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GI and Renal Exam 1 > 16 - Hypertension and Renal Artery Stenosis > Flashcards

16 - Hypertension and Renal Artery Stenosis Flashcards

1
Q

What do the kidneys do?

A
  • Filter waste
  • Hormone production (Vit D, erythropoetin)
  • BP control
  • Electrolyte balance
  • Water balance
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2
Q

What happens when the kidneys fail?

A
  • Electrolyte imbalances (phos gets high, potassium high, calcium low)
  • Anemia
  • Blood pressure irregularities
  • Meds hang around
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3
Q

Describe the relationship between hypertension and renal disease

A
  • Hypertension leads to renal disease

- Renal disease leads to hypertension

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4
Q

Give an example of a HTN case

A

60 y/o male known HTN, hasn’t been treating HTN, BP 220/110 “feels funny”

  • EKG left ventricular hypertrophy due to long-term HTN
  • Cr 16 (nml .6-1.2 – dialysis about 5)
  • Kidneys have failed
  • BP almost impossible to move because kidneys were not responding to meds
  • Sent to DSM – found likely autoimmune renal issue
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5
Q

Describe the prevalence of HTN in the US

A
  • 1 in 3 US adults have hypertension
  • > 1 in 2 adults over 60 have hypertension

With our culture, this will only increase

  • Increasing body weight
  • Decreasing activity levels (
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6
Q

What are the JNC 8 recommendations?

** KNOW FOR EXAM **

A

Recommendation

> or = 60 years (18 years with CKD (18 years with diabetes (

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7
Q

What do you need to do if you have a hypertensive patient?

A
  • Need to assess risk factors, co-morbidities and secondary causes – and start treatment
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8
Q

What are the risk factors for hypertension?

A
  • Age
  • Smoking
  • DM
  • High lipids
  • Inactivity/weight
  • Family history
  • Race
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9
Q

What are the secondary causes of hypertension?

A
  • Sleep apnea
  • Primary hyperaldosteronism (low K, htn resistant)
  • CRF
  • Thyroid
  • Renal vascular disease
  • Pheochromocytoma
  • Cushings or steroid therapy
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10
Q

What is the “new thing” that we look for in hypertensive patients?

A
  • Primary Hyperaldosteronism – Diagnose with a high aldosterone/renin ratio – their K will often be low
  • Consider in patients with resistant hypertension and a low potassium
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11
Q

When should you suspect a secondary cause?

A
  • Age extremes (very young or old)
  • Severity
  • Lack of family history
  • Does not respond to treatment
  • Sleep apnea
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12
Q

What tests should be run when you are diagnosed with hypertension?

A
  • EKG
  • UA
  • BMP
  • TSH
  • H&H
  • Ca
  • Cholesterol

This would help you to rule out

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13
Q

Describe the lifestyle changes that can make a difference

A
  • Wt reduction of 10 kg (5-20 mm)
  • Na restriction (2-8 mm)
  • Physical activity (4-9 mm)
  • Low fat/high veggie diet (8-14)

** Weight reduction is found to be the MOST effective **

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14
Q

Describe the Calcium Channel Blockers (CCBs) for the treatment of HTN

A

Not used much anymore

  • Decreases calcium influx into smooth and cardiac cells
  • Edema
  • Arrhythmias
  • Some lead to CHF

Not as popular as previously was; CHF plus no decrease in mortality

Short term CCB not recommended anymore

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15
Q

Describe beta blockers for the treatment of HTN

A
  • Beta blockers – antagonizes beta adrenergic receptors
  • Dizzy/syncope
  • Fatigue
  • Low HR***
  • Impotence
  • Makes working out difficult

Very effective; always used in MI or CAD

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16
Q

Describe the ACE inhibitors

A

Used in DM (regardless of BP) CHF and post MI – many beneficial effects

  • Decreases all CV causes of death in DM II
  • Think increases flexibility of vessels
  • Causes cardiac remodeling (repair)
17
Q

What are the side effects of ACE inhibitors?

