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Year 2 - Renal (DP) > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

How do diuretics increase urine flow?

A

Inhibit electrolyte reabsorption:

 - Mainly Na+ in nephron
           - > So reduced water reabsorption
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2
Q

What causes oedema?

A

Imbalance between:
- Rate of ISF formation
AND
- Rate of ISF absorption

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3
Q

What is ISF formation proportional to?

A 
(Pc - Pi) - (πp - πi)
Where:
     - Pc is capillary hydrostatic pressure
     - Pi is ISF hydrostatic pressure
     - πp is capillary oncotic pressure
     - πi is ISF oncotic pressure
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4
Q

What is the main constituent of πp?

A

Plasma proteins (Mainly albumin)

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5
Q

How does Nephrotic syndrome cause oedema?

A

Reduces πp

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6
Q

How does CHF cause oedema?

A

Increases Pc

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7
Q

How does hepatic cirrhosis cause ascites (intraperitoneal oedema)?

A

Reduced hepatic blood flow
-> Increased portal system pressure
-> Increased Pc -> Ascites
Reduced albumin production -> Decreased πp

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8
Q

How does increased ISF formation lead to further oedema?

A
  1. Blood volume and cardiac output reduced
  2. RAAS Activation (as there is renal hypoperfusion)
  3. Sodium and water retention
  4. Increased blood volume
  5. Increased Pc and further decreased πp
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9
Q

What sort of oedema does CHF cause?

A

Pulmonary (+/- peripheral)

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10
Q

What drugs block Na+ reabsorption in the PCT?

A

Carbonic anhydrase inhibitors

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11
Q

What drugs block Na+ reabsorption in the Loop of Henle?

A

Loop diuretics

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12
Q

What drugs block Na+ reabsorption in the DCT?

A

Thiazide diuretics

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13
Q

What drugs block Na+ reabsorption in the collecting duct?

A

Potassium-sparing diuretics

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14
Q

Where do most diuretics act, the apical membrane or the basolateral membrane?

A

Apical

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15
Q

What drugs are transported into the filtrate by Organic Anion Transporters (OATs)?

A

Acidic drugs:

 - Thiazides
 - Loop diuretics
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16
Q

What drugs are transported into the filtrate by Organic Cation Transporters (OATs)?

A

Basic drugs:

 - Triamterene
 - Amiloride
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17
Q

In regards to OATs, how do organic anions enter the cell at the basolateral membrane?

A

Diffusion

Exchange for α-ketoglutarate

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18
Q

How is the [α-ketoglutarate]i kept high?

A

Transported into cell via a Na+-dicarboxylate transporter:

- Na+ from Na+/K ATPase

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19
Q

How do organic anions enter the lumen at the apical membrane?

A

Via the Multidrug Resistant Protein 2 (MRP2)

And via OAT4 (in exchange for α-ketoglutarate)

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20
Q

Why do thiazides predispose to gout?

A

Uric acid competes with thiazides at MRP2:

- Increases [Uric acid]p -> Gout

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21
Q

How do organic cations move across the basolateral membrane?

A

Diffusion (if uncharged)
OR
Organic Cation Transporters

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22
Q

How do organic cations enter the lumen at the apical membrane?

A

Via MRP1
OR
Organic Cation+/H+ antiporters (OCTN)

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23
Q

What transporter do Loop diuretics block in the thick ascending loop of the Loop of Henle? How do they do this?

A

The Na+/K+/Cl- co-transporter:

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24
Q

Put the following steps of the pharmacophysiology of how loop diuretics work:

  • Filtrate is less dilute in thick ascending limb of Loop of Henle
  • Increased calcium and magnesium excretion
  • Reduced tonicity of medullary ISF
  • Diuretic binds to Cl- site on NKCC2
  • Increased Na+ load in DCT and CD
  • Potassium loss
A
  1. Diuretic binds to Cl- site on NKCC2 in TAL of Henle
  2. Reduced tonicity of medullary ISF
  3. Filtrate is less dilute in thick ascending limb of Loop of Henle
  4. Increased Na+ load in DCT and CD
  5. Potassium loss
  6. Increased calcium and magnesium excretion
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25
Q

What percentage of filtered Na+ is excreted on the use of IV loop diuretics?

