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Cardiology > Prevelance Of Hypertension > Flashcards

Prevelance Of Hypertension Flashcards

1
Q

How much of a blood pressure increase is needed to double your risk of heart attack/stroke?

A

20 systolic and 10 diastolic

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2
Q

How does renal artery stenosis cause hypertension?

A

High renin levels

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3
Q

How does pheochromocytoma cause hypertension?

A

Large amount of Catecholamines presence caused by increased norepinephrine release from the tumor

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4
Q

How does End stage renal disease (ESRD) cause hypertension?

A

Fluid overload causes increased volume levels.

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5
Q

Factors that increase blood pressure

A

Cardiac output: directly proportional

Blood volume: directly proportional

Flexibility of arteries: directly proportional

Blood viscosity: directly proportional

Diameter of arteries: inversely proportional

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6
Q

Primary vs secondary

A

Primary

  • mass majority of cases
  • caused idiopathically By age, genetics, alcohol consumption obesity

Secondary

  • minorities of cases
  • caused usually by an indirect issue such as drugs/medication, kidney disease, apnea, endocrine issues, etc.
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7
Q

What are common etiologies of 2nd HTN in people between 0-18 yrs?

A

Renal parenchyma disease

Aortic coarctation

Improper Medications

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8
Q

What are common etiologies of 2nd HTN in people between 19-39 yrs?

A

Thyroid dysfunction

Fibromuscular dysplasia

Renal parenchymal disease

Endogenous Cushing syndrome
- too much cortisol in blood caused by genetic and body abnormalities

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9
Q

What are common etiologies of 2nd HTN in people between 40-64 yrs?

A

Hyperaldosteronism

Thyroid dysfunction

Exogenous Cushing syndrome
- too much cortisol in the body caused by taking too much of a cortisol-like drug dose

Pheochromocytoma

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10
Q

What are common etiologies of 2nd HTN in people between greater than or equal to 65 yrs?

A

Renal artery stenosis

Hypothyroid

Chronic kidney disease

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11
Q

What is the most common cause of resistant hypertension?

A

Obstructive Sleep apnea

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12
Q

Aldosteronism

A

“Cons syndrome”

Resistant HTN due to adrenal tumors or bilateral adrenal hyperplasia

Causes hypocalemia in some of cases

Most commonly occurs in patients on 3+ medications with blood pressure that wont come down

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13
Q

What are the two most common causes of renal bruits?

A 
Fibromuscualr dysplasia (more common in younger females) 
- arteries look like “string of pearls “ and narrows the renal arteries due to muscular disorders

Renal artery stenosis (more common in elderly patients)

  • atherosclerosis from plaque build up involving renal arteries
  • will always show an increase in roughly 30% of serum Cr/K+ when starting ACEI/ARB
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14
Q

How to measure a renal artery bruit

A

Usually in the upper right or left quadrant in the abdominal wall.

Will sound like a “whoosh”

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15
Q

Examples of bad kidney diseases that often affect HTN

A

Recurrent UTIs

Kidney stones

Chronic HTN for other reasons

Glomerulonephritis

Polycystic kidney disease

  • all alter the renin-angiotensin system, inhibt nitric oxide production (vasodilator) and increase endothelium production*
  • all lead to HTN and vasoconstriction
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16
Q

Murmurs in the Aortic region can signify what?

A

Aortic stenosis

Flow mummers

Aortic valve sclerosis

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17
Q

Murmurs heard in the pulmonic area are indicative of what?

A

Pulmonic stenosis

Flow murmurs

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18
Q

What is the most common dietary issues for 2nd HTN?

A

Increased alcohol consumption and high sodium intake

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19
Q

What is alcohols affect on HTN?

A

Immediately after consumption causes vasodilation (1-2 hrs) and then vasoconstriction.
(biphasic effects)

Can cause HTN when sleeping

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20
Q

How to get an accurate measurement of BP

A

Make sure resting for 5 minutes and no caffeine/ tobacco/exercise 30 min prior

Arm and back are supported with feet on ground

Never measure BP over clothing

Arm is at heart level

No talking

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21
Q

Which measurement (DBP or SBP) is most determinetal for heart disease?

