Question 1

Define HTN

Accepted Answer

SBP > 140mmHg and DBP >90mmHg.

Any condition requiring antihypertensive RX

Question 2

Classification & Etiology of HTN

Accepted Answer

Essential- 90%. due to unknown cause.
Secondary-Renovascular, 
    Pheochromocytoma,
    Cushing’s syndrome,
    Primary aldosteronism,
    Coarctation of aorta,
    Obstructive sleep apnea,
    Parathyroid disease,
    Thyroid disease,
    Drugs

Question 3

Drugs that causes HTN

Accepted Answer

Steroids & OCP but HRT ok,
 OTC - NSAIDS&
               Decongestants,
Illicit -Cocaine, 
           Alcohol,
           Liquirce (chewable tobacco),
           St. John’s wort,
Erythropoietin,
Cyclosporine, tacrolimus,
TCA, 
Venlafaxine,
MAOI

Question 4

Hemodynamic definition of HTN

Accepted Answer

BP = CO x TPR ie,
Blood pressure = (stroke volume × heart rate) × peripheral resistance.
stroke volume (SV) is determined by venous return (VR), end diastolic volume and cardiac contractility. 

 CO= Volume / mit, CI= co/m2 or body surface area,
Stro

Question 5

Pathophysiology

Accepted Answer

Increased sympathetic activity,
Overproduction of sodium retaining hormones (ANG II and aldosterone),
Overproduction of vasoconstrictors (  ANG II, endothelin-1),
Underproduction of vasodilators(ex. NO, prostacyclin, & natriuretic peptide).

Question 6

Vasoconstriction caused by

Accepted Answer

increased  O2,
         sympathetic,
         Angio 2,
          Vasopresin,
          Endothelin,
         Ecosanoids (PGF2,
                              TXA2,
                                  Leukotriens)
          cold.
decreased CO2.

Question 7

Vasodilation is caused by.

remember BNP increased in fluid overload/ increased preload and measured in cardiogenic shock

Accepted Answer

decreased O2,
      Sympathetic flow.
Increased CO2,
    Nitric oxide,
    Ecosanoids (PGE2,PGI2),
    Histamin,
   Natriutetic peptide(ANP and BNP),
   Heat.

Question 8

Define Mean arterial pressure (MAP) 

know the normal value (90-110) & target value (>65)

Accepted Answer

average pressure throughout the cardiac cycle of contraction.

 During cardiac cycle 2/3 of the time is spent in diastole and 1/3 in systole.

Estimate of MAP: MAP=1/3(SBP)+2/3(DBP).CO x SVR or after load. Low MAP show hypoperfusion of organ.

Question 9

Pulse pressure

Accepted Answer

difference between SBP and DBP.

 indicator of arterial wall tension/ arterial “stiffness” (arteriosclerosis and/or atherosclerosis).

  can predict cardiovascular risk (isolated systolic hypertension).

Question 10

Short term regulation of BP

Accepted Answer

1.Baroreceptor-Strech receptor- in^adr & decre. ACH.

2.Chemoreceptor ( decre. O2 & PH, Incre. CO2,de^ BP) - In^ sympathy & decre.ACH to in^ BP.

3.adrenal medulla- in^ sympathy.

4.CNS ischemia  - decre. O2  few min- vasomotor stimulation - in^ adr

Question 11

Long term regulation of BP

Accepted Answer

1.Renin angio alodosterone system.
2.Vasopressin ADH.
3.fluid shift.
4.Natriuretic peptide ANP & BNP ( level of BNP shows fluid overload in HF).
5.Stress relaxation.

Question 12

CVD Risk Factors - Framingham CV risk score 10% or more

Accepted Answer

Hypertension,
Cigarette smoking,
Obesity,
Physical inactivity,
Dyslipidemia,
DM,
Microalbuminuria or estimated GFR <60 ml/min,
Age (older than 55 for men, 65 for women),
Family history of premature CVD 
	(men under age 55 or women under age 65)

Question 13

Diagnosis

Accepted Answer

2 or more properly measured  BP readings from 2 or more clinical encounters.

 rest - 5 min.
No caffeine or tobacco within prior 30 min.
Arm bared and supported at heart level.
cuff size appropriate.
rpt after 2 min if more than 5 mmHg differ.

