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ICOM-Cardio > Cardio-clinical-HTN-Bennet > Flashcards

Cardio-clinical-HTN-Bennet Flashcards

1
Q

HTN is considered what bp level :

A

>130/80

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2
Q

HTN trends have increased/decreased just about everywhere.

A

increased

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3
Q

The number one modifiable risk to early death is :

A

High BP or HTN

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4
Q

What is the average pressure within the patient’s arteries through one cardiac cycle?

A

MAP

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5
Q

What is a better predictor of stress on arterial walls?

A

MAP

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6
Q

What is a normal MAP?

A

70-100

>60 needed to maintain cerebral/renal/cardiac; MAP >100 is high)

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7
Q

For every mmHg increase in SBP or a mmHg increase in DBP: the risk of death from heart attack & stroke, and the risk of heart failure and aortic aneurysm

A

20; 10; DOUBLES; DOUBLES

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8
Q

What 3 things can lead to HTN:

A

Too much volume, renin, catecholamines

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9
Q

Pheochromocytoma increases which catecholamine? which can increase BP?

A

Norepinephrine

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10
Q

Primary HTN causes include:

A

Genetics

Age

High salt,

low potassium diet

Insulin resistance/diabetes

Inactivity

ETOH

Obesity

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11
Q

Secondary HTN (known cause) which may be reversible causes include:

A

Meds/drugs

Chronic kidney disease (RAS, FMD, PKD)*

Endocrine causes

Coarctation of Aorta

Sleep Apnea

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12
Q

Major causes of HTN for 0-18:

A

Renal parenchymal disease

Aortic coarctation

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13
Q

Major causes for HTN for ages 19-39

A

Thyroid dysfunction

Fibromuscular dysplasia

Renal parenchymal disease

Endogenous Cushing’s Syndrome

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14
Q

major causes for HTN in ages 40-64

A

Hyperaldosteronism

Thyroid dysfunction

OSA

Exogenous (Iatrogenic) Cushing’s Syndrome

Pheochromocytoma

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15
Q

Major causes of HTN in ages >65

A

Renal Artery Stenosis

Chronic Kidney Disease (CKD)

Hypothyroid

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16
Q

Cushing’s (iatrogenic) is caused by which drug?

A

steroids

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17
Q

Testosterone supplements can increase EPO which can lead to slurrying of blood and lead to:

A

HTN

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18
Q

What is a cause for resistant HTN caused by low K+ levels?

A

Aldosteronism (Conn’s Syndrome)

  • adrenal tumor
  • bilateral adrenal hyperplasia
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19
Q

What is the most common cause of resistant HTN?

A

sleep apnea

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20
Q

Obstructive sleep apnea (OSA) is also a common cause of :

A

hypertension

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21
Q

Fibromuscular dysplasia (string of pearls narrowed renal arteries) and tortuosity is a cause of HTN in which population?

A

younger women

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22
Q

Diffucult to control HTN involving renal arteries in older age?

A

renal artery stenosis

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23
Q

If treating FMD or Renal artery stenosis with ACE inhibitors, what happens to Cr lab values?

A

Serum creatinine rises 30%, significantly

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24
Q

FMD (renal string of pearls) and renal artery disease both can compromise sufficient to the glomerular complex and lead to kidney injury.

A

blood pressure

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25
Q

Kidney’ s issues lead to HTN problems in what manner?

A

messing with Na+

altered RAS system

increased endothelin (vasoconsticor)

inhib NO

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26
Q

Endocrine disorders -Pheochromocytoma, Carcinoid and other neuroendocrine tumors producing excess:

and have what effect on BP

A

EPI/NE/DOPAMINE/ SEROTONIN; SSRI/SNRI/TCA (ie antidepressants)-can also raise BP

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27
Q

Coarctation is another cause of HTN , there is a 75% mortality by age

A

46

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28
Q

Where do you listen for a possible coarctation of the aorta?

A

posterior, L inferior scapula

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29
Q

What is endogenous cushing’s syndrome?

A

excess cortisol production (due to tumor on adrenal gland->10-15%); overproduction of ACTH by pituitary tumor ( ie Cushing’s Disease -70% or extra-pituitary, ACTH-producing tumor->10-15%)

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30
Q

Exogenous (iatrogenic Cushing’s): leading to resistant HTN, truncal obesity, striae, elevated glucose, easy bruising, osteoporosis at young age. is more or less common than endogenous Cushing’s and is caused by?

