SlideShare a Scribd company logo
1 of 44
Download to read offline
HYPERTENSION
Evaluation of Hypertension - 2
Mohammad Ilyas, M.D.
Assistant Clinical Professor
University of Florida / Health Sciences Center
Jacksonville, Florida USA
1
Outline
1. Definition, Regulation and Pathophysiology
2. Measurement of Blood Pressure, Staging of Hypertension and Ambulatory Blood
Pressure Monitoring
3. Evaluation of Primary Versus Secondary
4. Sequel of Hypertension and Hypertension Emergencies
5. Management of Hypertension (Non-Pharmacology versus Drug Therapy)
6. The Relation Between Hypertension: Obesity, Drugs, Stress and Sleep Disorders.
7. Hypertension in Renal diseases and Pregnancies
8. Pediatric, Neonatal and Genetic Hypertension
2
Types of Hypertension
• Primary HTN:
• >95% cases of HTN in adult
• Cause Unknown.
• Multiple risk factors: including age,
family history, genetics, race,
environment etc…
• Secondary HTN:
• < 5% HTN in adult are secondary
• Secondary to other potentially
rectifiable causes.
• Often overlooked & under screen
3
Secondary HTN
Overview
• Testing for secondary HTN can be expensive and requires high
index of clinical suspicion.
• General principles:
• New onset HTN if <30 or >50 years of age
• HTN refractory to medical Rx (>3-4 meds)
• Specific clinical/lab features typical for dz :
4
Causes of Secondary HTN
• Common
1. Intrinsic renal disease
2. Renovascular disease
3. Mineralocorticoid excess
4. Sleep Breathing disorder
• Uncommon
1. Pheochromocytoma
2. Glucocorticoid excess
3. Coarctation of Aorta
4. Hyper/hypothyroidism
5
1. Renal Parenchymal Disease
• Common cause of secondary HTN (2-5%)
• HTN is both cause and consequence of renal disease
• Multifactorial cause for HTN including disturbances in Na/water balance,
vasodepressors/ prostaglandins imbalance
• Renal disease from multiple etiologies.
6
2. Renovascular HTN
•Incidence 1-3%
•Etiology
•Atherosclerosis 75-90% (elder)
•Fibromuscular dysplasia 10-25%
(younger)
•Other
•Aortic/renal dissection
•Takayasu’s arteritis
•Thrombotic/cholesterol emboli
•CVD
•Post transplantation stenosis
•Post radiation
7
Renovascular HTN – History
• History
• Onset HTN age <30 or >55
• Negative FH of HTN
• Sudden onset uncontrolled HTN in previously well controlled
patient
• Accelerated/malignant HTN
• Intermittent pulmonary edema with normal LV function
8
Renovascular HTN - Clinical
• Clinical exam. /Lab. findings
• Epigastric bruit, particularly systolic/diastolic
• Advanced fundal changes, grade III/IV retinopathy
• Azotemia induced by ACEI, ARBs or diuretics
• Paradoxical worsening of HTN with diuretics
• Secondary aldosteronism : ↑ plasma renin & ↓ s. Na & K
• Unilateral small kidney, difference >1.5cm, on sonography
9
Renovascular HTN – Diagnostic studies
• Physical findings (bruit)
• Duplex U/S
• Captopril renography
• Magnetic Resonance Angiography
• Renal Angiography
10
Fibromuscular dysplasia Atherosclerotic RAS
• Fibromuscular dysplasia
• 10-25% of all RAS
• Young female, age 15-40
• Medial disease 90%, often
involves distal RA
• Atherosclerotic RAS
• 75-90% of RAS
• Usually men, age >55,
• Other atherosclerotic
11
RAS screening/diagnostics
Sens Spec Limitation
Bruit 39-65% 90-99%
Insensitive, severe stenosis may be silent
Duplex U/S 90-95% 60-90%
Operator dependent, 10-20%
Captopril
Renography
83-91% 87-93%
Accuracy reduced in pt with renal insufficiency,
lacks anatomical info; good predictor of BP
response
MRA 88-95% 95%
False positive artifact resp, peristalsis, tortuous
vessels; cost
Angiography Gold std Gold std
Invasive, nephrotoxicity, little value in
predicting BP response
12
Fibromuscular Dysplasia, before and after PTRA
Atherosclerotic RAS before and after stent13
3. Primary Aldosteronism
• Primary Aldosteronism, previously felt to be an unlikely cause of secondary
HTP, now is more commonly observed depending on the severity of HTP :
• 8% Stage 2
• 13% of Stage 3 and
• 20% of those with resistant hypertension.
(10th Annual SMA-ASH Carolinas Georgia Chapter Meeting, 2006)
14
Primary Aldosteronism
• Prevalence 0.5- 2.0% (5-12% in referral centers)
• Etiology
• Adrenal adenoma
• Bilateral adrenal hyperplasia, glucocorticoid suppressible hyperaldo, adrenal carcinoma
• Clinical:
• May be asymptomatic.
• Headache, weakness, paralysis, polyuria
• Retinopathy, edema uncommon
• Hypokalemia (K normal in 40%), metabolic alkalosis, high-normal Na
15
Screening for Hyper aldosteronism
• Spontaneous hypokalemia (<3.5 mmol/L).
• Profound diuretic-induced hypokalemia (<3.0 mmol/L).
• Hypertension refractory to treatment with 3 or more drugs.
• Incidental adrenal adenomas.
16
17
4. Pheochromocytoma
• Catecholamine-producing neuroendocrine tumor that arises from
chromaffin cells
• Adrenal Medulla : 80-85% pheochromocytomas
• Extra-adrenal paragangliomas
• Often in head and neck (glomus jugulare) and rarely produce catecholamines.
• Some can be dopamine producing.
18
Epidemiology
• Incidence: 1 in 100,000 each year
• Prevalence among pts with HTP
• In adults – 0.1-0.6%
• In children – 1%
• Traditional rule of 10
• 10% bilateral, 10% familial, 10% extra-adrenal, and 10% malignant.
• Recent reports found 12-24% of sporadic pheochromocytoma with germline mutation.
19
Clinical Presentation
• Paroxysmal attacks of Headache, palpitations, and sweating.
• Adults more often have paroxysmal hypertension (50%).
• Children have sustained hypertension (70-90%).
• 20% of children will be normotensive at diagnosis.
20
Pheochromocytoma – Testing
• Best detected during or immediately after episodes
TEST Sensitivity Specificity
Plasma free metanephrine
>0.66nmol/L
99% 89%
24hr urine metanephrine
(>3.7nmol/d)
77% (95%) 93% (96%)
24 urine VMA 64% 95%
21
Lenders, et al. JAMA 2002 Mar 20;287(11):1427-34
Pheochromocytoma - Diagnosis
• Imaging for localization of tumor
TEST Sens Spec PPV NPV
MIBG scintigraphy
(metaiodobenzylguanidine)
78% 100% 100% 87%
CT Scan 98% 70% 69% 98%
MRI 100% 67% 83% 100%
22
Akpunonu, et al. Dis Month.October 1996, p688
5. Cushing’s syndrome
(Hypercortisolism)
• Rare cause of secondary HTN
(0.1- 0.6%)
• Etiology
• Pituitary micro adenoma,
• Iatrogenic (steroid use),
• Ectopic ACTH,
• Adrenal adenoma
• Clinical
• Sudden weight gain, truncal obesity,
moon faces, abdominal striae,
DM/glucose intolerance, HTN, prox
muscle weakness, skin atrophy,
hirsutism /acne
23
Cushings syndrome
24
Cushings syndrome - diagnosis
• Screen:
• 24 Hr Urine free cortisol
• >90ug/day is 100% sens and 98% spec
• False + in Polycystic Ovarian Syndrome, depression
• Confirm
• Low dose dexamethasone suppression test
• 1mg dexameth. midnight, measure am plasma cortisol (>100nmol is +)
• Other tests include dexa/CRH suppression test
• Imaging
• CT/MRI head (pit) chest (ectopic ACTH tumor)
25
6. Coarctation of Aorta
• Congenital defect, male>female
• Clinical
• Differential systolic BP arms v/s legs (=DBP)
• May have differential BP in arms if defect is prox to L subclavian art
• Diminished/absent femoral art pulse
• Often asymptomatic
• Echo-Doppler, CT angiography, aortography.
26
Coarctation of Aorta
27
Brickner, et al. NEJM 2000;342:256-263
7. Hyperthyroidism
• 33% of thyrotoxic pt develop HTN
• Usually obvious signs of thyrotoxicosis
• Dx: TSH, Free T4/T3, thyroid
28
8. Hypothyroidism
• 25% hypothyroid patient develop HTN
• Mechanism mediated by local control, as basal metabolism falls so
does accumulation of local metabolites; relative vasoconstriction
ensues
29
30
31
Summary
• Screening for 2ry HTN can be expensive and requires clinical suspicion and
knowledge of limitations of different tests
• General principles:
• New onset HTN if <30 or >50 years of age
• HTN refractory to medical Rx (>3-4 meds)
• Specific clinical/lab features typical for dz :
• Hypokalemia in the absence of diuretic therapy may indicate a state of mineralocorticoid excess
• Excess aldosterone production (Conn’s)
• Excess glucocorticoid production (Cushing’s)
• Excess T3 & T4 (hyperthyroidism)
• Epigastric bruits, differential BP in arms, episodic HTN/flushing/palp.
32
Time for quiz !!
Quiz 1. TRUE or FALSE
1. Renal Parenchymal diseases are the common cause of primary HTN.
2. Hypertension is both cause and consequence of renal parenchymal disease.
3. Renal Parenchymal HTN is only due to disturbances in Na/water balance.
4. Renal Vascular disease usualy cause resistive HTN
34
Quiz 1. TRUE or FALSE
1. Renal Parenchymal diseases are the common cause of primary HTN.
FALSE
2. Hypertension is both cause and consequence of renal parenchymal disease.
TRUE
3. Renal Parenchymal HTN is only due to disturbances in Na/water balance.
FALSE
4. Renal Vascular disease usualy cause resistive HTN. TRUE
35
Quiz 2. All of the following studies are helpful in
diagnosis of Renovascular HTN - EXCEPT
A. Urine pH
B. Doppler renal U/S
C. Captopril renography
D. Magnetic Resonance Angiography
E. Renal Angiography
36
Quiz 2. All of the following studies are helpful in
diagnosis of Renovascular HTN – EXCEPT?
A. Urine pH
B. Doppler renal U/S
C. Captopril renography
D. Magnetic Resonance Angiography
E. Renal Angiography
37
Quiz 3. Which of the following statement is not true
about Primary Aldosteronism?
A. May be asymptomatic.
B. Can cause headache, weakness, paralysis, and polyuria.
C. Retinopathy, edema are common finding.
D. Can cause hypokalemia, metabolic alkalosis and high-normal Na.
38
Quiz 3. Which of the following statement is not true
about Primary Aldosteronism?
A. May be asymptomatic.
B. Can cause headache, weakness, paralysis, and polyuria.
C. Retinopathy, edema are common finding.
D. Can cause hypokalemia, metabolic alkalosis and high-normal Na.
39
Quiz 4. Which of the following in NOT true about
Pheochromocytoma?
A. Clinical presentation includes paroxysmal attacks of headache,
palpitations, and sweating.
B. Adults more often have paroxysmal hypertension.
C. Children have sustained hypertension.
D. Majority of children could be normotensive at diagnosis.
E. MIBG scintigraphy (metaiodobenzylguanidine) is diagnostic study
for Pheochromocytoma
40
Quiz 4. Which of the following in NOT true about
Pheochromocytoma?
A. Clinical presentation includes paroxysmal attacks of headache,
palpitations, and sweating.
B. Adults more often have paroxysmal hypertension.
C. Children have sustained hypertension.
D. Majority of children could be normotensive at diagnosis.
E. MIBG scintigraphy (metaiodobenzylguanidine) is diagnostic study
for Pheochromocytoma
41
Quiz 5. Which of the following statement is FALSE
about Coarctation of Aorta?
A. Mostly present as Congenital defect
B. More common in male than female
C. BP in lower extremity is lower than upper extremity
D. Often symptomatic
E. Echo-Doppler, CT angiography, aortography.
42
Quiz 5. Which of the following statement is FALSE
about Coarctation of Aorta?
A. Mostly present as Congenital defect
B. More common in male than female
C. BP in lower extremity is lower than upper extremity
D. Often symptomatic
E. Echo-Doppler, CT angiography, aortography.
43
Mohammad Ilyas MD, FAAP44

