The kidney Flashcards

1
Q

Describe the anatomical position of the kidneys.

A
  • 3 vertebrae in length
  • Retroperitoneal
  • T12 to L3
  • Right kidney lower than left
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2
Q

Briefly describe arterial supply to the kidneys.

A

Via the renal arteries which arise from abdominal aorta, distal to superior mesenteric artery. The right renal artery is longer.

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3
Q

Briefly describe the venous drainage of the kidneys.

A

Via renal veins which empty into the inferior vena cava.

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4
Q

Briefly describe lymphatic drainage of the kidneys.

A

Lymph node drainage to para-aortic lymph nodes (aka. lateral aortic)

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5
Q

1) Where does ultrafiltration occur in the kidney?

2) Where does reabsorption occur in the kidney?

A

1) Renal corpuscle (glomerulus and Bowman’s capsule)

2) Nephrons (renal tubules).

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6
Q

Name the 7 main functions of the kidney.

A

1) excretion of waste products.
2) fluid and electrolyte balance.
3) acid-base balance.
4) control of BP
5) production of EPO
6) vitamin D synthesis
7) gluconeogenesis in times of starvation

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7
Q

1) What cells does the juxtaglomerular apparatus consist of?

2) What is the function the juxtaglomerular apparatus?

A

1) Macula dense cells, extraglomerular mesangial cells and juxtaglomerular cells.
2) Helps to regulate BP and GFR.

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8
Q

Generally, what is the function of macula densa cells?

A

Detect low sodium and low chloride so can detect hypovolaemia and hypotension. They then send signals to the juxtaglomerular cells.

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9
Q

What is the action of macula densa cells in the event of hypernatraemia?

A

They trigger the contraction of the afferent arteriole, reducing glomerular blood flow and GFR.

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10
Q

What is thought to be the function of extraglomerula mesangial cells?

A

They are thought to help with signalling between macula densa cells and juxtaglomerular cells.

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11
Q

What does intraglomerular mesangial cells do?

A

Aid neutrophils in phagocytosis of mesangial cells undergoing apoptosis and other debris.

They also remove trapped residues and aggregated protein from the basement membrane thus keeping the filter free of debris.

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12
Q

What is the function of the juxtaglomerular cells?

A

Receive a signal from macula densa cells and also detect hypotension themselves. They then secrete renin. This up regulates the RAAS, increasing sodium and water reabsorption, which increases BP.

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13
Q

What are podocytes?

A

Specialised cells which wrap around the basement membrane. Gaps between podocytes are filtration slits which only allow H2O, glucose and ionic salts to pass through.

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14
Q

Describe the 3 components of the glomeruli filtration system.

A

1) Capillary endothelium: has fenestrae.
2) Basement membrane: consists mainly of type IV collagen, heparin sulphate proteoglycans and lamina.
3) Epithelial cells (podocytes): form the visceral layer of the capsule. Foot projections from podocytes interdigitate to form filtration slits. Filtration slits are bridge by the slit diaphragm which has pores.

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15
Q

How does the capillary endothelium filter blood?

A

Fenestrae do not restrict movement of water, proteins or large molecules but limit filtration of cellular components such as RBCs.

The glycocalyx has negatively charged glycosaminoglycans surrounding the luminal surface. This hinders diffusion of negative molecules.

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16
Q

How does the basement membrane assist in blood filtration?

A

Heparan sulphate proteoglycans restrict movement of negatively charged molecules. Also prevents filtration of intermediate to large molecules.

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17
Q

How do podocytes help to filter blood?

A

Pores in the slit diaphragm prevent large molecules from crossing. Negatively charged proteins restrict filtration of large anions.

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18
Q

Why can albumin not be filtered?

A

Because it is negatively charged.

19
Q

Give the reason for minimal change disease causing nephrotic syndrome.

A

Proteinuria occurs because of effacement of the podocyte foot processes, causing the widening of filtration slits.

20
Q

What 2 factors can cause the adrenal cortex to release aldosterone?

A

Angiotensin II presence and increased potassium in extracellular fluid.

21
Q

1) Actions of angiotensin II are mainly exerted through which receptors?
2) What are the main functions of angiotensin II?

A

1) AT1 receptors.
2) Release of aldosterone from adrenal cortex, vasoconstriction of arterioles (greater effect in efferent arteriole). and increases ADH production.

22
Q

What are the 3 main functions of aldosterone?

A

1) Works on principal cells of collecting ducts, causing an increase in reabsorption of water and sodium.
2) Increases activity of Na+/K+ ATPase to increase release of Na+ from cells where it has been reabsorbed into.
3) Increases expression of apical ENaC and K+ channels

23
Q

Define GFR.

A

The volume of fluid that filters into the Bowman’s capsule per unit of time. Normal GFR is 100-120mL per minute.

24
Q

1) An increase in afferent arteriole resistance causes what?
2) An increase in efferent arteriole resistance causes what?
3) A decrease in afferent arteriole resistance causes what?

A

1) decreased GFR.
2) increased GFR.
3) increased GFR.

25
Q

2) Describe the function of angiotensin II on the following:

a) arterioles
b) kidneys
c) sympathetic nervous system
d) adrenal cortex
e) hypothalamus
f) mesangial cells

A

a) vasoconstriction (all arterioles. vasoconstriction happens in both afferent and efferent arterioles but is greater in the efferent).
b) Na+ reabsorption in PCT.
c) noradrenaline release.
d) aldosterone release.
e) ADH released from posterior pituitary.
f) mesangial cell contraction causing decreased filtration area.

