Hypertension PATHO Flashcards
Primary Hypertension
Definition, prevalence, risk Factors
Primary HTN
Essential HTN
Idiopathic HTN
Elevated BP with no identifiable cause
95% HTN
Risk factors
- old age
- obesity
- smoking
- alcoholism
- sedentary lifestyle
- Gender (men > women before 55; women > men after 55)
- african
- indigenous
- low SES
- high dietary sodium
- low dietary potassium, calcium, mangesium
- glucose intolerance
Secondary HTN
Definition, prevalence, risk factors
Secondary HTN
elevated BP with known cause
treat cause, reverse HTN
10% HTN
younger people
Risk Factors
- Renal disease
- coartication aorta
- OSA
- pheochromocytoma
- aldosteronism
- cushings syndrome
- hyperthyroid (high SBP), hypothyroid (High DBP)
- drug induced (NSAIDS, corticosteroids, immunosupressants, oral contraceptives, stimulants (amphetamines, cocaine), alcohol, smoking, SNRIs, lithium)
- Food induced (licorice, ginsing)
Risk Factors for HTN
- Lack of exercise (< 150 min per week moderate intensity)
- Diet ( < 5 servings fruit/vegetables per day, > 2000mg sodium, low potassium/calcium/magnesium)
- obesity ( BMI > 25, waist > 102/88cm)
- DIABETES
- KIDNEY DISEASE (GFR < 60mL/min)
- ALCOHOL (abstain)
Long term effect of HTN
- Microvascular 2. Macrovascular damage –> End organ damage
HTN -> damages capillaries, endothelial lining –> scaring –> atheroscelersosis –> narrowing –> ischemia
- Heart
- high BP increases afterload of heart
- high BP decreases RBP and increases RAAS and SNS
- collectively angiotensin II, aldosterone, SNS result in vascular and cardiac remodelling (increase ECM and fibrosis, increase atheroscelerosis, hypertrophy)
- vessel damage results in atheroscelerosis
- Increase demand for oxygen due to workload
- ischemia
–> CAD, angina, MI, HFrEF, LV hypertrophy - Kidney
- high BP reduces RBP
- reduction of GFR
- activation RAAS and SNS
- results in angiotensin II, aldosterone (cardiovascular remodelling; and SNS stimulation) –> + HTN
- reduced RBP ischemia
- ATN; increase intratubular pressure; damage glomerular basement membrane
- proteinuria - Brain
- high BP damages endothelial lining
- atheroscelerosis, narrowing, ischemia
- TIA, strokes, dementia - Eyes
- high BP damages capillaries
- flare hemorrhages, cotton wool spots, retinal scelerosis - Peripheral arteries
- intermittent claudication due to ischemia from atheroscelerosis
- gangrene due to ischemia
Pathophysiology
SNS and RAAS = HTN
SNS
1. Vascular/cardiac remodeling
2. insulin resistance
3. vascular resistance
4. coagulation
= HTN
- Heart
- beta 1 adrenergic receptors: HR, conduction, contraction = increase BP - Pancreas
- SNS inhibits release insulin, increase release glucagon, increase BP = endothelial dysfunction, inflammation, atheroscelerosis, narrowing = BP
- cortisol increases insulin resistance (released by adrenal medulla from SNS stimulation)
- epinephrine increases blood glucose (released by adrenal medulla from angiotensin II stimulation) - Kidney
- beta 1 receptors juxtaglomerular cells release renin
- high BP decreases RBP releases renin (+)
- RAAS pathway
- angiotensin II 1. vascular remodelling (narrowing, increase BP 2. cardiac remodelling (hypertrophy, HF) 3. vasoconstriction direct (BP) 4. release cortisol, aldosterone, epinephrine (insulin resistance, BP, cardiac remodeling) - Coagulation factors
- increase circulation of coagulation factors
Function of Natriuretic peptides
ANP/BNP
- atrial natriuretic peptide
- bone natriuretic peptide
- released from atrium/ventricle during stretch
- prevent kidney from reabsorbing sodium
- diuresis of water
CNP and urodilantin
- CNP released from vasculature
- urodilantin released from collecting duct
- during stretch
- promote dilation of renal arteriole
- promote GF and diuresis
*Dysfunction natriuretic peptides result in hypertension
Inflammation and HTN
Pro-inflammatory states
- hyperglycemia
- hypoglycemia (proinflammation, procoagulation)
- obesity
Inflammation = endothelial cell dysfunction
- doesn’t produce NO for vasodilation
- vaosoconstriction
- narrowing, atheroscelerosis, and HTN
Obesity and HTN
Obesity
- adipokines proinflammatory
- activation SNS (vasoconstriction ; release cortisol and NE)
- NE binds beta 1 adrenergic receptors on heart; increase HR, conduction, contractility; increase BP
- NE binds beta 1 adrenergic receptors on kidney; increase renin release; RAAS activation; increase BP
- cortisol increases blood glucose; inflammation; atheroscelerosis; narrowing; BP