More Related Content

What's hot

What's hot (20)

Hypertension management 2018
Hypertension  management 2018Hypertension  management 2018
Hypertension management 2018
 
L3..hypertension
L3..hypertensionL3..hypertension
L3..hypertension
 
Approach to secondary hypertension in young patients
Approach to secondary hypertension in young patientsApproach to secondary hypertension in young patients
Approach to secondary hypertension in young patients
 
GEMC: Hypertensive Urgency and Emergency: Resident Training
GEMC: Hypertensive Urgency and Emergency: Resident TrainingGEMC: Hypertensive Urgency and Emergency: Resident Training
GEMC: Hypertensive Urgency and Emergency: Resident Training
 
Hypertension
HypertensionHypertension
Hypertension
 
Hypertension (HTN)
Hypertension (HTN)Hypertension (HTN)
Hypertension (HTN)
 
management of hypertension
management of hypertensionmanagement of hypertension
management of hypertension
 
Hypertensive emergencies
Hypertensive emergenciesHypertensive emergencies
Hypertensive emergencies
 
Updated management of Hypertension
Updated management of HypertensionUpdated management of Hypertension
Updated management of Hypertension
 
Hypertension
HypertensionHypertension
Hypertension
 
Diagnosis of hypertension
Diagnosis of hypertension Diagnosis of hypertension
Diagnosis of hypertension
 
Hypertension Pro
Hypertension ProHypertension Pro
Hypertension Pro
 
3. research methodology
3. research methodology3. research methodology
3. research methodology
 
Hypertension management for primary health care
Hypertension management for primary health careHypertension management for primary health care
Hypertension management for primary health care
 
Hypertension
HypertensionHypertension
Hypertension
 
Hypertension
HypertensionHypertension
Hypertension
 
Hypertension
Hypertension Hypertension
Hypertension
 
RESISTANT HYPERTENSION
RESISTANT HYPERTENSIONRESISTANT HYPERTENSION
RESISTANT HYPERTENSION
 
Hypertension
Hypertension Hypertension
Hypertension
 
Best Presentation On Hypertension 2018
Best Presentation On Hypertension 2018Best Presentation On Hypertension 2018
Best Presentation On Hypertension 2018
 

Similar to Hypertension evaluation 2

Thrombotic Thrombocytopenic Purpura
Thrombotic Thrombocytopenic PurpuraThrombotic Thrombocytopenic Purpura
Thrombotic Thrombocytopenic Purpura
Shakeel Arif
 
Secondary Hypertension. final.ppt
Secondary Hypertension. final.pptSecondary Hypertension. final.ppt
Secondary Hypertension. final.ppt
AdelSALLAM4
 
Cushingssyndrome 160827080057
Cushingssyndrome 160827080057Cushingssyndrome 160827080057
Cushingssyndrome 160827080057
amnehmeno
 
hypertension guidelines.pptx management in ;peadiatrics
hypertension guidelines.pptx management in ;peadiatricshypertension guidelines.pptx management in ;peadiatrics
hypertension guidelines.pptx management in ;peadiatrics
drnishurai97
 
Pediatric Hypertension Nephrologist View
Pediatric Hypertension Nephrologist ViewPediatric Hypertension Nephrologist View
Pediatric Hypertension Nephrologist View
Dang Thanh Tuan
 

Similar to Hypertension evaluation 2 (20)

Secondary hypertension work up
Secondary hypertension work upSecondary hypertension work up
Secondary hypertension work up
 
Pheochromocytoma dr ashish nair
Pheochromocytoma dr ashish nairPheochromocytoma dr ashish nair
Pheochromocytoma dr ashish nair
 
Hypertension Emergencies and their managementpptx
Hypertension Emergencies and their managementpptxHypertension Emergencies and their managementpptx
Hypertension Emergencies and their managementpptx
 
Seminar on critical Congenital heart disease Dr Habibur Rahim | Dr Faria Yasmin
Seminar on critical Congenital heart disease Dr Habibur Rahim | Dr Faria YasminSeminar on critical Congenital heart disease Dr Habibur Rahim | Dr Faria Yasmin
Seminar on critical Congenital heart disease Dr Habibur Rahim | Dr Faria Yasmin
 
HYPERTENSIVE CRISIS IN PEDIATRICS
HYPERTENSIVE CRISIS IN PEDIATRICSHYPERTENSIVE CRISIS IN PEDIATRICS
HYPERTENSIVE CRISIS IN PEDIATRICS
 
Hypertension Hypertension types causes and management complications classific...
Hypertension Hypertension types causes and management complications classific...Hypertension Hypertension types causes and management complications classific...
Hypertension Hypertension types causes and management complications classific...
 
Hypertension, its causes, types and management
Hypertension, its causes, types and managementHypertension, its causes, types and management
Hypertension, its causes, types and management
 
Secondary hypertension by dr Raj kishor
Secondary hypertension by dr Raj kishor Secondary hypertension by dr Raj kishor
Secondary hypertension by dr Raj kishor
 
Thrombotic Thrombocytopenic Purpura
Thrombotic Thrombocytopenic PurpuraThrombotic Thrombocytopenic Purpura
Thrombotic Thrombocytopenic Purpura
 
Secondary Hypertension. final.ppt
Secondary Hypertension. final.pptSecondary Hypertension. final.ppt
Secondary Hypertension. final.ppt
 
Oncologic Emergencies and Symptom Management
Oncologic Emergencies and Symptom ManagementOncologic Emergencies and Symptom Management
Oncologic Emergencies and Symptom Management
 
Cushingssyndrome 160827080057
Cushingssyndrome 160827080057Cushingssyndrome 160827080057
Cushingssyndrome 160827080057
 
Cushing's syndrome
Cushing's syndromeCushing's syndrome
Cushing's syndrome
 
Pediatric hypertention
Pediatric hypertentionPediatric hypertention
Pediatric hypertention
 
Systemic lupus erythematosus2019
Systemic lupus erythematosus2019Systemic lupus erythematosus2019
Systemic lupus erythematosus2019
 
hypertension guidelines.pptx management in ;peadiatrics
hypertension guidelines.pptx management in ;peadiatricshypertension guidelines.pptx management in ;peadiatrics
hypertension guidelines.pptx management in ;peadiatrics
 
Pediatric Hypertension Nephrologist View
Pediatric Hypertension Nephrologist ViewPediatric Hypertension Nephrologist View
Pediatric Hypertension Nephrologist View
 
ADRENAL GLAND-Dr.Hamisi Mkindi.pptx
ADRENAL GLAND-Dr.Hamisi Mkindi.pptxADRENAL GLAND-Dr.Hamisi Mkindi.pptx
ADRENAL GLAND-Dr.Hamisi Mkindi.pptx
 
Systemic Hypertension
Systemic HypertensionSystemic Hypertension
Systemic Hypertension
 
Hypertensive crisis
Hypertensive crisisHypertensive crisis
Hypertensive crisis
 

More from University of Florida (15)

Lupus nephritis
Lupus nephritisLupus nephritis
Lupus nephritis
 
Hypertension neonatal
Hypertension   neonatalHypertension   neonatal
Hypertension neonatal
 
Pediatric hypertension
Pediatric hypertensionPediatric hypertension
Pediatric hypertension
 
Gestational hypertension
Gestational hypertensionGestational hypertension
Gestational hypertension
 
Hypertension and renal diseases
Hypertension and renal diseasesHypertension and renal diseases
Hypertension and renal diseases
 
Hypertension and obesity
Hypertension and obesityHypertension and obesity
Hypertension and obesity
 
Hypertension drug therapy
Hypertension   drug therapyHypertension   drug therapy
Hypertension drug therapy
 
Hypertension principle of drug therapy
Hypertension   principle of drug therapyHypertension   principle of drug therapy
Hypertension principle of drug therapy
 
Hypertension non pharmcolical management
Hypertension   non pharmcolical managementHypertension   non pharmcolical management
Hypertension non pharmcolical management
 
Hypertension sequel - 2
Hypertension   sequel - 2Hypertension   sequel - 2
Hypertension sequel - 2
 
Hypertension sequel 1
Hypertension   sequel 1Hypertension   sequel 1
Hypertension sequel 1
 
Hypertension BP mesurement
Hypertension   BP mesurementHypertension   BP mesurement
Hypertension BP mesurement
 
Hypertension regulation
Hypertension   regulationHypertension   regulation
Hypertension regulation
 
Hypertension introduction
Hypertension   introductionHypertension   introduction
Hypertension introduction
 
Ancient israelites
Ancient israelitesAncient israelites
Ancient israelites
 

Recently uploaded

The basics of sentences session 3pptx.pptx
The basics of sentences session 3pptx.pptxThe basics of sentences session 3pptx.pptx
The basics of sentences session 3pptx.pptx
heathfieldcps1
 
Seal of Good Local Governance (SGLG) 2024Final.pptx
Seal of Good Local Governance (SGLG) 2024Final.pptxSeal of Good Local Governance (SGLG) 2024Final.pptx
Seal of Good Local Governance (SGLG) 2024Final.pptx
negromaestrong
 
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in DelhiRussian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
kauryashika82
 
1029 - Danh muc Sach Giao Khoa 10 . pdf
1029 -  Danh muc Sach Giao Khoa 10 . pdf1029 -  Danh muc Sach Giao Khoa 10 . pdf
1029 - Danh muc Sach Giao Khoa 10 . pdf
QucHHunhnh
 

Recently uploaded (20)

ComPTIA Overview | Comptia Security+ Book SY0-701
ComPTIA Overview | Comptia Security+ Book SY0-701ComPTIA Overview | Comptia Security+ Book SY0-701
ComPTIA Overview | Comptia Security+ Book SY0-701
 
The basics of sentences session 3pptx.pptx
The basics of sentences session 3pptx.pptxThe basics of sentences session 3pptx.pptx
The basics of sentences session 3pptx.pptx
 
Seal of Good Local Governance (SGLG) 2024Final.pptx
Seal of Good Local Governance (SGLG) 2024Final.pptxSeal of Good Local Governance (SGLG) 2024Final.pptx
Seal of Good Local Governance (SGLG) 2024Final.pptx
 
Explore beautiful and ugly buildings. Mathematics helps us create beautiful d...
Explore beautiful and ugly buildings. Mathematics helps us create beautiful d...Explore beautiful and ugly buildings. Mathematics helps us create beautiful d...
Explore beautiful and ugly buildings. Mathematics helps us create beautiful d...
 
Unit-IV; Professional Sales Representative (PSR).pptx
Unit-IV; Professional Sales Representative (PSR).pptxUnit-IV; Professional Sales Representative (PSR).pptx
Unit-IV; Professional Sales Representative (PSR).pptx
 
Magic bus Group work1and 2 (Team 3).pptx
Magic bus Group work1and 2 (Team 3).pptxMagic bus Group work1and 2 (Team 3).pptx
Magic bus Group work1and 2 (Team 3).pptx
 
PROCESS RECORDING FORMAT.docx
PROCESS      RECORDING        FORMAT.docxPROCESS      RECORDING        FORMAT.docx
PROCESS RECORDING FORMAT.docx
 
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in DelhiRussian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
Russian Escort Service in Delhi 11k Hotel Foreigner Russian Call Girls in Delhi
 
ICT role in 21st century education and it's challenges.
ICT role in 21st century education and it's challenges.ICT role in 21st century education and it's challenges.
ICT role in 21st century education and it's challenges.
 
