Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Stage II HTN

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Severe HTN

A

> 180mmhg need hospital admission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pt under 40y/o with HTN

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Medications that can = HTN

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Monitoring HTN

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

White coat HTN

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CI loop diuretics

A

Severe hypokalemia or hyponatremia
Hypovolemia
Pregnancy - teratogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SE loop diuretics

A 
GI disturbance, postural hypotension
low Na+, K+, Ca2+, Mg2+
Ototoxicity
Hyperureamic = increased gout risk
Metabolic alkalosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Loop diuretics

A

Furosemide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CI thiazide diuretics

A

Addisons, renal impairment, gout, avoid in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Interactions of thiazide diuretics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
SE of spironolactone
Gynecomastia, hyperkalemia, GI upset, AKI
26
Indications for spironolactone
HF, ascites, nephrotic syndrome, 1 hyperaldosteronism, refractory HTN
27
B-blockers
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
B1 receptors
Cardiac muscle catacholeamines act as iontropes and chrontropes. Increase renin production from JGA
29
B2 receptors
Bronchi in lung = SM relaxation, skeletal muscle = vasodilation and glucogengesis
30
B3 receptors
Adipose lipolysis
31
Indications for B-blockers
Angina, AF or tachyarythmias, HF, symptomatic relief of hyperthyroid or anxiety Variceal prophylaxis. Glaucoma
32
CI of B-blockers
Asthma and COPD. Bradycardia or HB, hypotension, poorly controlled DM or PVD.
33
Cardioselective B-blockers
Bisproplol, atenolol and metaprolo. Have a reduced B2 effect act primarily on B1 receptors in the heart
34
Non-cardioselective B-blockers
Propanolol, carvediol, labetolol, timolol. Some of these have additional a1 blocking effect - arteriolar vasodilation to reduced PR
35
ISA
Intrinsic sympathomimetic activity. Certain B blockers show low level agonism while acting as antagonists
36
SE of B-blockers
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
Interactions of B-blockers
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
ACEi MOA
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
Indications for ACEi
HTN 1st line if <55y/o or DM Type 1 diabetic nephropathy Heart failure + post MI
40
CI to ACEi
Pregnancy, hypersensitivity, renal artery stenosis
41
SE ACEi
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
Interaction of ACEi
Increased hypoglycaemic effect with insulin, metformin and sulphonyureas Diuretics = increased hypotension risk K+ sparing diuretics = increased hyperkalemia risk
43
ARB
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
Calcium channel blockers
Dihydropyridines - amlopidine and nifedipine | Non-dihydropyridines - Verapamil, dilatazem
45
Dihydropyridine CCB MOA
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
Indications DHP's
HTN, Raynauds, prinzemetals angina
47
SE DHP CCB
Flushing, headache and ankle oedema due to vasodilation Hypotension and dizziness Nifedipine can = gingival hypertrophy
48
CI DHP CCB
Cardiogenic shock, AS, unstable angina
49
Non-dihydropyridines CCB MOA
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
NDHP CCB SE
Flushing, headache, constipation | SA and AV node block
51
Alpha blockers ( Tamulosin, prazosin) MOA
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
SE a1 blockers
postural hypotension, dizziness, fatigue.
53
Nitroprusside
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
Labetolol
Acts on both a and B adrenoreceptors to reduce BP in obstetric emergencies - preeclampsia SE postural hypotension, dizziness, hepatotoxicity, HB, fever
55
Antihypertensives safe in pregnancy
Methyl-dopa, nifedipine Labetolol can be used in pre-eclampsia as baby is fully formed
56
Pre-eclampsia
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
Unsafe antihypertensives in pregnancy
ACEi and ARBs = congenital abnormality in 1st trimester, Thiazide diuretics = oligohydramnios B-blockers = growth retardation
58
NNT
100/ARR
59
Acute HF Management
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
Resolved acute HF management
Daily wt and fluid chart DVT prophylaxis - tinzaparin ACEi, B blockers if new HF 2nd CXR and oral furosemide
61
Mx chronic HF
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
Clinical syndromes of acute heart HF
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions