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Theme 3 - 104 > Formation of Urine (L3+4) > Flashcards

Formation of Urine (L3+4) Flashcards

1
Q

What is glomerular filtration rate (GFR)?

A

The rate at which glomerular filtrate is produced. It can be used as an indicator

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2
Q

What small molecules get filtered in the glomerulus?

A
  • Electrolytes
  • Amino acids
  • Glucose
  • Some drugs
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3
Q

What large molecules remain in the blood and don’t get filtered at the glomerulus?

A
  • Red blood cells
  • Lipids
  • Proteins
  • Most drugs
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4
Q

What two factors can have an effect on glomerular filtration?

A
  • Renal blood flow

- Blood pressure

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5
Q

What is the sequence of what filtrate passes through during glomerular filtration?

A

1) Pores in the endothelium of the glomerular capillary
2) Basement membrane of the Bowman’s capsule
3) Epithelial cells of the Bowman’s capsule (podocytes) via filtration slits

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6
Q

What are the two theories of the auto regulation of renal blood flow (RBF)?

A
  • Caused by the stretching of renal arterioles (myogenic)

- Caused by renal metabolites which modulate the contracting/dilation of the afferent and efferent arterioles

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7
Q

What causes afferent arteries to constrict and dilate?

A
  • Constriction can be caused by noradrenalin, endothelin, adenosine and ADH
  • Dilation can be caused by prostaglandins, NO and dopamine
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8
Q

What caused efferent arterioles to constrict and dilate?

A
  • Constriction can be caused by angiotensin II

- Dilation can be caused by adenosine and NO

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9
Q

Where does glomerular filtrate enter?

A

Proximal tubule

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10
Q

Which small molecules get almost fully reabsorbed in the PT, and what is the driving force for this reabsorption?

A
  • Glucose and amino acids

- Driving force is Na+/K+ ATPase

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11
Q

Which ion enters the blood from the PT via facilitated diffusion?

A

Cl-

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12
Q

What are aquaporins (AQP)?

A

Specific water channels in cell membranes that offer a transcellular route for water movement.

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13
Q

What are the 4 main renal APQs?

A
  • AQP1 which is abundant in the proximal tubule
  • AQP2 which is controlled by ADH and present on the apical surface of the collecting duct
  • AQP3/4 which is in the basolateral surface of the collecting duct
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14
Q

How does glucose enter the blood from the PT?

A

By co-transport with Na+ via glucose transporters

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15
Q

How does glucose from the filtrate enter the PT?

A

Via sodium-glucose transporters (SGLTs) which also transport Na+ into the PT.

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16
Q

What are the two types of SGLT?

A
  • SGLT1: High affinity but low capacity

- SGLT2: Low affinity but high capacity

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17
Q

What are SGLT2 inhibitors?

A

These are drugs that inhibit SGLT2, leading to less glucose being reabsorbed into the blood (hypoglycaemic effect). Therefore, it could be used to treat type II diabetes.

18
Q

Examples of SGLT2 inhibitors?

A
  • Dapagliflozin
  • Canagliflozin
  • Empagliflozin

(All end in gliflozin)

19
Q

How are proteins reabsorbed from the PT?

A
  • First get broken down into amino acids by lysosomes

- Then enter the blood

20
Q

What is the role of specialised pumps in the PT?

A

To transport substances and drugs into the nephron that may not be able to enter normally due to their size or protein binding

21
Q

What are the two stages of reabsorption in the loop of Henle (LOH)?

A

1) Extraction of water in the descending limb

2) Extraction of Na+ and Cl- in the ascending limb

22
Q

Why is reabsorption more important in juxtamedullary nephrons than cortical nephrons?

A

Because they have longer loops of Henle

23
Q

What are the differences between the thin descending limb and thick ascending limb?

A
  • Thin descending limb is permeable to water via AQP1 whereas the thick descending limb is impermeable to water
  • No active transport of salts in thin ascending limb but active transport occurs in thick ascending limb via NKCC2 co-transporters
24
Q

What is the NKCC2 co-transporter?

A

Transports Na+, K+ and 2Cl- from the tubular fluid so that they can. then be absorbed into the blood.

25
Q

What is countercurrent multiplication?

A

The creation of a large osmotic gradient, via NKCC2 in the thin ascending loop, so that passive reabsorption can occur. Urea also plays a part in it.

26
Q

What are principal cells?

A

Specialised cells that exchange Na+ for K+ in the late DT and early collecting duct.

27
Q

What are principal cells sensitive to?

A

Aldosterone - which increases Na+ reabsorption and so increases blood pressure because water follows it into the blood.

28
Q

What are intercalated cells?

A
  • Specialised cells that exchange Na+ for H+ in the DT and early collecting duct
  • They are involved in acid-base regulation
29
Q

What are the 2 types of intercalated cells?

A

alpha and beta

30
Q

What do alpha intercalated cells do?

A
  • Secrete H+ via H+/Na+ATPase or H+/K+ATPase

- Reabsorb HCO3-

31
Q

What do beta intercalated cells do?

A
  • Reabsorb H+

- Secrete HCO3- via Pendrin (anion exchanger)

32
Q

What is the permeability of the collecting duct to water?

A
  • The collecting duct is impermeable to water

- ADH can increase its permeability to water

33
Q

What does ADH stand for?

A

Anti Diuretic Hormone

34
Q

How does ADH increase water uptake in the DT and collecting duct?

A

Acts on vasopressin 2 receptors on the basal membrane of principal cells, leading to the activation of AQP2 water channels

35
Q

Where is ADH stored and released from?

A

Pituitary glands

36
Q

What is diabetes insipidus?

A

A lack of ADH, meaning the urine is very dilute.

37
Q

What is nephrogenic diabetes insipidus?

A
  • The inability of the kidney to respond to ADH normally

- It can be treated by Chloritalidone (diuretic) and Indometacin (anti-inflammatory)

38
Q

What is neurogenic diabetes insipidus?

A
  • Lack of ADH production by the brain

- Can be treated by Desmopressin, Vasopressin and Carbamezapine

39
Q

Where is ADH synthesised?

A

Hypothalamus

40
Q

What increase ADH release?

A
  • Nicotine
  • Ether
  • Morphine
  • Barbiturates
41
Q

What inhibits ADH release?

A

Alcohol

Theme 3 - 104 (3 decks)

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