Mixin Classes in Odoo 17 How to Extend Models Using Mixin Classes
Mixin Classes in Odoo 17  How to Extend Models Using Mixin ClassesMixin Classes in Odoo 17  How to Extend Models Using Mixin Classes
Mixin Classes in Odoo 17 How to Extend Models Using Mixin Classes
 
psychiatric nursing HISTORY COLLECTION .docx
psychiatric  nursing HISTORY  COLLECTION  .docxpsychiatric  nursing HISTORY  COLLECTION  .docx
psychiatric nursing HISTORY COLLECTION .docx
 
Third Battle of Panipat detailed notes.pptx
Third Battle of Panipat detailed notes.pptxThird Battle of Panipat detailed notes.pptx
Third Battle of Panipat detailed notes.pptx
 
Python Notes for mca i year students osmania university.docx
Python Notes for mca i year students osmania university.docxPython Notes for mca i year students osmania university.docx
Python Notes for mca i year students osmania university.docx
 
Key note speaker Neum_Admir Softic_ENG.pdf
Key note speaker Neum_Admir Softic_ENG.pdfKey note speaker Neum_Admir Softic_ENG.pdf
Key note speaker Neum_Admir Softic_ENG.pdf
 
Asian American Pacific Islander Month DDSD 2024.pptx
Asian American Pacific Islander Month DDSD 2024.pptxAsian American Pacific Islander Month DDSD 2024.pptx
Asian American Pacific Islander Month DDSD 2024.pptx
 
1029 - Danh muc Sach Giao Khoa 10 . pdf
1029 -  Danh muc Sach Giao Khoa 10 . pdf1029 -  Danh muc Sach Giao Khoa 10 . pdf
1029 - Danh muc Sach Giao Khoa 10 . pdf
 
SOC 101 Demonstration of Learning Presentation
SOC 101 Demonstration of Learning PresentationSOC 101 Demonstration of Learning Presentation
SOC 101 Demonstration of Learning Presentation
 
Grant Readiness 101 TechSoup and Remy Consulting
Grant Readiness 101 TechSoup and Remy ConsultingGrant Readiness 101 TechSoup and Remy Consulting
Grant Readiness 101 TechSoup and Remy Consulting
 
This PowerPoint helps students to consider the concept of infinity.
This PowerPoint helps students to consider the concept of infinity.This PowerPoint helps students to consider the concept of infinity.
This PowerPoint helps students to consider the concept of infinity.
 
Introduction to Nonprofit Accounting: The Basics
Introduction to Nonprofit Accounting: The BasicsIntroduction to Nonprofit Accounting: The Basics
Introduction to Nonprofit Accounting: The Basics
 