A
  • Increases K
  • Angioedema (.2%, Asians/Blacks 3-4X more likely)
  • Cough (>8%)
  • Increase Creatinine
18
Q

Describe the increase in creatinine

A
  • Can increase 30% before stop or big w/u

- Small increase means intraglomular pressure has been reduced

19
Q

Describe the treatment of HTN with thiazides

A

Thiazides - inhibits NaCl reabsorption

Side effects

  • K/Na reduction
  • Renal damage
  • Increased glucose, Ca+

Back in favor; cheap, few side effects, decreases mortality.

Will see more Chlorthiadone (same dose as HCTZ)

20
Q

Further describe the JNC 8 recommendations for medications

A

General nonblack population (thiazides, CCB, ACEi or ARB)

General black population (thiazides or CCB initially)

Chronic kidney disease
(treatment should include ACEi or ARB)

Up-titrate or add therapy after 1 month if BP goal is not met

  • Do NOT use ACEi and ARB together
  • If 3 or more drugs are needed, refer to hypertension specialist
21
Q

Describe the use of ARBs in the use of treating HTN

A
  • Block angiotensin II at the receptor
  • Many similar effects as ACE – not as well studied
  • Pt not to be on both ACE and ARB
22
Q

What other medication can be used for HTN?

A

Clonidine
– alpha 2 agonist (centrally acting)
– fast acting, pts can titrate
– can have rebound

23
Q

Describe polypharmacy for HTN

A
  • The large majority of people require 2 or 3 or more meds.

- If >160/100 to start, just start 2 meds

24
Q

What is the “take away”

A
  • Beta Blockers are NOT first line (unless post MI)
  • Whites – start almost anything else (Thiazides, ACE/ARB, CCB)
  • Blacks – avoid ACE (know why - chance of angioedema is 3-4x higher than whites)
  • Diabetics/CRF – ACE
  • Post MI/CVA – beta blocker/ACE
  • CHF – Beta Blocker + ACE, plus thiazide plus spiranolactone
25
Q

Describe hypertensive emergencies

A
  • “malignant hypertension”
  • Any increase in BP that results in acute end organ damage

Still want to lower BP SLOWLY

26
Q

What type of organ damage do we see?

A
  • Encephalopathy, stroke, chf, aortic dissection, MI, ARF

- Nosebleed

27
Q

What is a hypertensive urgency?

A
  • > 180 or >110
  • No symptoms or vague symptoms
  • Disagreement in how urgent treatment needs to be; what is their normal?
  • Tricky to treat in ER – do you start them on something at d/c? What if incidental finding?
  • Titinilli (ER Text) says d/c and lower over 24-48 hrs
  • You can send them home and have them come back the next day for a BP check
28
Q

What do you need to remember about treating HTN?

A

Shouldn’t drop BP too quickly

29
Q

Describe renal artery stenosis

A
  • When renal arteries are constricted to the point that the kidneys have a decreased blood flow.
  • Kidney thinks body is hypovolemic and secretes renin which increases BP
30
Q

What should you suspect renal artery stenosis?

A
  • Doesn’t respond to treatment
  • Intermittent claudication
  • Sudden worsening of HTN
  • Image abnormality
  • ACE leads to worsening creatinine
31
Q

What is the risk for renal artery stenosis?

A
  • HTN
  • Obesity
  • Vascular disease of any kind
  • Age
  • Smoking
  • Anything that increases risk of vascular problems anywhere else
32
Q

What causes renal artery stenosis?

A
  • Usually caused by atherosclerosis (older)
  • Also due to fibromuscular dysplasia (younger)
  • Problems occur at 70% blockage
33
Q

What happens to the kidneys if renal artery stenosis is uncontrolled?

A
  • Affected kidney gets small, ischemic (Ischemic nephropathy)
  • Other kidney gets injured from the increased BP (hypertensive nephrosclerosis)
34
Q

What is the treatment for renal artery stenosis?

A
  • Angioplasty – often wont last
  • Stent – sometimes wont last
  • Bypass
  • Nephrectomy if affected kidney very damaged
35
Q

What is fibromuscular dysplasia?

A
  • A specific type RAS
  • Angiopathy of medium sized vessels; mainly seen in women of childbearing age.
  • Seems to increase just before menopause
  • Genetic link as well
  • Symptoms occur where artery occluded (brain, periphery – kidneys mainly)
  • Rare – less than 1% of population
36
Q

How do you treat fibromuscular dysplasia?

A

Angioplasty or stent

GI and Renal Exam 1 (16 decks)

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