1) Filtration
2) Renin production
3) EPO production
4) Vit D activation
Functions of Glomerulus
1) Filtration
2) Renin production
3) EPO production
4) Vit D activation
What is Glomerular Filtration barrier made off
1) Endothelial Cells
2) Glomerular Basement Membrane
- Type 4 collagen with 3 layers - lamina densa, lamina rara interna and externa
- GENEs = COL4A3,4 & 5
3) Podocytes
- foot processes with filtration slits
4) Mesangial cells
- supportive role (can contract and regulate pressure through capillary)
Important Channels in PCT
H+ & HCO3 exchanger via Carbonic Anhydrase
Active Reabsorption of most things
- 90-100% glucose & amino acids
70% Na+/K+/ Ca2+ and Mg2+
85% HCO3
Important Channels in Loop of Henle
Na+K+Cl2 (NKCC2)
frusemide works on this and one of the Batters defects
15-25% Na+/Cl-/K+ reabsorbed
Important Channels in DCT
NCC
Thiazides act on this
Gittleman syndrome
Collecting Duct Important Channels
EnAC
Aldosterone Receptor
Spiro - antagonises Aldo receptor
Amiloride antagonises ENac
Liddles Syndrome activates ENac
Pseudohypoaldosteronism inactivates Aldo receptor
Regulators of Sodium Homeostasis
Increase Sodium (Volume contraction, Low BP)
- Angiotensin 2 in PCT
- Aldosterone in CD
Noradrenaline in changing flow to kidney (slow it down for more reabsorption)
ADH for H20 reabsorption
Decrease Sodium ( High salt diet and high BP)
- ANP - suppresses renin
Potassium homeostasis
increased secretion
- due to increased aldosterone
increased flow and Na+ delivery to CD
K+ inhibited by acidosis
Calcium Homeostasis in Kidney
Monitored at each section of Kidney
Most is reabsorbed
Increased reabsorption
- PTH release
- Vitamin D
Calcitonin
Thiazide diuretics
Low BP/ hypovolaemia
metabolic alkalosis
Decreased Reabsorption
- Metabolic acidosis
Frusemide
volume expansion
increased sodium intake
Phosphate Homeostasis in the Kidney
most is reabsorbed however there is a Threshold and hence if that is overwhelmed excess will be excreted
Increased Reabsorption
- GH
volume contraction
dietary restriction
Decreased Reabsorption
PTH
Volume expansion
What is Plasma Osmolality equation
2 x Na + Glucose & Urea (normally 270-290)
Voiding Control mechanisms
Sympathetic Nervous System (T10-11) inhibits urination - supplied by the hypogastric nerve
- Noradrenaline Alpha Receptors
- contraction of bladder neck and posterior urethra
- Noradrenaline Beta Receptors
- Relaxation of bladder fundus
Parasympathetic NS (S2-S4) facilitates urination
-ACh inhibits SNS
filling activates mechanoreceptors
ascending signal is sent to pontine micturition centre which sends signals via pelvic splanchnic nerves to inhibit SNS and cause detrusor muscle contraction
MCUG
IDC to place contrast into bladder & then Lateral and AP films
used to look for VUR, urethral pathology (PUV), ureteric dilatation
DMSA
Used to look for renal scarring
can also provide differential renal function information
ectopic renal tissue and non functioning kidney tissue
DTPA/MAG 3
Can differentiate between obstructive and non-obstructive causes of hydronephrosis
Can identify differences between the two kidneys
Given IV frusemide midway and time to excrete is documented
