Formation of Urine (L3+4) Flashcards Preview

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Flashcards in Formation of Urine (L3+4) Deck (41):
1

What is glomerular filtration rate (GFR)?

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

2

What small molecules get filtered in the glomerulus?

- Electrolytes
- Amino acids
- Glucose
- Some drugs

3

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

- Red blood cells
- Lipids
- Proteins
- Most drugs

4

What two factors can have an effect on glomerular filtration?

- Renal blood flow
- Blood pressure

5

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

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

6

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

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

7

What causes afferent arteries to constrict and dilate?

- Constriction can be caused by noradrenalin, endothelin, adenosine and ADH
- Dilation can be caused by prostaglandins, NO and dopamine

8

What caused efferent arterioles to constrict and dilate?

- Constriction can be caused by angiotensin II
- Dilation can be caused by adenosine and NO

9

Where does glomerular filtrate enter?

Proximal tubule

10

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

- Glucose and amino acids
- Driving force is Na+/K+ ATPase

11

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

Cl-

12

What are aquaporins (AQP)?

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

13

What are the 4 main renal APQs?

- 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

14

How does glucose enter the blood from the PT?

By co-transport with Na+ via glucose transporters

15

How does glucose from the filtrate enter the PT?

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

16

What are the two types of SGLT?

- SGLT1: High affinity but low capacity
- SGLT2: Low affinity but high capacity

17

What are SGLT2 inhibitors?

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

Examples of SGLT2 inhibitors?

- Dapagliflozin
- Canagliflozin
- Empagliflozin

(All end in gliflozin)

19

How are proteins reabsorbed from the PT?

- First get broken down into amino acids by lysosomes
- Then enter the blood

20

What is the role of specialised pumps in the PT?

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

21

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

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

22

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

Because they have longer loops of Henle

23

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

- 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

What is the NKCC2 co-transporter?

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

25

What is countercurrent multiplication?

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

What are principal cells?

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

27

What are principal cells sensitive to?

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

28

What are intercalated cells?

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

29

What are the 2 types of intercalated cells?

alpha and beta

30

What do alpha intercalated cells do?

- Secrete H+ via H+/Na+ATPase or H+/K+ATPase
- Reabsorb HCO3-

31

What do beta intercalated cells do?

- Reabsorb H+
- Secrete HCO3- via Pendrin (anion exchanger)

32

What is the permeability of the collecting duct to water?

- The collecting duct is impermeable to water
- ADH can increase its permeability to water

33

What does ADH stand for?

Anti Diuretic Hormone

34

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

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

35

Where is ADH stored and released from?

Pituitary glands

36

What is diabetes insipidus?

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

37

What is nephrogenic diabetes insipidus?

- The inability of the kidney to respond to ADH normally
- It can be treated by Chloritalidone (diuretic) and Indometacin (anti-inflammatory)

38

What is neurogenic diabetes insipidus?

- Lack of ADH production by the brain
- Can be treated by Desmopressin, Vasopressin and Carbamezapine

39

Where is ADH synthesised?

Hypothalamus

40

What increase ADH release?

- Nicotine
- Ether
- Morphine
- Barbiturates

41

What inhibits ADH release?

Alcohol