Hypertension evaluation 2

  • 1. HYPERTENSION Evaluation of Hypertension - 2 Mohammad Ilyas, M.D. Assistant Clinical Professor University of Florida / Health Sciences Center Jacksonville, Florida USA 1
  • 2. Outline 1. Definition, Regulation and Pathophysiology 2. Measurement of Blood Pressure, Staging of Hypertension and Ambulatory Blood Pressure Monitoring 3. Evaluation of Primary Versus Secondary 4. Sequel of Hypertension and Hypertension Emergencies 5. Management of Hypertension (Non-Pharmacology versus Drug Therapy) 6. The Relation Between Hypertension: Obesity, Drugs, Stress and Sleep Disorders. 7. Hypertension in Renal diseases and Pregnancies 8. Pediatric, Neonatal and Genetic Hypertension 2
  • 3. Types of Hypertension • Primary HTN: • >95% cases of HTN in adult • Cause Unknown. • Multiple risk factors: including age, family history, genetics, race, environment etc… • Secondary HTN: • < 5% HTN in adult are secondary • Secondary to other potentially rectifiable causes. • Often overlooked & under screen 3
  • 4. Secondary HTN Overview • Testing for secondary HTN can be expensive and requires high index of clinical suspicion. • General principles: • New onset HTN if <30 or >50 years of age • HTN refractory to medical Rx (>3-4 meds) • Specific clinical/lab features typical for dz : 4
  • 5. Causes of Secondary HTN • Common 1. Intrinsic renal disease 2. Renovascular disease 3. Mineralocorticoid excess 4. Sleep Breathing disorder • Uncommon 1. Pheochromocytoma 2. Glucocorticoid excess 3. Coarctation of Aorta 4. Hyper/hypothyroidism 5
  • 6. 1. Renal Parenchymal Disease • Common cause of secondary HTN (2-5%) • HTN is both cause and consequence of renal disease • Multifactorial cause for HTN including disturbances in Na/water balance, vasodepressors/ prostaglandins imbalance • Renal disease from multiple etiologies. 6
  • 7. 2. Renovascular HTN •Incidence 1-3% •Etiology •Atherosclerosis 75-90% (elder) •Fibromuscular dysplasia 10-25% (younger) •Other •Aortic/renal dissection •Takayasu’s arteritis •Thrombotic/cholesterol emboli •CVD •Post transplantation stenosis •Post radiation 7
  • 8. Renovascular HTN – History • History • Onset HTN age <30 or >55 • Negative FH of HTN • Sudden onset uncontrolled HTN in previously well controlled patient • Accelerated/malignant HTN • Intermittent pulmonary edema with normal LV function 8
  • 9. Renovascular HTN - Clinical • Clinical exam. /Lab. findings • Epigastric bruit, particularly systolic/diastolic • Advanced fundal changes, grade III/IV retinopathy • Azotemia induced by ACEI, ARBs or diuretics • Paradoxical worsening of HTN with diuretics • Secondary aldosteronism : ↑ plasma renin & ↓ s. Na & K • Unilateral small kidney, difference >1.5cm, on sonography 9
  • 10. Renovascular HTN – Diagnostic studies • Physical findings (bruit) • Duplex U/S • Captopril renography • Magnetic Resonance Angiography • Renal Angiography 10
  • 11. Fibromuscular dysplasia Atherosclerotic RAS • Fibromuscular dysplasia • 10-25% of all RAS • Young female, age 15-40 • Medial disease 90%, often involves distal RA • Atherosclerotic RAS • 75-90% of RAS • Usually men, age >55, • Other atherosclerotic 11
  • 12. RAS screening/diagnostics Sens Spec Limitation Bruit 39-65% 90-99% Insensitive, severe stenosis may be silent Duplex U/S 90-95% 60-90% Operator dependent, 10-20% Captopril Renography 83-91% 87-93% Accuracy reduced in pt with renal insufficiency, lacks anatomical info; good predictor of BP response MRA 88-95% 95% False positive artifact resp, peristalsis, tortuous vessels; cost Angiography Gold std Gold std Invasive, nephrotoxicity, little value in predicting BP response 12
  • 13. Fibromuscular Dysplasia, before and after PTRA Atherosclerotic RAS before and after stent13
  • 14. 3. Primary Aldosteronism • Primary Aldosteronism, previously felt to be an unlikely cause of secondary HTP, now is more commonly observed depending on the severity of HTP : • 8% Stage 2 • 13% of Stage 3 and • 20% of those with resistant hypertension. (10th Annual SMA-ASH Carolinas Georgia Chapter Meeting, 2006) 14
  • 15. Primary Aldosteronism • Prevalence 0.5- 2.0% (5-12% in referral centers) • Etiology • Adrenal adenoma • Bilateral adrenal hyperplasia, glucocorticoid suppressible hyperaldo, adrenal carcinoma • Clinical: • May be asymptomatic. • Headache, weakness, paralysis, polyuria • Retinopathy, edema uncommon • Hypokalemia (K normal in 40%), metabolic alkalosis, high-normal Na 15
  • 16. Screening for Hyper aldosteronism • Spontaneous hypokalemia (<3.5 mmol/L). • Profound diuretic-induced hypokalemia (<3.0 mmol/L). • Hypertension refractory to treatment with 3 or more drugs. • Incidental adrenal adenomas. 16
  • 17. 17
  • 18. 4. Pheochromocytoma • Catecholamine-producing neuroendocrine tumor that arises from chromaffin cells • Adrenal Medulla : 80-85% pheochromocytomas • Extra-adrenal paragangliomas • Often in head and neck (glomus jugulare) and rarely produce catecholamines. • Some can be dopamine producing. 18
  • 19. Epidemiology • Incidence: 1 in 100,000 each year • Prevalence among pts with HTP • In adults – 0.1-0.6% • In children – 1% • Traditional rule of 10 • 10% bilateral, 10% familial, 10% extra-adrenal, and 10% malignant. • Recent reports found 12-24% of sporadic pheochromocytoma with germline mutation. 19
  • 20. Clinical Presentation • Paroxysmal attacks of Headache, palpitations, and sweating. • Adults more often have paroxysmal hypertension (50%). • Children have sustained hypertension (70-90%). • 20% of children will be normotensive at diagnosis. 20
