Large Group 2 Flashcards

1
Q

What things can contribute to Essential HTN?

A

Increased Intravascular Volume

Up-regulation of the sympathetic nervous system

Increased RAAS activity

Increased vascular function from vascular disease

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2
Q

What things do we want to check in a pt with HTN?

A

Renal: UA, albumin excretion, serum creatinine

Endocrine: serum sodium, LDL, HDL, Triglycerides, thyroid function, fasting glucose

EKG, Hematocrit, CBC, chem panel

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3
Q

Where does most Na+ intake come from? What is Na+ intake correlated with? What is the goal Na+ intake/day?

A

processed and restaurant foods

Left ventricular mass

goal: <2.3g/day

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4
Q

Is HTN more prevalent among men or women? Does this change with age.

A

yes

Before age of 55 HTN prevalence men > women after 55 women > men

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5
Q

What is the goal for a pre-HTN pt?

A

get the BP as low as can –> no set number

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6
Q

What can uncontrolled HTN lead to?

A
end organ damage!! 
CVA 
retinopathy 
vascular disease 
nephropathy 
heart disease
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7
Q

How is the risk for Coronary Artery Disease affected by BP?

A

each increment of 20/10 DOUBLES the risk of CAD across the entire BP range (starting at 115/75)

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8
Q

What is the treatment for stage 2 HTN?

A

2 drug combination

usually thiazide diuretic and ACEI or ARB or BB or CCB

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9
Q

Are beta blockers one of the preferred treatments in pts without CHF or CAD?

A

NO

use of thiazides, ACEIs, ARBs, CCBs are preferred

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10
Q

What is Conn’s syndrome? What are the symptoms? how is it diagnosed?

A

hyperaldosteronism

symptoms: HTN, hypokalemia, Na+/H2O retention (due to expression of ENaC), metabolic alkalosis

•PAC (plasma aldosterone concentration) and PRA (plasma renin activity) elevated
•Aldo/Renin > 30
•Serum aldosterone > 15 ng/dL
•Confirm w/ salt load and 24 hours urine Na+ (>200) and ALDO (>12)
-High-resolution CT –> determine adrenal adenoma (surgery) or bilateral hyperplasia (medical therapy–> spiranolactone or eplerenone)
•Adrenal vein sampling (determine between hyperplasia and adenoma)

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11
Q

What is the preferred tx of HTN in African descent without CKD?

A

CCB or thiazides

has to do with salt sensitivity

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12
Q

When should you follow up with a pt with pre-HTN? Stage 1? Stage 2? BP >180/110?

A
normal=2 years
pre-HTN=1 year
Stage 1=2 months confirm 
Stage 2=1 month 
BP >180/110=evaluate and treat immediately or within 1 week
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13
Q
55 yo female present for annual visit. BP 150/95 and begins therapy for HTN and gets a cough. The drug that most likely caused this is: 
A. captopril
B. clonidine 
C. hydralazine
D. nifedipine 
E. propranolol
A

A. captopril

ACE Inhibitor

cough due to the increase in bradykinin

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14
Q

What are potential causes of secondary HTN?

A

Conn’s syndrome

sleep apnea

renal artery stenosis (cut off blood supply–> increase in RAAS)

polycystic kidney disease

liddle’s syndrome

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15
Q

What are potential causes of secondary HTN?

A

Conn’s syndrome

sleep apnea

renal artery stenosis (cut off blood supply–> increase in RAAS)

polycystic kidney disease

liddle’s syndrome

Cushings

pheochromocytoma (HA< palpitations, diaphoresis)

thyroid dysfunction

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16
Q

What tests should be ordered if secondary HTN is suspected?

A

Aldo/Renin
-Aldo/Renin > 30
+
-Serum aldosterone greater than 15 ng/dL.

MRA vs. US with doppler (for Renal Artery stenosis)

24 hr urine fractionated metanephrines + chatecholamines

  • For suspected Pheochromocytoma
  • Patients present with the Triad: Headache, Diaphoresis, and Palpitations.

Sleep study

17
Q
52 yo male w/uncontrolled HTN. BP 195/105. Brachial A pulses=symmetrical. Elecated serum creatinine, BUN and AG II. Treated with ACE Inhibitor or 2 days and BP decrease to 135/85. causes renal function to worsen. Further testing leads to treatment of a stent placement of renal arteries. Normalizes blood pressure and returns the kidney function to normal
Most likely dx is:
1. coarctation of the aorta 
2. essential HTN 
3. pheochromocytoma
4. renal A stenosis 
5. renin-secreting tumor
A
  1. renal A stenosis
18
Q

Treament with the ACE Inhibitor will most likely cause increased serum levels of:

  1. aldosterone
  2. AG II
  3. Epinephrine
  4. norepinephrine
  5. renin
A
  1. renin
19
Q

What is hypertensive urgency? how is this treated? How is this different from HTN emergency?

A
  • Subacute rise in blood pressure >180/110
  • No evidence of end organ damage
  • manage in 24-48 hours

-can be treated with oral meds: Captopril
Nicardipine or Nifedipine
Labetalol

-HTN emergency if there is end organ damage

20
Q

What are some findings with hypertensive emergency? How should these pts be managed?

A

BP>180/120
symptoms:
Retinal hemorrhages, exudates, and papilledema
Acute pulmonary edema, left ventricular failure (CHF)
Headache, nausea, vomiting, CNS (lacunar infarcts,, intra-cerebral bleed, cortical blindness, seizures, coma, and death)
Acute Kidney Injury; 2˚ to thrombotic microangiopathy

keep in the ICU

21
Q

What is the preferred treatment for hypertensive emergency?

A

depends on system affected

  • neuro: Nitroprusside
  • cardiac: NTG
  • autonomic:Phentolamine (Pheo)
  • vascular: Esmolol+NTP
  • renal: Fenoldepam
  • OB: Hydralazine, MgSO4

post-op: Esmolol

22
Q

What is the preferred treatment for hypertensive emergency?

A

IV meds! type depends on system affected

  • neuro: Nitroprusside
  • cardiac: NTG
  • autonomic:Phentolamine (Pheo)
  • vascular: Esmolol+NTP
  • renal: Fenoldepam
  • OB: Hydralazine, MgSO4

post-op: Esmolol

23
Q

What is resistant HTN?

A
  • Office BP >140/90 or 130/80 mm Hg in patients with DM or chronic kidney disease and
  • Patient prescribed 3 or more antihypertensive medications at optimal doses, including if possible a diuretic or
  • Office BP at goal but patient requiring 4 or more antihypertensive medications.
24
Q

What is the algorithm for managing resistant HTN?

A
  • Confirm treatment resistance based on resistant HTN diagnosis criteria.
  • Exclude Pseudo-resistance: patient doesn’t take their meds.
  • Identify any contributing lifestyle factors (obesity, no exercise, etc.)
  • Reduce interfering drugs and other substances
  • Screen for secondary causes of hypertension.