26
Q

Acute tubular necrosis mainly affects which cells?

A

Simple cuboidal epithelial cells in the PCT.

27
Q

1) Where does 70-80% reabsorption of bicarbonate happen?
2) What 2 types of cells in the DCT help to maintain acid-base balance?
3) When are type A intercalated cells active?
4) When are type B intercalated cells active?

A

1) PCT.
2) Type A and type B intercalated cells.
3) When the body is in a state of academia (secrete more H+ into urine).
4) When the body is in a state of alkal emia (secrete more H+ into capillaries).

28
Q

Name 3 factors which may increase the potential for drug toxicity.

A
  • reduced GFR
  • reduced drug clearance
  • longer half life of drugs
  • increased bioavailability due to reduced pre-systemic elimination.
  • hypoalbuminaemia
  • reduced non-renal clearance due to reduced activity of CYP450 enzymes.
29
Q

1) When there is an increased potential for drug toxicity, what action may need to be taken?
2) How does hypoalbuminaemia cause accumulation of endogenous substances?

A

1) Smaller drug doses may be needed as toxic levels may occur at normal dosage.
2) Hypoalbuminaemia causes accumulation of endogenous substances that competitively displace acidic drugs from their albumin binding sites.

30
Q

What is obstructive nephropathy?

A

Kidney impairment occurring secondary to functional or anatomical obstructive uropathy. It is an interruption of urine flow by a blockage or narrowing of some part of the urinary tract.

31
Q

Name 4 common causes of obstructive uropathy,

A

Renal calculi
BPH
Prostate cancer
Bladder tumours.

32
Q

1) What is unilateral obstructive nephropathy normally caused by?
2) What is bilateral obstructive nephropathy normally caused by?
3) What can obstructive nephropathy lead to?

A

1) Renal calculi.
2) BPH.
3) The conditions causing obstructive nephropathy prevent the normal flow of urine, causing back pressure and then hydronephrosis.

33
Q

Describe the cascade of consequences which can occur as a result or hydronephrosis.

A

Reduced renal blood flow > decreased GFR > ischaemia > upregulation of RAAS.

34
Q

1) What can hydronephrosis lead to with regards to renal tubules and interstitial tissues?
2) What causes a decrease in GFR in hydronephrosis?
3) What else does high pressure in renal tubules cause?

A

1) Atrophy and apoptosis of renal tubules and interstitial tissue fibrosis due to macrophage infiltration.
2) Backflow of urine = increased pressure in renal tubules = decrease in glomerular pressure gradient = decreased GFR.
3) Increased reabsorption of sodium, water and urea, leading to azotemia, hypernatraemia, decreased urinary sodium and a low FeNa.

35
Q

Give 3 potential symptoms of obstructive nephropathy.

A
  • Unilateral flank pain
  • Increased frequency, increased urgency, post-terminal dribbling, incomplete emptying
  • Distended abdomen/ palpable bladder
  • Enlarged or nodular prostate
  • Anuria, polyuria, nocturne.
36
Q

Describe the electrolyte imbalances commonly seen in patients with an AKI.

A
Hyponatraemia
Hyperkalaemia
Hypermagnesaemia
Hypocalcaemia
Hyperphosphataemia.
37
Q

What causes Hyperkalaemia in patients with an AKI?

A

Decreased GFR
Less sodium filtered into tubules
Less activation of Na+/K+ co-transporters in DCT
Less K+ secretion.

38
Q

What causes metabolic acidosis in patients with an AKI?

A

High serum potassium level
Activation of K+/K+ transporters
Increased release of protons into blood
Metabolic acidosis

39
Q

Describe the change in amylase levels in patients with an AKI.

A

There is a marked elevation in serum amylase when creatinine clearance falls below a certain level.

** In renal failure there is an increase in S-type and P-type iso-amylases.

40
Q

In patients with an AKI, what normally happens to urea and creatinine?

A

Usually BUN:Cr is >20:1, especially in conditions that enhance reabsorption of of urea such as prerenal causes of AKI.

41
Q

What happens to urea and creatinine in patients with interstitial nephritis?

A

BUN:Cr is normally <15:1 because the damage affects tubular reabsorption and secretion, so urea cannot be reabsorbed alongside Na.

42
Q

1) What is urine osmolarity determined by?
2) What is meant by a high urine osmolarity?
3) Describe osmolarity in a patient with a prerenal AKI.
4) Describe osmolarity in patients with acute tubular necrosis/

A

1) The concentration of solutes and electrolytes in urine.
2) There is a high concentration of electrolytes and particles suspended in the urine.
3) There is a low urinary sodium, so low urinary water and so a high osmolarity as the urine is concentrated.
4) There is high urinary sodium due to impairment of tubular reabsorption and secretion, causing a low urine osmolarity <500.

43
Q

How is fraction of excreted sodium calculated?

A

Calculated by the fraction of sodium filtered in the glomerulus compared to the fraction of sodium excreted in the urine.

44
Q

1) When will FeNa be <1%?
2) What does a low FeNa mean?
3) When might FeNa be >1%

A

1) In prerenal AKI or contrast induced nephropathy.
2) That there is sodium retention by the kidneys.
3) In intrinsic AKI such as ATN where N sodium is lost due to tubular damage (there is sodium wasting).