  • 21. Pheochromocytoma – Testing • Best detected during or immediately after episodes TEST Sensitivity Specificity Plasma free metanephrine >0.66nmol/L 99% 89% 24hr urine metanephrine (>3.7nmol/d) 77% (95%) 93% (96%) 24 urine VMA 64% 95% 21 Lenders, et al. JAMA 2002 Mar 20;287(11):1427-34
  • 22. Pheochromocytoma - Diagnosis • Imaging for localization of tumor TEST Sens Spec PPV NPV MIBG scintigraphy (metaiodobenzylguanidine) 78% 100% 100% 87% CT Scan 98% 70% 69% 98% MRI 100% 67% 83% 100% 22 Akpunonu, et al. Dis Month.October 1996, p688
  • 23. 5. Cushing’s syndrome (Hypercortisolism) • Rare cause of secondary HTN (0.1- 0.6%) • Etiology • Pituitary micro adenoma, • Iatrogenic (steroid use), • Ectopic ACTH, • Adrenal adenoma • Clinical • Sudden weight gain, truncal obesity, moon faces, abdominal striae, DM/glucose intolerance, HTN, prox muscle weakness, skin atrophy, hirsutism /acne 23
  • 25. Cushings syndrome - diagnosis • Screen: • 24 Hr Urine free cortisol • >90ug/day is 100% sens and 98% spec • False + in Polycystic Ovarian Syndrome, depression • Confirm • Low dose dexamethasone suppression test • 1mg dexameth. midnight, measure am plasma cortisol (>100nmol is +) • Other tests include dexa/CRH suppression test • Imaging • CT/MRI head (pit) chest (ectopic ACTH tumor) 25
  • 26. 6. Coarctation of Aorta • Congenital defect, male>female • Clinical • Differential systolic BP arms v/s legs (=DBP) • May have differential BP in arms if defect is prox to L subclavian art • Diminished/absent femoral art pulse • Often asymptomatic • Echo-Doppler, CT angiography, aortography. 26
  • 27. Coarctation of Aorta 27 Brickner, et al. NEJM 2000;342:256-263
  • 28. 7. Hyperthyroidism • 33% of thyrotoxic pt develop HTN • Usually obvious signs of thyrotoxicosis • Dx: TSH, Free T4/T3, thyroid 28
  • 29. 8. Hypothyroidism • 25% hypothyroid patient develop HTN • Mechanism mediated by local control, as basal metabolism falls so does accumulation of local metabolites; relative vasoconstriction ensues 29
  • 30. 30
  • 31. 31
  • 32. Summary • Screening for 2ry HTN can be expensive and requires clinical suspicion and knowledge of limitations of different tests • General principles: • New onset HTN if <30 or >50 years of age • HTN refractory to medical Rx (>3-4 meds) • Specific clinical/lab features typical for dz : • Hypokalemia in the absence of diuretic therapy may indicate a state of mineralocorticoid excess • Excess aldosterone production (Conn’s) • Excess glucocorticoid production (Cushing’s) • Excess T3 & T4 (hyperthyroidism) • Epigastric bruits, differential BP in arms, episodic HTN/flushing/palp. 32
  • 34. Quiz 1. TRUE or FALSE 1. Renal Parenchymal diseases are the common cause of primary HTN. 2. Hypertension is both cause and consequence of renal parenchymal disease. 3. Renal Parenchymal HTN is only due to disturbances in Na/water balance. 4. Renal Vascular disease usualy cause resistive HTN 34
  • 35. Quiz 1. TRUE or FALSE 1. Renal Parenchymal diseases are the common cause of primary HTN. FALSE 2. Hypertension is both cause and consequence of renal parenchymal disease. TRUE 3. Renal Parenchymal HTN is only due to disturbances in Na/water balance. FALSE 4. Renal Vascular disease usualy cause resistive HTN. TRUE 35
  • 36. Quiz 2. All of the following studies are helpful in diagnosis of Renovascular HTN - EXCEPT A. Urine pH B. Doppler renal U/S C. Captopril renography D. Magnetic Resonance Angiography E. Renal Angiography 36
  • 37. Quiz 2. All of the following studies are helpful in diagnosis of Renovascular HTN – EXCEPT? A. Urine pH B. Doppler renal U/S C. Captopril renography D. Magnetic Resonance Angiography E. Renal Angiography 37
  • 38. Quiz 3. Which of the following statement is not true about Primary Aldosteronism? A. May be asymptomatic. B. Can cause headache, weakness, paralysis, and polyuria. C. Retinopathy, edema are common finding. D. Can cause hypokalemia, metabolic alkalosis and high-normal Na. 38
  • 39. Quiz 3. Which of the following statement is not true about Primary Aldosteronism? A. May be asymptomatic. B. Can cause headache, weakness, paralysis, and polyuria. C. Retinopathy, edema are common finding. D. Can cause hypokalemia, metabolic alkalosis and high-normal Na. 39
  • 40. Quiz 4. Which of the following in NOT true about Pheochromocytoma? A. Clinical presentation includes paroxysmal attacks of headache, palpitations, and sweating. B. Adults more often have paroxysmal hypertension. C. Children have sustained hypertension. D. Majority of children could be normotensive at diagnosis. E. MIBG scintigraphy (metaiodobenzylguanidine) is diagnostic study for Pheochromocytoma 40
  • 41. Quiz 4. Which of the following in NOT true about Pheochromocytoma? A. Clinical presentation includes paroxysmal attacks of headache, palpitations, and sweating. B. Adults more often have paroxysmal hypertension. C. Children have sustained hypertension. D. Majority of children could be normotensive at diagnosis. E. MIBG scintigraphy (metaiodobenzylguanidine) is diagnostic study for Pheochromocytoma 41
  • 42. Quiz 5. Which of the following statement is FALSE about Coarctation of Aorta? A. Mostly present as Congenital defect B. More common in male than female C. BP in lower extremity is lower than upper extremity D. Often symptomatic E. Echo-Doppler, CT angiography, aortography. 42
  • 43. Quiz 5. Which of the following statement is FALSE about Coarctation of Aorta? A. Mostly present as Congenital defect B. More common in male than female C. BP in lower extremity is lower than upper extremity D. Often symptomatic E. Echo-Doppler, CT angiography, aortography. 43