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CPTP > Heart failure and HTN > Flashcards

Heart failure and HTN Flashcards

1
Q

Stage I HTN

A

Clinic BP > 140/90mmhg or >135/85 ON ABPM

Treat all pt <80y/o or with evidence of:
Target organ damage, CVD, DM, RVD and Q risk >10%

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2
Q

Stage II HTN

A

Clinic BP >160/100 or >155/95 on ABPM

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3
Q

Severe HTN

A

> 180mmhg need hospital admission

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4
Q

Lifestyle interventions for HTN

A 
Reduced Na+ (5-6g) and fat in diet, more fruit and vegetable
30 mins of exercise a day
Reduced alcohol intake <14U 
Smoking cessation
BMI < 25
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5
Q

Targets for HTN

A

<130/90 for DM, evidence of atherosclerosis, CVD, renal
<140/90 in pt < 80y/o
<150/90 elderly over 80y/o

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6
Q

Pt under 40y/o with HTN

A

If no risk factors referral to specialist to exclude 2ndary causes of HTN

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7
Q

Medications that can = HTN

A

COCP, cold and flu remedies, corticosteroids, EPO, caffeine and cocaine

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8
Q

Mx of HTN

A

1st line if <55y/o = ACEi
>55y/o or afrocarribean- CCB (DHP - amlodipine)

2nd line = add CCB or ACEi
3rd line = Thiazide diuretic

Specialist care

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9
Q

Monitoring HTN

A

BP, urine dipstick for protein/blood
Albumin:Creatinine <2 = normal
Fundoscopy

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10
Q

Large vessel complications of HTN

A

Blood vessels = atherosclerosis, aneurysms, aortic dissections
Heart = MI, LVH - HF and pul oedema
Brain = Stroke, TIA, intracerebral haemorrhage, vascular dementia

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11
Q

Hypertensive retinopathy

A

I - tortuous retinal arteries with increased reflectiveness = silver wiring

II - AV nipping produced when thickened retinal arteries pass over the retinal veins. The arteries compress the veins causing collapse and bulging when they cross

III - Flame haemorrhages from burst blood vessels, cotton wool spots due to ischemia, hard exudate deposits = cholesterol

IV - III + papilloedma - blurring of the optic disc

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12
Q

Hypertensive nephrosclerosis

A

Most common cause of CKD. Due to hyaline deposition in the walls of small arterioles leading to thickening and reduced blood flow to areas of renal tissue. This leads to tubular atrophy and fibrosis of the glomeruli. Compensatory increase in GFR by remaining nephrons perpetuates their destruction.

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13
Q

White coat HTN

A

Difference of 20/10mmhg between clinic and daytime monitoring. ABPM is crucial to prevent over diagnosis and treatment

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14
Q

Malignant vs severe HTN

A

Severe >180/110 no evidence of organ damage

Malignant >180/110mmhg with evidence of papilloedema, retinal haemorrhages, ACS, acute dissection, hypertensive encephalopathy

Mx = sodium nitroprusside

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15
Q

Loop diuretics MOA

A

These act to competitively inhibit Na+/K+/Cl- transporter @ the ascending limb of the loop of Henle

This leads to K+ Na+, Cl- excretion so h2o is lost and BP falls. 2ndary inhibition of Mg2+ and Ca2+ reabsorption due to disruption of +ve lumen gradient
Therefore = hypercalciuria

Also increases prostaglandin production leading to afferent arteriole vasodilation and increased renal blood flow

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16
Q

CI loop diuretics

A

Severe hypokalemia or hyponatremia
Hypovolemia
Pregnancy - teratogenic

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17
Q

SE loop diuretics

A 
GI disturbance, postural hypotension
low Na+, K+, Ca2+, Mg2+
Ototoxicity
Hyperureamic = increased gout risk
Metabolic alkalosis
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18
Q

Loop diuretics

A

Furosemide

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19
Q

Interactions of loop diuretics

A

Aminoglycosides and vancomycin = increase risk of ototoxicity
NSAIDs = reduced efficacy and increased AKI risk
Increased risk of digoxin and lithium toxicity

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20
Q

Thiazide diuretics (Bendroflumathaizide) MOA

A

Inhibit Na/Cl- symporter @ DCT. This leads to reduced Na+ reabsorption and water loss. Conversely to correct the membrane potential Ca2+ and urate are reabsorbed

Hypokalemia and metabolic alkaloid due to increased Na+ delivery to the collecting duct hence ENac leads to increased Na+/K+/H+ activity = K+ and H+ excretion. Na+ retention.

