Renal 2 Flashcards

1
Q

What are the Urine & Blood findings in pyloric stenosis

A

Metabolic Alkalosis
Hypochloraemia, Hypokalaemia
Urine
pH High
Low urine Cl-
High urine K+ and sodium

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2
Q

Most common cause of fanconi syndrome

A

Cystinosis
Rx - cysteamine

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3
Q

What is Liddle’s Syndrome

A

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

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4
Q

Where does the kidney Lie

A

retroperitoneal T12-L3

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5
Q

How much of the cardiac output does the kidney take

A

22%

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6
Q

Mechanism of action ADH

A

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

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7
Q

What Does ANP do into Kidney

A

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

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8
Q

Action of Endothelin & Prostaglandin on Kidney

A

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).

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9
Q

PTH affects on Kidney

A

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

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10
Q

Functions of Glomerulus

A

1) Filtration
2) Renin production
3) EPO production
4) Vit D activation

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10
Q

Functions of Glomerulus

A

1) Filtration
2) Renin production
3) EPO production
4) Vit D activation

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11
Q

What is Glomerular Filtration barrier made off

A

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)

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12
Q

Important Channels in PCT

A

H+ & HCO3 exchanger via Carbonic Anhydrase
Active Reabsorption of most things
- 90-100% glucose & amino acids
70% Na+/K+/ Ca2+ and Mg2+
85% HCO3

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13
Q

Important Channels in Loop of Henle

A

Na+K+Cl2 (NKCC2)
frusemide works on this and one of the Batters defects
15-25% Na+/Cl-/K+ reabsorbed

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14
Q

Important Channels in DCT

A

NCC
Thiazides act on this
Gittleman syndrome

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15
Q

Collecting Duct Important Channels

A

EnAC
Aldosterone Receptor

Spiro - antagonises Aldo receptor
Amiloride antagonises ENac
Liddles Syndrome activates ENac
Pseudohypoaldosteronism inactivates Aldo receptor

16
Q

Regulators of Sodium Homeostasis

A

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

17
Q

Potassium homeostasis

A

increased secretion
- due to increased aldosterone
increased flow and Na+ delivery to CD
K+ inhibited by acidosis

18
Q

Calcium Homeostasis in Kidney

A

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

19
Q

Phosphate Homeostasis in the Kidney

A

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

20
Q

What is Plasma Osmolality equation

A

2 x Na + Glucose & Urea (normally 270-290)

21
Q

Voiding Control mechanisms

A

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

22
Q

MCUG

A

IDC to place contrast into bladder & then Lateral and AP films
used to look for VUR, urethral pathology (PUV), ureteric dilatation

23
Q

DMSA

A

Used to look for renal scarring
can also provide differential renal function information
ectopic renal tissue and non functioning kidney tissue

24
Q

DTPA/MAG 3

A

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