A

15-25%

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26
Q

Loop diuretics have an indirect vasodilator action which makes them useful in pulmonary oedema. What are the possible mechanisms by how this works?

A

Increase levels of vasodilating prostaglandins?
Reduce response to Angiotensin II and NA?
Open K+ channels in resistance vessels?
-> Hyperpolarisation
-> Reduced Calcium influx -> Relaxation

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27
Q

Loop diuretics are strongly bound to plasma proteins, how does this affect their transport into the nephron lumen?

A

They rely heavily on OATs

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28
Q

True or false; Loop diuretics are poorly absorbed from the GI tract?

A

False

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29
Q

Which of the following is not a major use of loop diuretics:

  • Acute pulmonary oedema (IV)
  • CHF
  • Chronic kidney failure
  • Ankle oedema
  • Hepatic cirrhosis with ascites
  • Nephrotic syndrome
A

Ankle oedema

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30
Q

Why do loop diuretics have a reduced effect in nephrotic syndrome?

A

There is protein in the tubules so the diuretics bind to them

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31
Q

Which of the following is not an adverse effect of loop diuretics:

  • Hypokalaemia
  • Impaired glucose tolerance
  • Metabolic alkalosis
  • Hypovolaemia and Hypotension
  • Hypocalcaemia and Hypomagnesaemia
  • Hyperuricaemia
A

Impaired glucose tolerance

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32
Q

How can hypokalaemia be prevented when diuretics are used?

A

K+ supplement
OR
Add a K+-sparing diuretic

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33
Q

What drugs have increased toxicity when a patient is hypokalaemic?

A

Digoxin
Class III antidysrhythmic drugs:
- Amiodarone and Sotalol

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34
Q

How can diuretics cause metabolic alkalosis?

A

H+ secretion is increased in the collecting ducts

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35
Q

What do thiazide diuretics block?

A

Na+/Cl- co-transporter in the early DCT

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36
Q

What are the two best examples of thiazide diuretics?

A

Bendroflumethiazide

Hydrochlorothiazide

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37
Q

What are the two best examples of thiazide-like diuretics?

A

Metolazone

Indapamide

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38
Q

Put the following steps of the pharmacophysiology of how thiazide diuretics work:

  • Prevent dilution in early DCT
  • Increased Na+ load in late DCT
  • Increased calcium reabsorption
  • Inhibit Na+/Cl- carrier by binding to Cl- site
  • Potassium loss
A
  1. Inhibit Na+/Cl- carrier by binding to Cl- site
  2. Prevent dilution in early DCT
  3. Increased Na+ load in late DCT
  4. Potassium loss
  5. Increased calcium reabsorption
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39
Q

What percentage of filtered Na+ do thiazides cause to be excreted?

A

~5%

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40
Q

How do thiazide diuretics enter the PCT?

A

Via OATs

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41
Q

Which of the following is not a use for thiazide diuretics:

  • Hypertension
  • Mild CHF
  • Nephrolithiasis
  • Chronic hepatitis
  • Nephrogenic Diabetes Insipidus
  • Severe pulmonary oedema
A

Chronic hepatitis

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42
Q

True or false; Thiazide diuretics can cause erectile dysfunction?

A

True

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43
Q

True of false; Thiazide diuretics do not affect glucose tolerance?

A

Fale - They impair it

44
Q

What does aldosterone do in the late DCT and collecting duct?

A

Increases the synthesis of Na+/K+ ATPase via increased gene transcription
Increases the synthesis of a protein that activates Epithelial Na+ Channel on the apical membrane:
- Makes them open more frequently
These result in Na+ and water retention and K+ excretion

45
Q

How does ADH work in the collecting ducts?