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21
Q

CI thiazide diuretics

A

Addisons, renal impairment, gout, avoid in pregnancy

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22
Q

SE of thiazide diuretics

A 
low Na+, low K+,
high Ca2+, urate = gout!
hypovolemia and postural hypotension
hypercholestrolemia and hyperglycaemia
metabolic alkalosis
TIN
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23
Q

Interactions of thiazide diuretics

A

Increased risk of lithium and digoxin toxicity
B-blocker potentiate hyperglycaemia and hyperlipidemia
Reduced efficacy with NSAIDs

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24
Q

Potassium sparing diuretics (Spironolactone)

A

Competitive antagonist at the intracellular aldosterone receptor in distal tubule. This indirectly reduces Na+/K+ATPase in distal tubule leading to less Na+ reabsorption and K+ excretion

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25
Q

SE of spironolactone

A

Gynecomastia, hyperkalemia, GI upset, AKI

26
Q

Indications for spironolactone

A

HF, ascites, nephrotic syndrome, 1 hyperaldosteronism, refractory HTN

27
Q

B-blockers

A

Competitive antagonists of B adrenoreceptors preventing endogenous catecholamines binding and eliciting a sympathetic response. This leads to inhibitor in adenyl cyclase reducing cAMP and intracellular Ca2+ hence reduced contractility, SM relaxation and bronchoconstriction

28
Q

B1 receptors

A

Cardiac muscle catacholeamines act as iontropes and chrontropes. Increase renin production from JGA

29
Q

B2 receptors

A

Bronchi in lung = SM relaxation, skeletal muscle = vasodilation and glucogengesis

30
Q

B3 receptors

A

Adipose lipolysis

31
Q

Indications for B-blockers

A

Angina, AF or tachyarythmias, HF, symptomatic relief of hyperthyroid or anxiety
Variceal prophylaxis. Glaucoma

32
Q

CI of B-blockers

A

Asthma and COPD. Bradycardia or HB, hypotension, poorly controlled DM or PVD.

33
Q

Cardioselective B-blockers

A

Bisproplol, atenolol and metaprolo. Have a reduced B2 effect act primarily on B1 receptors in the heart

34
Q

Non-cardioselective B-blockers

A

Propanolol, carvediol, labetolol, timolol. Some of these have additional a1 blocking effect - arteriolar vasodilation to reduced PR

35
Q

ISA

A

Intrinsic sympathomimetic activity. Certain B blockers show low level agonism while acting as antagonists

36
Q

SE of B-blockers

A

Slowing down, fatigue, cold extremities esp in Raynuads and PVD, bradycardia, hypotension
Sleep intolerance esp in lipid soluble B-blckers such as metoprolol and propranolol as they cross BBB
erectile dysfunction
Increased TG, low HDL

37
Q

Interactions of B-blockers

A

Increased hypotensive effect when combined with other antihypertensives
NSAIDs and steroids reduce efficacy
Mask warning signs of hypoglycaemia
CI with verapamil or diltiazem = HB

38
Q

ACEi MOA

A

Ramipril, lisinopril

They inhibit angiotensin converting enzyme which is needed to convert angiotensin I to angiotensin II. This leads to

reduced vasoconstrictive effect on blood vessels,
reduced aldosterone = Na+ loss and K+ retention h20 loss and BP reduction
reduced ADH release = h20 loss due to no aquaporin insertion
high bradykinin as no enzyme to facilitate breakdown

39
Q

Indications for ACEi

A

HTN 1st line if <55y/o or DM
Type 1 diabetic nephropathy
Heart failure + post MI

40
Q

CI to ACEi

A

Pregnancy, hypersensitivity, renal artery stenosis

41
Q

SE ACEi

A

Chronic dry cough due to increased bradykinin levels
Hypotension
Hyperkalemia
Initially can lead to a decline in renal function if creatinine >30% increase stop . Monitor U+E before and for 1st 2 wks

42
Q

Interaction of ACEi

A

Increased hypoglycaemic effect with insulin, metformin and sulphonyureas
Diuretics = increased hypotension risk
K+ sparing diuretics = increased hyperkalemia risk

43
Q

ARB

A

Angiotensin receptor blockers antagonise the angiotensin II receptor. This doesn’t give dry cough as bradykinin metabolism isn’t effected.