A

more common, steroids

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31
Q

Which top 3 diet involved issues can affect blood pressure (not including cholesterol)?

A

High salt, low potassium, and high ETOH

32
Q

Alcohol has a biphasic affect with BP, how?

A

low BP ( vasodilation) for the first few hours, followed by vasoconstiction (while sleeping)

33
Q

EPO is a treatment for chronic renal failure, however, it can worsen HTN in 2 ways:

A

increases blood viscosity

has direct pressor effect

34
Q

Hyperthyroidism/hypothroidism can cause HTN?

A

both actually, via different mechanisms

35
Q

Other endocrine issues that can cause HTN other than cushings and throid issues include:

A

hyperparathyroidism and acromegaly-growth hormones excess (fluid retention)

36
Q

Normally, there is about a 10-20% drop of BP while you sleep which is called the nocturnal dip except which two populations:

of which both have a higher risk of HTN

A

African americans and those with sleep apnea

37
Q

What are the things we do clinically when someone is diagnosed with HTN:

A

look at optic discs for HTN retinopathy

auscultate for cardiac murmurs or bruits

palpate thyroid

check peripheral pulses

directed neuro exam (visual and cognitive changes)

38
Q

First choice antihypertensives include which 4?

and of those 4, are usually started first because of cost and they are highly tolerated

A

ace inhibitors (-pril)

angiotensin receptor blockers (-aratns)

CCBs

diuretics (thiazides)

diuretics are used

39
Q

What diuretic is most commonly prescribed for treatment of HTN?

A

Hydrochlorothiazide

40
Q

Though Hydrochlorothiazide is more often prescribed, which diuretic is most effective?

A

chlorthalidone

more expensive

41
Q

Continually and repetitively emphasize which lifestyle changes for treatment of HTN:

A

a diet low in Na+ & high in K+ (DASH), aerobic exercise 3-5 x/wk, limit ETOH, stress management, sleep adequacy

42
Q

Labs to check and why when diagnosed with primary HTN:

A

Chem panel: gluclose, electrolytes

CBC: polycythemia

lipids: hyperlipidemia

TSH: thyroid function

UA- leaking protein, renal dz

EKG

43
Q

If you suspect secondary HTN, what are some important labs to consider:

A
  1. BNP (brain natriuretic peptide) and/or echo (ie heart failure)
  2. Aldosterone/Renin Ratio (hyperaldosteronism)
  3. Urinary catecholamines (pheo), 5-HIAA (carcinoid)
  4. Sleep study (OSA)
  5. AM Cortisol (Cushing’s)
  6. Magnetic Resonance Angiography of renal arteries (RAS, FMD)
44
Q

What is the first line treatment for African Americans for HTN as they dont respond as well to ACE inhib, and angiotensin receptor blockers (ARBs)?

A

start off with diurectics and CCB

45
Q

What is the first line therapy with diabetics?

A

ACE ihibs, and ARBs (especially with kidney disease)

46
Q

Which first line therapy is not used for diabetics?

A

diuretics, as they can raise blood gluclose levels

47
Q

Those with kidney disease (like many diabetics) we use:

A

ACEs and ARBs because they are renal sparing

48
Q

What is first line HTN therapy for coronary artery disease sufferers:

A

BBlockers (especially after MI) , add ACE or ARB if BP not at goal, or have LV heart failure

49
Q

What is the first line therapy for those with or without HTN for those with migraines?

A

BB and CCB, this can be with or w/o HTN

50
Q

What first line HTN therapy is contraindicated for those with GOUT?

A

diuretics, as they can increase uric acid and worsen gout

51
Q

At what age in kids should one follow ACC/AHA guidelines for treating HTN?

A

13

52
Q

you should suspect secondary HTN if child has symptoms under the age of , with no fam hx of HTN, failure to , and thin body

A

6; thrive; habitus

53
Q

Common conditions that cause HTN in kids under six with no fam hx of HTN are which 3 conditions:

A

Suspected or known kidney disease, endocrine disorder or congenital cardiac disorder

54
Q

What end organ damage can be caused by poorly controlled or undiagnosed HTN?

