Pharmacology 3

Question 1

Are osmotic diuretics membrane permeable? And where is their major site of action?

Answer 1

They are membrane IMPERMEABLE = given IV

Major site of action is the proximal tubule (because this is where most iso-osmotic reabsorption of water occurs_

Question 2

Mannitol

Answer 2

i.v. osmotic diuretic

Question 3

Hyperglycemia and the use of iodine-based radiocontrast dyes in imaging may also result in which type of diuresis?

Answer 3

Osmotic diuresis

Question 4

Acetazolamide

Answer 4

Carbonic anhydrase inhibitor

Question 5

Type of drug used in

• glaucoma and following eye surgery
• prophylaxis of altitude sickness
• some forms of infantile epilepsy

Answer 5

Carbonic anhydrase inhibitors

Question 6

Increase excretion of HCO3- with Na+, K+ and H2O – alkaline* diuresis and metabolic acidosis result

Answer 6

Carbonic anhydrase inhibitors

Question 7

Lack of vasopressin secretion from the posterior pituitar

Answer 7

Neurogenic diabetes insipidus

Question 8

Treatment for neurogenic diabetes insipidus?

Answer 8

Desmopressin

Question 9

Does desmopressin increase blood pressure?

Answer 9

No

Question 10

Ethanol and nicotine effects on vasopressin?

Answer 10

Ethanol inhibits secretion of vasopressin and nicotine enhances

Question 11

Inability of the nephron to respond to vasopressin?

Answer 11

Nephrogenic diabetes insipidus

-no current pharmacological treatment

Question 12

Nephrogenic diabetes insipidus inheritance?

Answer 12

X-linked recessive

Question 13

Drugs which inhibit vasopressin?

Answer 13

Lithium
Demeclocycline
Vaptana

Question 14

Canagliflozin, dpagliflozin and empaglifolzin

Answer 14

SGLT2 inhibtors

Question 15

Most common adverse effects of SGLT2 inhibitors?

Answer 15

Genital bacterial and fungal infections

Question 16

Treatment for acute urinary retention?

Answer 16

Immediately catheterise men and then offer alpha blocker before removing catheter

alpha blockers: alfuzosin, tamsulosin

Question 17

Often presents in patients with chronic bladder outflow obstruction in association with uraemia, oedema, CCF, hypertension

Answer 17

Post-obstructive diuresis

This happens because you have retained urea, sodium and water =need to be diluted on excretion and you also have a defect in the concentrating ability of the kidney

Question 18

Role of prostaglandins in obstruction

Answer 18

Ureter becomes blocked (e.g. by calculus) and then ureter releases prostaglandins in response

Question 19

After how many months would calculus need intervention?

Answer 19

If not passed in 1 month then likely to require intervention

Question 20

Treatment for infected hydronephrostomy?

Answer 20

Percutaneous nephrostomy

Question 21

Indications to treat calculus urgently?

Answer 21

Pain unrelieved
Pyrexia
Persistent nausea/vomitting
High-grade obstruction

Question 22

Treatment for clot retention?

Answer 22

3-way irrigating haematuria catheter

Question 23

Investigations for frank haematuria?

Answer 23

CT urogram and cystoscopy

Question 24

Torsion of spermatic cord presentation?

Answer 24

Usually sudden onset of pain, sometimes previous episodes of self limiting pain

Question 25

Act as competitive antagonists of vasopressin receptors?

Answer 25

Aquaretics

Vaptans

Question 26

These receptors mediate vasoconstriction

Answer 26

V1a

Question 27

These receptors mediate H20 reabsorption in collecting tubule by directing aquaporin 2 (AQP2)-containing vesicles to the apical membrane

Answer 27

V2

Question 28

Blockade of V2 receptors and the effect on water and Na+?

Answer 28

ade of V2 receptors causes excretion of water without accompanying Na+ and thus raises plasma Na+ concentration

Question 29

Tolvaptan use?

Answer 29

Used in SIADH to correct hyponatremia

Question 30

Where is SGLT1 expressed?

Answer 30

In the intestine (enterocytes) and the kidney

Question 31

Where is SGLT2 expressed?

Answer 31

Almost exclusively confined to the proximal tubule

Question 32

S1 vs S2 segment of proximal tubule and glucose reabsorption?

Answer 32

S1 segment –> 90% of glucose reabsorption

S2/S3 segment –> reabsorb up to 10% of filtered glucose, respectively

Question 33

Method of glucose reabsorption at apical membrane?

Answer 33

secondary active transport

Question 34

Reabsorption of glucose at basolateral membrane?

Answer 34

Facilitated diffusion

Question 35

Inhibition of SGLT2 results in glucosuria and this mimics which condition?

Answer 35

Familial renal glucosuria (FRG)

Question 36

Canagliflozin, dapagliflozin and empagliflozin are what type of drug?

Answer 36

SGLT2 inhibitors

Question 37

What are prostaglandins formed from?

Answer 37

Formed from fatty acid arachidonic acid (by the cyclo-oxygenase enzymes)

Question 38

Where is PGE2 made?

Answer 38

Medulla

Question 39

Where is PGI2 (prostacyclin) made?

Answer 39

Glomeruli

Question 40

Act as vasodilators, are natriuretic, and are synthesised in response to ischaemia, mechanical trauma, angiotenin II, ADH and bradykinin?

Answer 40

Prostaglandins

Question 41

Prostaglandins and afferent and efferent arteriole?

Answer 41

Vasodilator effect on AFFERENT arteriole

Vasoconstrictor effect on efferent arteriole (because releases renin that leads to increased levels of angiotensin II)

Question 42

Which type of drug may precipitate acute renal failure?

Answer 42

NSAIDS

Question 43

“triple whammy effect”

Answer 43

ACEI