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Year 1: Patho/Pharm > Hypertension PATHO > Flashcards

Hypertension PATHO Flashcards

1
Q

Primary Hypertension
Definition, prevalence, risk Factors

A

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

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2
Q

Secondary HTN
Definition, prevalence, risk factors

A

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)

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3
Q

Risk Factors for HTN

A
  1. Lack of exercise (< 150 min per week moderate intensity)
  2. Diet ( < 5 servings fruit/vegetables per day, > 2000mg sodium, low potassium/calcium/magnesium)
  3. obesity ( BMI > 25, waist > 102/88cm)
  4. DIABETES
  5. KIDNEY DISEASE (GFR < 60mL/min)
  6. ALCOHOL (abstain)
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4
Q

Long term effect of HTN

A
  1. Microvascular 2. Macrovascular damage –> End organ damage

HTN -> damages capillaries, endothelial lining –> scaring –> atheroscelersosis –> narrowing –> ischemia

  1. 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
  2. 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
  3. Brain
    - high BP damages endothelial lining
    - atheroscelerosis, narrowing, ischemia
    - TIA, strokes, dementia
  4. Eyes
    - high BP damages capillaries
    - flare hemorrhages, cotton wool spots, retinal scelerosis
  5. Peripheral arteries
    - intermittent claudication due to ischemia from atheroscelerosis
    - gangrene due to ischemia
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5
Q

Pathophysiology
SNS and RAAS = HTN

A

SNS
1. Vascular/cardiac remodeling
2. insulin resistance
3. vascular resistance
4. coagulation
= HTN

  1. Heart
    - beta 1 adrenergic receptors: HR, conduction, contraction = increase BP
  2. 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)
  3. 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)
  4. Coagulation factors
    - increase circulation of coagulation factors
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6
Q

Function of Natriuretic peptides

A

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

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7
Q

Inflammation and HTN

A

Pro-inflammatory states
- hyperglycemia
- hypoglycemia (proinflammation, procoagulation)
- obesity

Inflammation = endothelial cell dysfunction
- doesn’t produce NO for vasodilation
- vaosoconstriction
- narrowing, atheroscelerosis, and HTN

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8
Q

Obesity and HTN

A

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
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9
Q

Insulin Resistance and HTN

A

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
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10
Q

Shift in pressure-natriuresis relationship
HTN

A
  1. SNS
  2. RAAS
  3. dysfunction natriuretic peptides
  4. insulin resistance
  5. obesity
  6. diet
  7. glomerular and tubular inflammation
  8. endothelial dysfunction
  9. genetics

*retention sodium and water
HTN

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11
Q

HTN
Treatment Goals based on Risk Stratification

A

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

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12
Q

Pharmacological Treatment
Diabetes
with microalbuminuria, CVD, CV risk factors, renal disease

A

First line:
ACEi/ARB (nephroprotective, cardioprotective)

Combination:
ACEi/ARB + CCB dihydropyridine

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13
Q

Pharmacological Treatment
Diabetes
without TOD

A

First line:
ACEi/ARB/CCB/Thiazide diuretic

Combination therapy:
ACEi/ARB + CCB dihydropyridine

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14
Q

Pharmacological treatment
Non-Diabetic CKD / proteinuria

A

First Line:
ACEi/ARB

Combination:
ACEi/ARB + Diuretic

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15
Q

Pharmacological treatment
Past stroke/TIA

A

First Line:
ACEi + Thiazide Diuretic
Ex. Perindopril + Indapamide (reduce stroke 4 years)

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16
Q

Pharmacologial treatment
Coronary Artery Disease

A

First line:
ACEi/ARB

CAD with stable angina
First line:
Beta blocker/CCB

Combination therapy:
ACEi/CCB added

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17
Q

Pharmacological treatment
Recent MI
HF LEF < 40%

A

First line:
Beta blocker + ACEi
OR
CCB + ARB

Addition:
Aldosterone antagonist (elevated BNP, hospitalization, acute MI, HF symptoms II-IV)
Thiazide diuretic

18
Q

HTN
Candian Prevalence

A

Increases with age
> 70 years 70%

Men = Women

< 40 years
untreated, silent, undermanaged

19
Q

Goal of HTN Treatment

A

Prevent TOD
- microvascular and macrovascular changes
1. heart 2. kidney 3. eyes 4. peripheral arteries 5. brain

20
Q

Pathophysiology HTN

A

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

21
Q

SNS and HTN

A

SNS activation releases NE, E, cortisol

  1. heart
    increase HR, CO, conduction = increase BP
  2. 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
  3. pancreas
    - inhibtion insulin release, increase glucoagon release, BG, inflammation
    - SNS insulin resistance periphery
    - obesity inflammation pancreatic beta cell dysfunciton decrease insulin
  4. pro-coagulation
    virchow triad: endothelial dysfunction, inflammation, increased blood viscosity = increase thrombosis
  5. Endothelial dysfunction
22
Q

Accurately diagnosing HTN
Measurement Techniques

A
  • 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
23
Q

Diagnosis cut offs in office/out of office HTN

A

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)