Reduced efficacy in afro-carribeans due to ACEi polymorphisms

44
Q

Calcium channel blockers

A

Dihydropyridines - amlopidine and nifedipine

Non-dihydropyridines - Verapamil, dilatazem

45
Q

Dihydropyridine CCB MOA

A

Act on arterial SM to inhibit influx of Ca2+ via L type Ca2+ channels reducing SM contractility and leading tp vasodilation

This reduced TPR, increasing sympathetic tone and leading to reflex tachycardia

46
Q

Indications DHP’s

A

HTN, Raynauds, prinzemetals angina

47
Q

SE DHP CCB

A

Flushing, headache and ankle oedema due to vasodilation
Hypotension and dizziness

Nifedipine can = gingival hypertrophy

48
Q

CI DHP CCB

A

Cardiogenic shock, AS, unstable angina

49
Q

Non-dihydropyridines CCB MOA

A

Acts on cardiac a1 subunits of L-type Ca2+ channels preventing influx of Ca2+. They have a -ve inotropic effect and can slow conduction at the SA/AV node

50
Q

NDHP CCB SE

A

Flushing, headache, constipation

SA and AV node block

51
Q

Alpha blockers ( Tamulosin, prazosin) MOA

A

Act to inhibit the a1 adrenoreceptors in arterioles reducing the tone of vascular SM and overall TPR. They inhibit binding of noradrenaline hence preventing the phosphorylation cascade and Ca2+ influx. Can help relief obstructive urinary symptoms by relaxing the periurethral prostatic stroma

52
Q

SE a1 blockers

A

postural hypotension, dizziness, fatigue.

53
Q

Nitroprusside

A

Used IV for hypertensive crisis. Nitric oxide release reduces both TPR and venous return dropping preload and after load

SE - bradycardia, hypotension, rash, swelling, ileus, haemorrghe, increased ICP

54
Q

Labetolol

A

Acts on both a and B adrenoreceptors to reduce BP in obstetric emergencies - preeclampsia

SE postural hypotension, dizziness, hepatotoxicity, HB, fever

55
Q

Antihypertensives safe in pregnancy

A

Methyl-dopa, nifedipine

Labetolol can be used in pre-eclampsia as baby is fully formed

56
Q

Pre-eclampsia

A

BP >140mmhg + proteinuria > 1+ on dipstick
Mx = 75mg aspirin OD

>150/100 = oral labetolol
>160/110 = IV labetolol (Magnesium sulphate to reduced risk of eclampsia)
57
Q

Unsafe antihypertensives in pregnancy

A

ACEi and ARBs = congenital abnormality in 1st trimester,
Thiazide diuretics = oligohydramnios
B-blockers = growth retardation

58
Q

NNT

A

100/ARR

59
Q

Acute HF Management

A

Sit upright high flow 02
IV furosemide 80mg bolus x2

SBP >100 - Vasodilator (GT)
SBP <85 - Noradrenaline, inotropes

If decline consider CPAP and ITU

60
Q

Resolved acute HF management

A

Daily wt and fluid chart
DVT prophylaxis - tinzaparin
ACEi, B blockers if new HF
2nd CXR and oral furosemide

61
Q

Mx chronic HF

A

low Na+ diet, stop smoking, cardiac rehab, 5x 30mins exercise a week
ACEi and B-blockers for all
Spironolactone for worsening HF
Diuretics = no survival benefits used symptomatically for oedema

62
Q

Clinical syndromes of acute heart HF

A

Acute pul oedema - tachypnoea, pulmonary crackles, sats<90%, bilateral infiltrates on CXR

Cardiogenic shock systolic BP <90, HR >60bpm, urine output <0.5ml/kg/hr, cold periphery, long CRT

High output HF = warm periphery, pulmonary congestion, low BP - septic shock

CPTP (11 decks)

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