A

Both are, so MAP is more important

MAP = SBP + 2(DBP)/3

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22
Q

Nocturnal Dip

A

Normal drop in blood pressure of 10-20% when sleeping

  • if this doesn’t happen (i.e sleep apnea/being black) there is a higher risk of CV events.
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23
Q

White coat HTN

A

BP naturally goes up when people know they are being monitored in the office

Because of this, 24-hr monitoring is the best source for determine BP

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24
Q

Masked HTN

A

Usually young males who have normal BP when in the office but outside of the office they have high BP during daily activities

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25
Q

First choices for Tx of HTN

A

ACE/ARBs/CCB/ diuretics

Most effective diuretic is chlorthalidone*

  • hydrochlorothiazide is more commonly used since cheaper, but is less effective*
  • try to keep to QD dosing (once a day) or less*
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26
Q

Lifestyle treatments

A

Diet low in sodium and high in potassium (DASH)

Recommend aerobic exercise 3-5x wk

Limit ETOH and stress

Get 8 hrs of sleep

27
Q

Tx for HTN in African American populations

A

Usually start w/ diuretics and CCBs

Don’t respond well to ACE inhibitors and ARBs

28
Q

Tx for HTN in patients with migraine

A

Beta Blockers and CCBs are first line

29
Q

Tx for HTN in patients with Gout

A

DONT use diuretics since it increases Uric acid levels

Anything else is okay

30
Q

Tx for HTN in diabetic populations

A

W/ nephropathy = ACE and ARBs

Without nephropathy = ACE ARB and CCBs

  • dont use diuretics much since they raise glucose levels*
31
Q

Measurements for chronic mild/moderate and severe HTN in pregnancy

A

Chronic = known history or HTN for the 1st 20 weeks of gestation

Mild/ moderate = 140-159/90-109

Severe = >160/>110

  • most agencies (especially ACOG) suggest to not treat/ discontinue current HTN drugs unless severe HTN is present (160/110) or greater*
  • this is because these limit blood supply to the placenta and therefore the child
32
Q

ACOGs definition of Pre-eclampsia

A 
Severe HTN (>160/>110) w/ any of the following 
1) platelet leaves <100K

2) liver enzymes 2x normal level
3) serum creatine levels are double normal level
4) Serve RUQ pain
5) Pulmonary edema
6) Visual dysfunctions starting along side pregnancy

33
Q

Lifestyle Tx for HTN in pregnancy

A

DASH diet and cutting off tobaccos/alcohol w/ mild exercise

DONT use low salt or weight loss recommendations

This is used in mild-severe HTN, but meds are only used in Severe HTN

34
Q

HELLP syndrome

A

Hemolysis

Elevated Liver enzymes

Low Platelets

When these symptoms arise, can be considered a subset of severe pre-eclampsia that can develop eclampsia

30% mortality rate and needs to be treated w/ magnesium sulfate, IV HTN drugs and corticosteroids

35
Q

Antihypertensives safe for pregnancy

A

Beta blockers (except for atenolol which causes growth retardation)

Centrally acting agents (a-methyldopa)

CCBs

DONT USE ACEIs/ARBs, NITROPRESSIDE AND SPIRONOLACTONE

36
Q

Is the majority of pediatrics HTN primary or secondary?

A

Primary now due to rising obesity and type 2 diabetes

37
Q

Hypertensive crisis

A

HTN emergency and urgency

Urgency: Categorized as severe HTN without end organ damage

  • SBP > 180 and/or DBP > 110mmHg
  • NO acute end organ injury
  • more common in men

Emergency: categorized as severe HTN with end organ damage
- can’t envelop malignant HTN (HTN that is widespread and affects at least 3 organs)

38
Q

Most common systems affected in “end-organ” damage during HTN emergency

A

Cerebral and cardiac

Includes the one or more of the following:

1) stroke
2) vascular dementia (silent strokes)
3) chronic kidney disease/ ESRD
4) MI
5) LVH
6) CHF
7) Aortic aneurysm
8) retinopathy and retinal artery thrombosis

39
Q

Treatment of HTN emergency

A

Follow PEARLS protocol
- lower BP SLOWLY (prevent hypotension and increased baroreflex)

  • 3 exceptions to this*
  • eclampsia
  • ischemic/hemorrhagic stroke
  • aortic dissection
40
Q

Tx for HTN emergency in aortic dissections

A

Lower HR to under 60 bpm immediately and SBP under 120 within 20 min
- usually IV beta blocker then nitroprusside or Nicardipine

41
Q

Tx for HTN of hemorrhagic stokes

A

Aggressively lower SBP to 140-160 within 2 hrs

Spontaneous intracranial hemorrhagic stoke occurs if SBP is 220 mmHg or higher

42
Q

Broad definition of HTN

A

> 130 SBP

> 80 DBP

43
Q

How has the prevelance of HTN changed from 2000-2017?