Question 14

Symptoms

Accepted Answer

Asymptomatic.

Signs/symptoms of Target organ damage-  
    1.Brain- TIA, stroke,
    2.Eye- retinopathy ,
   3. Heart-CHF,LVH, CAD,angina, MI, 
    4.Kidney- CKD,
   5. Peripheral vasculature- PAD.

Question 15

Goals of therapy and Goal BP

Accepted Answer

reduce EOD.JNC 8<140/90- age < 60 years or DM or CKD.
 <150/90 for  age ≥ 60 years. <140/80 mmHg for DM (ADA ).
 <130/80 mmHg for DM,CKD, CAD(Framingham)score >10%).
<120/80 mmHg LVH -AHA.
<140/90 CKD no protetin urea.
<130/80 with protein - KDIEGO.

Question 16

Treatment - pharmacologic & non pharmacologic

Accepted Answer

Life style modification,
Antihypertensive RX.

Question 17

Life style modification

Accepted Answer

Weight reduction,

Reduce dietary fat and cholesterol,

DASH diet,

Reduce dietary Na- No more than 1.5gm Na in severe restriction ( normal<2.3gm Na) or 6gm NaCl per day)

Increase aerobic exercise,

Limit EtOH.

Question 18

Drug Therapy - initial

Accepted Answer

Initial Therapy-Use of lifestyle modifications, 
thiazide diuretics in non–African American patient,
CCBs /thiazide diuretics in African American,
 ACEIs or ARBs if CKD.

Question 19

Drug Therapy - if not controlled by initial

Accepted Answer

Aldosteron Antagonist, Beta blockers,  direct vasodilators, α1-receptor antagonists,  central α2-receptor agonists, and postganglionic adrenergic neuron blockers,direct renin inhibitors

Question 20

Hypertensive Emergecy

Accepted Answer

Severe elevation in BP > 180/120 with acute TOD .
Treat initially with IV agents to decre. MAP by 25% with in min to hr. and 160/100 in 2-6 hr. goal BP in 1-2 days.

Question 21

Hypertensive Urgency

Accepted Answer

Severe elevation in BP without acute TOD. 
immediate lowering of BP not required.
treated outpatient with PO combination- AVOID nifedipine SL.
Onset of action 15-30 min peak 2-3 hr.

