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CPR Exam 1 > HTN and HTN urgency/emergency > Flashcards

HTN and HTN urgency/emergency Flashcards

1
Q

what are the modifiable risk factors of HTN?

A 
current cigarette smoking
secondhand smoke
DM
HLD
obesity
low physical activity
unhealthy diet
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2
Q

what are the fixed risk factors of HTN?

A 
CKD
family history
increased age
low SES
male
obstructive sleep apnea
psychosocial stress
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3
Q

what are the cardiac consequences of HTN?

A 
LVH
HF
atherosclerotic CAD
microvascular dz
arrhythmias (Afib)
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4
Q

what are the cerebral consequences of HTN?

A

CVA
dementia
HTN-encephalopathy

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5
Q

what are the renal consequences of HTN?

A

renal injury

ESRD

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6
Q

what are the arterial consequences of HTN?

A

PAD

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7
Q

what is primary/essential HTN?

A

elevated BP with no specific underlying disorder

80-90% of cases

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8
Q

what is secondary HTN?

A

elevated BP with a specific underlying disorder

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9
Q

what is hypertensive urgency?

A

severe BP elevation (>180/110) without symptoms of end organ damage

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10
Q

what is a hypertensive emergency?

A

severe BP elevation (>180/110) WITH symptoms of end organ damage

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11
Q

what physiological factors raise blood pressure?

A 
Na retention 
vasoconstriction
endothelin 1 
activation of SNS
pro-inflammatory Th1 cells
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12
Q

what is normal BP?

A

<120/80

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13
Q

what is elevated BP?

A

120-129/<80

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14
Q

what is stage 1 HTN?

A

130-139/80-89

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15
Q

what is stage 2 HTN?

A

≥ 140/90

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16
Q

what are signs of secondary HTN?

A 
features of Cushing syndome
neurofibromatosis
enlarged kidneys
abdominal bruits
precordial murmurs
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17
Q

what are signs of target-organ damage?

A 
motor or sensory deficit
retinopathy
Afib/arrhythmia
pulmonary edema/congestion
absent, reduced or asymmetrical pulses
ischemic skin lesions
carotid murmurs
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18
Q

what lab tests need to be ordered when primary HTN is suspected?

A 
CBC
CMP
lipid panel
TSH
UA
EKG
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19
Q

what is the treatment for elevated BP?

A

nonpharmacologic therapy (lifestyle changes)

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20
Q

what is the treatment for stage 1 HTN in patients without other risk factors for CVD?

A

nonpharmacological therapy (lifestyle changes)

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21
Q

what is the treatment for stage 1 HTN in patients WITH other risk factors for CVD? (HLD, DM, CKD, old)

A

nonpharmacologic therapy
AND
BP lower medication (RAS inhibitor or diuretic)

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22
Q

what is the treatment for stage 2 HTN?

A

nonpharmacologic therapy
AND
BP lower medication (RAS inhibitor or diuretic)

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23
Q

what are the nonpharmacological therapies?

A 
weight reduction
salt reduction
DASH diet
alcohol reduction
increase physical activity
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24
Q

which nonpharmacological therapy can most significantly lower BP?

A

DASH diet

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25
Q

what are the first line anti-HTN?

A

RAAS inhibitors
CCBs
thiazide diuretics

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26
Q

what anti-HTN is best for white ppl?

A

ACEI or ARBs

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27
Q

what anti-HTN is best for black ppl?

A

CCBs or diuretics

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28
Q

what anti-HTN is best for patients with DM2?

A

ACEI or ARBs

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29
Q

what anti-HTN is best for patients with CHF?

A

ACEI or ARBs or B-blockers

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30
Q

what anti-HTN is best for patients with BPH?

A

a-blockers

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31
Q

what anti-HTN is best for patients with Afib?

A

CCBs or B-blockers

32
Q

what factors are important when reassessing BP?

A 
detection of orthostasis
ID white coat syndrome
document adherence
monitor response
reinforce importance of treatment
33
Q

what is the protocol for HTN urgency?

A

BP should be lowered gradually <160/100 but not acutely >20-25% of MAP over several days-weeks

34
Q

what are the most common presentations of HTN emergency?

A

cerebral infarction

pulmonary edema

35
Q

what labs/imaging should be ordered for suspected HTN emergency?

A 
EKG
CXR
UA
serum electrolytes 
creatinine
36
Q

what is the protocol for HTN emergency?

A

lower MAP gradually:
10-20% in 1st hour
5-15% over next 24 hours

37
Q

in primary htn what is the source of the HTN

A

increase in total peripheral resistance

38
Q

How does limit of Na intake influence a decrease in blood pressure

A

reduction in salt intake reduces fluid retention which lowers BP. In addition, lack of salt will activate RAAS which can be blocked pharmacologically.