A

All areas have gotten worse except for canada

44
Q

Are there gender disparities for HTN?

A

Generally no, however men do have slightly higher incidence rates

45
Q

How has HTN guidelines changed?

A

Before 2017:

  • HTN = > 140/90
  • 25-30% of population

After 2017 (NOW)

  • HTN = > 130/80
  • > 140/90 is now equivalent to Stage 2 HTN
  • 46% of population
46
Q

What three organizations dont adhere to the new 2017 HTN guidelines?

A

AAFP, ACP and European Union

47
Q

“A” causes for 2nd HTN

A

Improper accuracy of measurement

Aldosteronism

Sleep apnea (MOST COMMON)

48
Q

“B” causes for 2nd HTN

A

Bruits

Bad kidneys

49
Q

“C” causes for 2nd HTN

A

Catecholamines

Coarctation of aorta

Cushing’s syndrome

50
Q

“D” causes for 2nd HTN

A

Improper drug use

Diet (increased salt/alcohol consumption, decreases activity levels)

51
Q

“E” causes for 2nd HTN

A

Erythropoietin (blood doping)

Endocrine

52
Q

How do ACE inhibitors and ARBs cause renal function to decline in renal artery stenosis?

A

Blocks angiotensin 1 -> angiotensin 2 conversion

Prevents glomerulus from maintaining pressure = poor kidney perfusion (poor filtration since the fluid does not stay in the glomerulus long enough)

53
Q

Cushing syndrome explanation

A

Excess cortisol production due to tumors on the adrenal gland or pituitary gland (most common).
- pituitary gland tumor: causes overproduction of ACTH

Leads to resistant HTN, obesity, elevated glucose levels, easy bruising and osteoporosis.
- shows really prominent stretch mark lines (striae) in the stomach and breasts.

More common in 20-40 year olds and females vs males.

54
Q

Cushing disease vs syndrome

A

Syndrome = Cushing disease caused by a multitude of reasons

  • caused by direct overproduction of cortisol due to adrenal gland tumors
  • less common

Disease = Cushing disease caused by genetics only.

  • is caused by over production of ACTH in the pituitary which leads to overproduction of cortisol is the adrenal glands
  • more common
55
Q

Erythropoietin causes HTN how?

A

Stimulates over production of erythrocytes in the blood which jacks up blood viscosity.

  • illegal blood doping is an example of this.
  • even more common in chronic renal failure

testosterone supplementation can also cause the same thing

56
Q

What are examples of endocrine issues that can cause HTN?

A

Hyper/hypothyroidism

Hyper-parathyroidism

Acromegaly: growth hormone excess

Cushing’s syndrome

57
Q

Physcial exam specifics for HTN patients

A

Question compliance

Confirm readings of HTN (2-3 measurements)

Check optic discs for hypertensive retinopathy

Check for cardiac murmurs or peripheral bruits

Palpate the thyroid (check for tenderness, enlargement and nodules

Check peripheral pulses

Breif neuro exam checking for visual or cognitive changes

58
Q

Labs to order in evaluating primary HTN

A

Chem panel (w/ fasting)

CBC

Lipid panel

TSH panel

UA

EKG

59
Q

Labs to order for suspicion of secondary HTN

A

BNP and possible echos

Aldosterone/renin ratio (aldosteronism)

Urinary catecholamines

Sleep studies

cortisol panel

MRI angiogram or renal arteries

60
Q

Tx for HTN in patients with chronic kidney disease

A

ACE inhibitors and ARBs

  • DONT use diuretics
61
Q

Tx for HTN in patients with coronary artery disease

A

BBs first line after the MI

ACE/ARBs for stable CAD or only Left ventricular heart failure

  • add thiazides diuretics or dihydropyridine if treatment is a failure at first*
62
Q

4 types of HN in pregnant patients

A

1) Chronic HTN
- cause with known history of HTN or is present during the 1st 20 weeks of gestation

severe is classified as >160mmHg/ > 110mmHg

2) pre-eclampsia or eclampsia only
- HTN with increased renal/liver enzymes in the blood
* eclampsia is w/ seizures*

3) pre-eclampsia/eclampsia superimposed on chronic HTN

4) gestational HTN
- new HTN developing >20 was

63
Q

Treatment of HTN in patients with chronic kidney disease

A

ACEIs and ARBs are 1st line therapy

64
Q

Treatment of HTN in patients with coronary artery disease

A

If MI is present: BBs

If stable ACD or LV heart failure: ACEIs and ARBs

can add thiazides if the above uses dont solve the HTN

Cardiology (46 decks)

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