Cardio Medications

Question 1

Does Bendroflumethiazide cause Hyperkalaemia or Hypokalaemia and does it cause Hyponatraemia or Hypernatraemia ?

Answer 1

Hypokalaemia & Hyponatraemia

Question 2

What mineralocorticoid receptor antagonists can be used in patients with troublesome gynaecomastia on spironolactone

Answer 2

Eplerenone

Question 3

type 2 diabetes mellitus + chronic kidney disease (CKD) is reviewed in the nephrology clinic.

His blood tests and urine analysis reveal he has an eGFR of 43ml/min/1.73m 2 and an albumin creatinine ratio (ACR) of 34mg/mmol.

taking ramipril at the maximum dose of 10mg per day.

what additional class of medication should be added to manage his chronic kidney disease?

Answer 3

SGLT2 INHIBITORS-

SGLT-2 inhibitors are beneficial in proteinuric CKD, regardless of diabetic status

Question 4

Warfarin’s high INR monitoring…

Answer 4

To summarise management of high INR:

Bleeding:
MINOR bleed: IV vitamin K
MAJOR bleed: IV vitamin K + prothrombin complex concentrate

NOT bleeding:
INR >8: oral vitamin K
INR 5-8: miss next dose of warfarin

Question 5

Thiazide Diuretics MoA

Answer 5

inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Clˆ’ symporter

Question 6

What condition does Thiazide make it worse?

Answer 6

Gout

Question 7

MoA ACE Inhibitors

Answer 7

inhibits the conversion angiotensin I to angiotensin II

→ decrease in angiotensin II levels → to vasodilation and reduced blood pressure

→ decrease in angiotensin II levels

→ reduced stimulation for aldosterone release

→ decrease in sodium and water retention by the kidneys

Question 8

MoA ARB

Answer 8

block effects of angiotensin II at the AT1 receptor

Question 9

Side effects of ARB

Answer 9

Side-effects include hypotension and hyperkalaemia.

Question 10

MoA of Statins

Answer 10

Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.

Question 11

MoA of Aspirin

Answer 11

Aspirin works by blocking the action of both cyclooxygenase-1 and 2.

Cyclooxygenase is responsible for prostaglandin, prostacyclin and thromboxane synthesis.

The blocking of thromboxane A2 formation in platelets reduces the ability of platelets to aggregate which has lead to the widespread use of low-dose aspirin in cardiovascular disease.

Question 12

MoA of Clopidogrel

Answer 12

antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets

Question 13

MoA of Warfarin

Answer 13

inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form

this in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.

Question 14

MoA of LWM Heparin

Answer 14

Activates antithrombin III. Forms a complex that inhibits factor Xa

Question 15

MoA of DOACs

Answer 15

-Xaban

Direct factor Xa inhibitor

Dabigatran

Direct thrombin inhibitor

Question 16

MoA Loop Diuretics

Answer 16

inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.

Question 17

Statins + erythromycin/clarithromycin - an important and common interaction

Answer 17

increasing the risk of hepatotoxicity and a potentially grave condition known as rhabdomyolysis

an important and common interaction

Question 18

adverse effects of statins

Answer 18

myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase. Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)

liver impairment: NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range

there is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who’ve previously had a stroke.

Question 19

Contraindications of statins

Answer 19

macrolides (e.g. erythromycin, clarithromycin) are an important interaction. Statins should be stopped until patients complete the course

pregnancy

Question 20

Statins should be taken, when

Answer 20

at NIGHT as this is when the majority of cholesterol synthesis takes place. This is especially true for simvastatin which has a shorter half-life than other statins.

Question 21

Intracranial haemorrhage on warfarin →

Answer 21

give IV vitamin K 5mg + prothrombin complex concentrate

Question 22

Is pregnancy is a contraindication to statin therapy?

Answer 22

Yes, Pregnancy is a contraindication to statin therapy

Question 23

Calcium channel blockers - side-effects:

Answer 23

headache, flushing, ankle oedema

Question 24

ECG features of digoxin toxicity

Answer 24

down-sloping ST depression (‘reverse tick’, ‘scooped out’)

flattened/inverted T waves

short QT interval

arrhythmias e.g. AV block, bradycardia

Question 25

mechanism of action of aspirin to achieve an antiplatelet effect

Answer 25

‘inhibits the production of thromboxane A2’

Aspirin is an acetylsalicylic acid, which irreversibly inhibits the cyclooxygenase-1 (COX-1) enzyme in platelets.

This prevents the conversion of arachidonic acid to thromboxane A2, a potent vasoconstrictor and platelet aggregator.

By reducing its production, aspirin achieves its antiplatelet effect.

Question 26

talk through the process of the moa of aspirin

Answer 26

inhibit COX-1

inhibits conversions of arachidonic acid to thromboxane A2

Question 27

talk through the process of the moa of clopidogrel

Answer 27

P2Y12 inhibitors like clopidogrel, prasugrel and ticagrelor that inhibit ADP from binding to its platelet receptor.

Preventing activation and aggregation of platelets.