CVS - HTN pathophys

HTN pathophysiology & Treatment

Question	Answer
Define HTN	SBP > 140mmHg and DBP >90mmHg. Any condition requiring antihypertensive RX
Classification & Etiology of HTN	Essential- 90%. due to unknown cause. Secondary-Renovascular, Pheochromocytoma, Cushing’s syndrome, Primary aldosteronism, Coarctation of aorta, Obstructive sleep apnea, Parathyroid disease, Thyroid disease, Drugs
Drugs that causes HTN	Steroids & OCP but HRT ok, OTC - NSAIDS& Decongestants, Illicit -Cocaine, Alcohol, Liquirce (chewable tobacco), St. John’s wort, Erythropoietin, Cyclosporine, tacrolimus, TCA, Venlafaxine, MAOI
Hemodynamic definition of HTN	BP = CO x TPR ie, Blood pressure = (stroke volume × heart rate) × peripheral resistance. stroke volume (SV) is determined by venous return (VR), end diastolic volume and cardiac contractility. CO= Volume / mit, CI= co/m2 or body surface area, Stro
Pathophysiology	Increased sympathetic activity, Overproduction of sodium retaining hormones (ANG II and aldosterone), Overproduction of vasoconstrictors ( ANG II, endothelin-1), Underproduction of vasodilators(ex. NO, prostacyclin, & natriuretic peptide).
Vasoconstriction caused by	increased O2, sympathetic, Angio 2, Vasopresin, Endothelin, Ecosanoids (PGF2, TXA2, Leukotriens) cold. decreased CO2.
Vasodilation is caused by. remember BNP increased in fluid overload/ increased preload and measured in cardiogenic shock	decreased O2, Sympathetic flow. Increased CO2, Nitric oxide, Ecosanoids (PGE2,PGI2), Histamin, Natriutetic peptide(ANP and BNP), Heat.
Define Mean arterial pressure (MAP) know the normal value (90-110) & target value (>65)	average pressure throughout the cardiac cycle of contraction. During cardiac cycle 2/3 of the time is spent in diastole and 1/3 in systole. Estimate of MAP: MAP=1/3(SBP)+2/3(DBP).CO x SVR or after load. Low MAP show hypoperfusion of organ.
Pulse pressure	difference between SBP and DBP. indicator of arterial wall tension/ arterial “stiffness” (arteriosclerosis and/or atherosclerosis). can predict cardiovascular risk (isolated systolic hypertension).
Short term regulation of BP	1.Baroreceptor-Strech receptor- in^adr & decre. ACH. 2.Chemoreceptor ( decre. O2 & PH, Incre. CO2,de^ BP) - In^ sympathy & decre.ACH to in^ BP. 3.adrenal medulla- in^ sympathy. 4.CNS ischemia - decre. O2 few min- vasomotor stimulation - in^ adr
Long term regulation of BP	1.Renin angio alodosterone system. 2.Vasopressin ADH. 3.fluid shift. 4.Natriuretic peptide ANP & BNP ( level of BNP shows fluid overload in HF). 5.Stress relaxation.
CVD Risk Factors - Framingham CV risk score 10% or more	Hypertension, Cigarette smoking, Obesity, Physical inactivity, Dyslipidemia, DM, Microalbuminuria or estimated GFR <60 ml/min, Age (older than 55 for men, 65 for women), Family history of premature CVD (men under age 55 or women under age 65)
Diagnosis	2 or more properly measured BP readings from 2 or more clinical encounters. rest - 5 min. No caffeine or tobacco within prior 30 min. Arm bared and supported at heart level. cuff size appropriate. rpt after 2 min if more than 5 mmHg differ.
Symptoms	Asymptomatic. Signs/symptoms of Target organ damage- 1.Brain- TIA, stroke, 2.Eye- retinopathy , 3. Heart-CHF,LVH, CAD,angina, MI, 4.Kidney- CKD, 5. Peripheral vasculature- PAD.
Goals of therapy and Goal BP	reduce EOD.JNC 8<140/90- age < 60 years or DM or CKD. <150/90 for age ≥ 60 years. <140/80 mmHg for DM (ADA ). <130/80 mmHg for DM,CKD, CAD(Framingham)score >10%). <120/80 mmHg LVH -AHA. <140/90 CKD no protetin urea. <130/80 with protein - KDIEGO.
Treatment - pharmacologic & non pharmacologic	Life style modification, Antihypertensive RX.
Life style modification	Weight reduction, Reduce dietary fat and cholesterol, DASH diet, Reduce dietary Na- No more than 1.5gm Na in severe restriction ( normal<2.3gm Na) or 6gm NaCl per day) Increase aerobic exercise, Limit EtOH.
Drug Therapy - initial	Initial Therapy-Use of lifestyle modifications, thiazide diuretics in non–African American patient, CCBs /thiazide diuretics in African American, ACEIs or ARBs if CKD.
Drug Therapy - if not controlled by initial	Aldosteron Antagonist, Beta blockers, direct vasodilators, α1-receptor antagonists, central α2-receptor agonists, and postganglionic adrenergic neuron blockers,direct renin inhibitors
Hypertensive Emergecy	Severe elevation in BP > 180/120 with acute TOD . Treat initially with IV agents to decre. MAP by 25% with in min to hr. and 160/100 in 2-6 hr. goal BP in 1-2 days.
Hypertensive Urgency	Severe elevation in BP without acute TOD. immediate lowering of BP not required. treated outpatient with PO combination- AVOID nifedipine SL. Onset of action 15-30 min peak 2-3 hr.

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