24
Q

Diagnostic and laboratory investigations
Suspected HTN

A
  • 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.
25
Q

Approach to treatment of HTN
Stratify based on RISK

A

Framingham risk Score
- age
- gender
- SBP
- smoking status
- HDL
- TC

High risk > 15%
moderate risk 10-15%
low risk < 10%

*High risk and moderate will also start statin therapy for lipids

26
Q

Lifestyle modifications
HTN

A

Exercise
> 150minutes / week moderate-intense

Diet
< 2000mg/ day sodium
increase potassium, calcium, magnesium
DASH
> 5x fruits, vegetables, fibres, low fat, whole grain, plant protien

Weight loss
BMI < 25
waist circumference < 102cmm < 88cm women

Abstain alcohol and smoking
< 2 drinks per day

Stress management
CBT and relaxation

27
Q

Pharmacotherapy
Things to remember

A
  • long acting thiazide diuretics > short acting
  • beta blockers should not be used as monotherapy OR >/= 60 years of age
  • RAAS drugs (ACEi , ARBs) are teratogenic 2nd and 3rd trimester
  • Do not combine ACEi or ARBs
  • Caution combining beta blockers and CCB (cardiosupression toxic as same mechanism for non-dihydropyridines)
  • beta blockers and ACEi together have limited therapeutic effect (preferrable is CCB)
  • single pill combinations are preferred
  • ACEi + CCB
  • ACEi/ARB + thiazide diruetics
  • low dose multiple drugs > one drug high dose (less SE)
  • > 3 drugs, uncontrolled, referral
28
Q

Pregnancy
HTN pharmacotherapy

A

First line: Beta blockers
labetalol (third generation beta blocker, block beta 1, 2 and alpha 1)
acebutolol
metoprolol
pindolol
propranolol

Others:
long acting nifedipine
methyldopa ( Brainstem, supression SNS)

Additive:
Thiazide diuretic

29
Q

R/O before resistant HTN

A
  • white coat syndrome
  • non adherence medication / lifestyle
  • secondary hypertension
  • inadequate drug/combination
30
Q

Poor response to HTN therapy
causes

A
  • inaccurate measurement
  • inappropriate treatment
  • dosage
  • combination drugs
  • poor adherence diet, exercise, medication
  • Drugs that cause HTN
  • Undiagnosed secondary conditions
31
Q

Follow up HTN
pharmacological and lifestyle management

A

Follow up
1-2 months until BP in target
2 consecutive visits below target
3-6 month intervals

Lifestyle modification and adherence
3-6 month visits
not in target 1-2 months

32
Q

Pathophysiology of
HTN baroreceptor reflex

A

High baroreceptor reflex in HTN
keeps BP high

  • sense low BP, carotid arch, and aorta baroreceptors
  • signal brain
  • activation SNS
  • beta 1 receptors increase HR, conduciton, contraciton
  • beta 1 receptors kidney, release renin (RAAS pathway)
  • alpha 1 receptors vasoconstriction peripheral arteries/veins
  • increase BP to higher set point
33
Q

MOA
Thiazide diuretics

A
  1. prevention Na/K/Cl reabsorption at the early distal tubules
  2. promotion vascular muscle relaxation / vasodilation
34
Q

Can you cure HTN?

A

No
Therapy is life long
lifestyle +/- drug therapy

35
Q

Why start low and go slow with dosing?

A

Everyone has different sensitivity (receptors)

prevents triggering baroreceptor reflex

resets the setpoint

36
Q

Benefit of multiple drug therapy

A

Lower dosage of each drug needed

lower SE profiles

37
Q

Treatment considerations African American

A

First line: diuretic

Do not use beta blocker / ACEi monotherapy
*exception is risk profile

38
Q

Why don’t we use beta blockers with older people >/= 60 years?

A

blunt the baroreceptor reflex
results in orthostatic hypotension and falls

39
Q

HTN in pregnancy

A

10% pregnancies
Screen all pregnancies
High risk pre-eclampsia
Treat 160/110

Risk
- placental abruption
- fetal malformation and growth restrictions
- premature delivery
- death

40
Q

Pre-eclampsia
Pathophysiology, diagnosis, treatment

A

HTN > 140/90
proteinuria
eclampsia = seizures
after 20 weeks gestation
6 weeks after pregnancy

Pathophysiology
- hyperperfused placenta (narrowing spiral arteries)
- pro-inflammatory proteins released from placenta
- endothelial cells dysfunctional in mom
- kidney retain salt
- arteries narrow

Risk factors
- HTN
- diabetes
- black
- first pregnancy
- family history
- > 35 years
- obesity

Complications
- Seizures “eclampsia”
- Renal failure - damaged glomerulus
- Damage retina - blurred vision
- Liver damage - RUQ pain (cardinal symptom)
- Third spacing fluid - edema, legs, face, hands, pulmonary, cerebral edema (HA, seizures)
- stroke - micro-thrombi, hemolysis (HELP syndrome)
- placental abruption, intrauterine growth restriction
- HELP - hemolysis, elevated liver, low platelets

Treatment
- delivery baby and placenta (source of dysfunction)

Year 1: Patho/Pharm (39 decks)

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