- SNS inhibits insulin release from pancreas, increases glucagon release; increase BG; increase inflammation, atheroscelerosis, narrowing: BP
Insulin Resistance and HTN
Insulin Resistance
- Obesity is the driver for insulin resistance MSK
- increase BG
- damages blood vessels
- atheroscelerosis, narrowing
- obesity adipokines also damage beta cells resulting in dysfunction
- decrease insulin and amylin release
- increase gulcagon release; increase BG, inflammation, atheroscelerosis, narrowing
Shift in pressure-natriuresis relationship
HTN
- SNS
- RAAS
- dysfunction natriuretic peptides
- insulin resistance
- obesity
- diet
- glomerular and tubular inflammation
- endothelial dysfunction
- genetics
*retention sodium and water
HTN
HTN
Treatment Goals based on Risk Stratification
High Risk
- Diabetes (>130/80mmHg)
- >/= 75 years
- >/= 50 years with SBP > 130mmHg and:
- CVRF > 15%
- CKD (GFR < 60mL/min)
- CVD
Diabetes HTN: > 130/80
Goal: < 130/80
Other HTN: >130
Goal: < 120
Moderate - High Risk
- CVRF > 10%
- TOD present
- HTN: >140/90
- Goal: < 140/90
Low risk
- CVRF none
- TOD none
- HTN > 160/100
- Goal < 140/90
Pharmacological Treatment
Diabetes
with microalbuminuria, CVD, CV risk factors, renal disease
First line:
ACEi/ARB (nephroprotective, cardioprotective)
Combination:
ACEi/ARB + CCB dihydropyridine
Pharmacological Treatment
Diabetes
without TOD
First line:
ACEi/ARB/CCB/Thiazide diuretic
Combination therapy:
ACEi/ARB + CCB dihydropyridine
Pharmacological treatment
Non-Diabetic CKD / proteinuria
First Line:
ACEi/ARB
Combination:
ACEi/ARB + Diuretic
Pharmacological treatment
Past stroke/TIA
First Line:
ACEi + Thiazide Diuretic
Ex. Perindopril + Indapamide (reduce stroke 4 years)
Pharmacologial treatment
Coronary Artery Disease
First line:
ACEi/ARB
CAD with stable angina
First line:
Beta blocker/CCB
Combination therapy:
ACEi/CCB added
Pharmacological treatment
Recent MI
HF LEF < 40%
First line:
Beta blocker + ACEi
OR
CCB + ARB
Addition:
Aldosterone antagonist (elevated BNP, hospitalization, acute MI, HF symptoms II-IV)
Thiazide diuretic
HTN
Candian Prevalence
Increases with age
> 70 years 70%
Men = Women
< 40 years
untreated, silent, undermanaged
Goal of HTN Treatment
Prevent TOD
- microvascular and macrovascular changes
1. heart 2. kidney 3. eyes 4. peripheral arteries 5. brain
Pathophysiology HTN
BP = CO x PVR
HTN =
1. increase CO
2. increase peripheral resistance
3. BOTH
Increase CO
- CO = Stroke volume x HR
- SNS
- RAAS
PVR
- Diameter
- Vascular compliance
- blood viscosity
SNS and HTN
SNS activation releases NE, E, cortisol
- heart
increase HR, CO, conduction = increase BP - kidney
release renin
RAAS pathway
reabsorption water, sodium = BP
angiotensin II = vasoconstriction, + SNS, remodeling heart, VSM, release aldosterone
aldosterone = reabsorption sodium, water, remodellig heart, prevent NE degredation + SNS, baroreceptor setpoint higher - pancreas
- inhibtion insulin release, increase glucoagon release, BG, inflammation
- SNS insulin resistance periphery
- obesity inflammation pancreatic beta cell dysfunciton decrease insulin - pro-coagulation
virchow triad: endothelial dysfunction, inflammation, increased blood viscosity = increase thrombosis - Endothelial dysfunction
Accurately diagnosing HTN
Measurement Techniques
- sitting
- rest for 5 minutes before start
- back supported
- arm supported
- cuff at heart level
- cuff 40% diameter, 80-100% length
- 3 cm above elbow
- no talking, moving
- feet flat
- legs uncrossed
- measurements 1-2 minutes apart
- provider out of room
- arm with higher blood pressure used
- automated, provider out of room preferred
Diagnosis cut offs in office/out of office HTN
HTN
BP > 180/110mmHg ==> Hypertention
AOBP >/= 135/85mmHg
OBPM >/= 140/90mmHg (*in room)
diabetics >/= 130/80mmHg
*3 readings average second two
*3-5 office visits if ABPM or HBPM is not available
*probable HTN suspected then you proceed to out of office measurements
ABPM >/= 135/85mmHg (daytime average)
>/= 130/80mmHg (24 hour average)
*readings are taken every 20-30 minutes for 24 hours?
HBPM >/= 135/85mmHg (7 days, 2x AM 2x PM, discard first day)
Diagnostic and laboratory investigations
Suspected HTN
- urinalysis (Proteinuria, hematuria, glucosuria)
- ECG
- lipid pannel
- A1C and FPG (r/o pre-diabetes, diabetes)
- lytes (sodium, potassium, calcium, magnesium)
- kidney function (BUN, creatinine)
- liver function
- pregnancy screen
*
r/o secondary causes
- TSH, free T3, free T4
- 24 hour urine corticosteroids
- Drugs etc.