A

Stroke or TIA

Vascular dementia (#2 cause of dementia)-“silent strokes”

Chronic kidney disease/renal failure

Myocardial infarction

Left ventricular hypertrophy

Heart failure (diastolic and systolic)

Aortic aneurysm

Retinopathy and retinal artery thrombosis

55
Q

What do we consider HTN urgency (a type of HTN crisis)?

A

severe but asymptomatic HTN

SBP ≥ 180 OR DBP ≥ 110 mmHg

NO ACUTE, END-ORGAN INJURY

often caused by noncompliance

men 2:1

56
Q

What do we consider a hypertensive emergency?

A

end organ damage

SBP ≥ 180 OR DBP ≥ 110 mmHg

severe chest pain, SOB, headache with confusion or blurred vision, severe back pain, nausea/vomiting, seizures, unresponsive, severe anxiety or sense of impending doom

57
Q

What is malignant HTN?

A

subset of HTN Emergency with widespread arteriolar injury of at least 3 organs commonly involving retina, kidneys and brain —>death rates approach 100% if inadequately treated

worst hypertensive emergency

58
Q

What end organ damage is most common?

A

cardiac then cerebral

59
Q

if there is a 20mmhg difference in BP when measuring both arms, asymmetrical bilateral pulses, what pathology would you consider?

A

aortic dissection

60
Q

What are some things to look for in a retinal exam with someone in HTN crisis?

A

(exudates, cotton wool spots

61
Q

A new S3 sound during auscultation could indicate what?

A

Heart failure or torn chordae tendinae

62
Q

How would you treat HTN urgency (no end organ failure, asymptomatic)?

A

compliance with medications and followup within 24 /48 hours

if compliant, increase dose and/or add another med and f/u

63
Q

How would you treat a HTN emergency?

A

Lower BP SLOWLY by 25% in first 60min;

Then 10-15% more over next 6-23 hrs with the goal:

160/100-110mmHg) ICU admission

64
Q

What are the 3 exceptions to the normal treatment of HTN emergency:

Lower BP SLOWLY by 25% in first 60min;

Then 10-15% more over next 6-23 hrs with the goal:

160/100-110mmHg) ICU admission

A

Aortic Dissection *

Stroke (Hemorrhagic or Ischemic) *

Eclampsia(HTN+Seizure+Pregnancy

65
Q

How to treat the HTN emergency aortic dissection:

Lower HR to <60 bpm within

+

SBP to <120 mmHg within minutes

start on an IV

if BP still not at <120 add or nitroprusside or NTG

A

minutes; 20; BB (esmolol, labetolol); nicardipine

66
Q

Why is it so important to focus on HR first if an aortic dissection is suspected/occuring?

A

slow down the amount of blood getting into the pocket to prevent tearing and/or occlusion

67
Q

How do we treat hypertension emergency with acute ischemic stroke if using tPA?

A

If thrombolytics indicated (ie tPA) and BP is >220 mmHg:

then use

IV antihypertensives to lower BP to <185/110 before tPA and maintain BP <180/105 mmHg for 24 hrs after tPA

68
Q

When do we not treat hypertensive emergent acute ischemic stroke with IV antihypertensives:

A

if not using tPA and BP less than 220/100

69
Q

What is the BP range that we need to get to in order to treat ischemic stroke with tPA to lower risk of hemorrhagic stroke?

A

<180-185/110-105

70
Q

If acute ischemic stroke with >220 mmHg and not using tPA, then tx to get a 15% reduction in 24 hours

A

slowly

71
Q

What are the recommendations of high BP (over 220) with hemorrhagic stroke?

A

Aggressively lower SBP to between 140-160mmHg within first 2-4 hours, but not lower so as not to compromise perfusion

72
Q

CV risks rise linearly/nonlinearly with BP elevations over 115/75 mmHg

A

linearly

73
Q

What effect do NSAIDS have on BP?

A

they can elevate BP

74
Q

In a HTN emergency, it is important to bring BP down slowly, with three exceptions:

A

stroke, eclampsia and aortic dissection

75
Q
A

ICOM-Cardio (32 decks)

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