39
Q

Why are ACE inhibitors less likely to work in African Americans with primary HTN

A

they have low renin primary HTN so there is nothing to block (in addition, allergies)

40
Q

What conditions are likely to indicate secondary HTN

A

Abrupt onset
HTN <30 y/o
Accelerated/malignant HTN

41
Q

What are the categories of the first line drugs used to treat HTN

A

Thiazides
ACEi
ARBs
CCB dihydropyridines or nondihydropyridines

42
Q

What is the mechanism of the thiazide diuretics?

A

block Na-Cl cotransporters in the distal convoluted tubule

43
Q

A low GFR would make what class of drugs less effective?

A

Thiazides

44
Q

What drug is long lasting and used by many HTN experts for this reason?

A

Chlorthalidone

45
Q

what is the mechanism of action of furosemide

A

blocks Na-K-Cl cotransporter in the thick ascending loop of henle

46
Q

What are loop diuretics indicated for

A

HF
Pulmonary Edema
HTN

47
Q

What are notable toxicities of furosemide

A

Hypo-“saltemia” lose all salts

ototoxic

48
Q

You need a loop diuretic but cyka blyat your patient has a sulfa allergy because they are weak. what loop diuretic can you give your weak baby patient

A

ethacrynic acid

49
Q

how do potassium sparing diuretics work?

A

block Na the ENaC channel or Aldosterone at the collecting duct after K+ has been reabsorbed

50
Q

What are the Potassium sparing diuretics

A

Amiloride - blocks ENaC

Spironolactone - Blocks aldosterone

51
Q

What is the clinical indication of Amiloriode

A

Offsets K+ loss from other diuretics

hyperkalemia risk

52
Q

What is the clinical application of spironolactone?

A

counteracts K+ loss from other diuretics

reduce fibrosis in HFrEF post MI

53
Q

Where does aliskirin work on the RAAS

A

blocks renin

54
Q

what is a universal process that occurs in people recently put on ACE inhibitors

A

Decrease in GFR -> increase in serum creatinine

55
Q

What is the clinical application of captopril and other ACEi

A

HTN
Acute HTN/Emergency
HFrEF
Diabetic nephropathy

56
Q

What are two notable side effects of ACEi

A

cough

angioedema

57
Q

What is the mechanism of the -sartan drugs

A

block angiotensin II receptors

58
Q

What is candesartan notable for

A

irreversible binding and longer half life.

59
Q

Which AT receptors do -sartan drugs have a higher affinity

A

AT1

60
Q

What is the mechanism of action of aliskirin

A

blocks direct effects of renin

61
Q

What is a disadvantage of aliskirin

A

its new and expensive but does have few toxicities

62
Q

You have a pregnant lady with HTN, what will you not giver her 100 percent

A

ACEi

63
Q

What are the dihydropyridine CCB

A

Nifedipine

Amlodipine

64
Q

What are the uses Amlodipine is limited to

A

CAD

HTN

65
Q

Which category of CCB is cardioactive

A

non-dihydropyridine - verapamil; diltiazem

66
Q

When taking dihydropyridine CCB what interaction is important to look for

A

CYP3A4 active drugs

67
Q

What is the key difference between Nifedipine and Verapamil

A

nifedipine at therapeutic doses exerts smaller direct ionotropic effects and no chronotropic, but DOES have large vasodilation, HR, and CO because of reflex SNS

68
Q

What a-blockers were used early but not tolerated due to their extensive adverse effects

A

Phentolamine

Phenoxybenzamine

69
Q

What is the mechanism of action for propranolol

A

nonselective beta blockers (class II antiarrhythmic)

70
Q

what is the mechanism of action of atenolol or metoprolol

A

B1 selective blocker

71
Q

What is the risk of abruptly stopping a or B blockers

A

Tachycardia and HTN spike -> death

72
Q

why are B blockers no longer a first line therapy for HTN

A

dont prevent MI, HF, or death

higher incidence of stroke

73
Q

What is the clinical use of hydralazine

A

hypertensive emergency in pregnancy

HFrEF

74
Q

What is the mechanism of action of nitroprusside

A

venous and arteriolar dilation

75
Q

How does renal HTN affect systemic hypertension

A

stenosis decreases renal perfusion which activates RAAS

76
Q

Presence of what effects indicated BL renovascular HTN

A

Flash Pulmonary Edema
Progressive Renal Failure
Refractory Congestive Cardiac Failure

77
Q

What drug is classically used for IV HTN emergency

A

Sodium Nitroprusside

CPR Exam 1 (19 decks)

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