A

Acts via GPCRs to increase the number of aquaporins to allow more water reabsorption

46
Q

What channels excrete K+ into the lumen at the apical membrane?

A

Renal outer medullary K+ channels (ROMK)

47
Q

What causes the lumen to become more negative?

A

Increased Na+ reabsorption:

 - Depolarizes basolateral vs apical membrane
           - > As Cl- reabsorption
48
Q

As the lumen becomes more negative, how is this corrected?

A

Increased K+ driving force:

 - Increased K+ secretion to balance charge
           - > H+ secretion also increased
49
Q

How do Amiloride and Triamterene work?

A

Block apical ENaC:

 - Reduces Na+ reabsorption
 - Lumen is less negative
 - Reduced K+ secretion
           - > As charge doesn't need balanced
50
Q

How do Spironolactone and Eplerenone work?

A

Compete with intracellular aldosterone receptors:

 - Reduces ENaC activating protein synthesis
 - Reduces Na+/K+ ATPase synthesis
           - > Both cause reduced K+ excretion
51
Q

What is spironolactone metabolised to that has the most diuretice action?

52
Q

How do spironolactone and eplerenone gain access to the cells of the DCT and collecting duct?

A

Via basolateral membrane:

- They are lipophilic

53
Q

What is the GI absorption like for Triamterene and Amiloride?

A

Triamterene -> Good

Amiloride -> Poor

54
Q

When are aldostereone antagonists indicated?

A

CHF
Conn’s
Resistant hypertension
Secondary hyperaldosteronism (in hepatic cirrhosis)

55
Q

What type of diuretic is Mannitol?

A

An osmotic diuretic

56
Q

What is the structure of Mannitol?

A

A membrane impermeant polyhydric alcohol

57
Q

True or false, osmotic diuretics are pharmacologically inert?

58
Q

How does Mannitol enter the nephron?

A

By glomerular filtration

59
Q

Are osmotic diuretics reabsorbed?

60
Q

How do osmotic diuretics work?

A

Increase filtrate osmolarity which results in the opposition of water reabsorption

61
Q

Where is the primary site of action of Mannitol and why is this the primary site?

A

PCT:

- Most iso-osmotic water reabsorption

62
Q

What is a secondary effect of Mannitol?

A

Reduces Na+ reabsorption in PCT

63
Q

What type of renal failure can mannitol prevent?

A

Acute hypovolaemic renal failure

64
Q

Apart from renal failure, when else is mannitol used? How does it help these states?

A

Increased ICP
Increased IOP
Increased plasma osmolality extracts water from these components

65
Q

What type of drug is Acetazolomide?

A

Carbonic Anhydrase inhibitor

66
Q

What does Acetazolomide do?

A

Increases the excretion of:

 - Bicarbonate
 - Na+
 - K+
 - Water
67
Q

What does Acetazolomide result in due to the effect it has on urine excretion?

A

Alkaline diuresis:
- Relieve dysuria
Metabolic acidosis

68
Q

How does Acetazolomide work in the treatment of glaucoma and post-ocular surgery?

A

Reduces IOP by reducing aqueous humour production

69
Q

What ekse can Acetazolomide be used to treat?

A

Altitude sickness prophylaxis

Infantile epilepsy

70
Q

What causes Neurogenic DI?

A

Lack of ADH secretion from posterior pituitary

71
Q

How is Neurogenic DI treated?

A

Desmopressin:

 - V₂-Selective GPCR
           - > Avoids increased BP associated with V₁
72
Q

What causes Nephrogenic DI?

A

Nephrons become insensitive to ADH:

 - Usually due to recessive/X-linked mutations
           - > In V₂ receptor
73
Q

How is Nephrogenic DI treated?

A

It can’t be

74
Q

What drugs inhibit ADH?

A

Lithium
Demeclocycline
‘Vaptans’

75
Q

How do ‘Vaptans’ work?

A

Competitive antagonists of ADH receptors (V₁ₐ, V₁ᵇ and V₂)

76
Q

What does activation of V₁ₐ receptors cause?

A

Vasoconstriction

77
Q

What does activation of V₂ receptors cause?

A

Water reabsorption

78
Q

Where does the activation of V₂ receptors have its affects and how?

A

In collecting duct:

Aquaporin-containg vesicles directed to apical membrane

79
Q

What happens if V₂ receptors are blocked?

A

Increased water excretion

No Na+ accompanies the water so increased [Na+]p

80
Q

What are some examples of ‘Vaptans’ and what receptors do they block?

A

Conivaptan (V₁ₐ and V₂)

Tolvaptan (V₂)

81
Q

When might ‘Vaptans’ be used?

A

CHF

Most value in Hypervolaemic Hyponatraemia by reducing preload

82
Q

What channels is glucose absorbed through in the PCT?

83
Q

When is glycosuria present?

A

If [Glucose]filtrate >11mmol/L

84
Q

Where is SGLT1 expressed?

A

Intestines and kidneys

85
Q

Where is SGLT2 expressed?

A

Almost exclusively in the nephron PCT

86
Q

Describe the process and features of glucose reabsorption by SGLT2?

A

S1 segment
90% of reabsorption
Low affinity
High capacity

87
Q

Describe the process and features of glucose reabsorption by SGLT1?

A

S2/3 segment
10% of reabsorption
High affinity
Low capacity

88
Q

How is glucose reabsorbed at the apical membrane?

A

Secondary active transport

89
Q

How is glucose reabsorbed at the basolateral membrane?

A

Facilitated diffusion

90
Q

What is the stoichiometry of each SGLT receptor?

A

SGLT1 -> 2 Na+ : 1 Glucose

SGLT2 -> 1 Na+ : 1 Glucose

91
Q

What does SGLT2 inhibition result in?

A

Glycosuria

92
Q

What are some examples of SGLT2 inhibitors?

A

Canagliflozin
Dapagliflozin
Empagliflozin

93
Q

What effects do SGLT2 inhibitors have in T2DM?

A

Glucose excretion
Reduces HbA1c
Reduces weight

94
Q

What are some side effects of SGLT2 inhibitors?

A

Glycosuria -> Increases bacterial and fungal UTI risk

95
Q

Where is PGE₂ formed?

A

Renal medulla

96
Q

Where is PGI₂ (Prostacyclin) formed?

97
Q

What are the functions of prostaglandins?

A

Vasodilate

Natriuretic

98
Q

Which of the following does not result in prostaglandin synthesis:

  • Ischaemia
  • Mechanical trauma
  • Angiotensin II
  • Hyperkalaemia
  • ADH
  • Bradykinin
A

Hyperkalaemia

99
Q

How much of an effect do prostaglandins have on RBF and GFR in normal people?

A

Very little

100
Q

When do prostaglandins become more important?

A

In vasoconstriction

If there is a decrease in effective arterial BP

101
Q

How do prostaglandins affect GFR?

A
  1. Direct vasodilator effect on afferent arteriole
  2. Increase renin release -> Increased Ang II levels -> Efferent arteriole vasoconstricts -> Increased filtration pressure
  3. Both increase GFR
102
Q

How do NSAIDs precipitate acute renal failure?

A

Inhibit COX so decrease prostaglandin synthesis

103
Q

When especially do NSAIDs reduce GFR?

A

In conditions were renal blood flow depends on prostaglandins:

 - Liver cirrhosis
 - CHF
 - Nephrotic syndrome
104
Q

What drug combination can be bad?

A

ACEi + Diuretic + NSAIDs

105
Q

What do Probenecid and Sulfinpyrazole do?

A

Block reabsorption of urate in PCT

Year 2 - Renal (DP) (15 decks)

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