Hypertension Flashcards
What is Hypertension? • Elevated blood pressure (BP) • General Guide: – Diastolic > \_\_\_\_ mm Hg – Systolic > \_\_\_\_ mm Hg • Affects more than 25% of population – Increases with \_\_\_\_ – Twice as prevalent in \_\_\_\_
• Anything above 140/90 > seek treatment; but there are stages (I, II; prehypertension) • Anything above 120/80 needs to be monitored • There are ethnic variabilities ○ Genetic principles behind that!
90
140
age
AA
Classification of Hypertension
• Primary or Essential
– ____ (95%)
– Often ____
• Secondary (5%)
– ____, endocrine, neurologic, etc.
• Benign
– Stable at higher level
– Better ____
• Malignant
– Rises rapidly
– Poor ____
• Primary or essential ○ Don't know what causes; state of person combined with genetics and environment ○ Asymptomatic - why screenings are important • Secondary ○ Secondary to a preexisting condition § Renal - BP and kidney function are tightly linked ○ Pituitary, thyroid, etc. • Benign ○ High BP but around the same level; doesn't increase at dramatic rates ○ Responsive to treatment • Malignant ○ Erratic changes in BP § At very high levels § 200/120 BP § Risk for serious symptoms
idiopathic asymptomatic renal prognosis prognosis
Regulators of Hypertension
BP = ____ x ____
cardiac output
peripheral resistane
Cardiac Output
• Blood volume
– ____ homeostasis
• Cardiac factors – \_\_\_\_ – \_\_\_\_ ○ Neurologic ○Renal
Na+
heart rate
contractility
Peripheral Resistance
- Constrictors Vs Dilators
- Constriction increases BP
- Dilation decreases BP
– Autoregulation of resistance vessel
• Prevent ____
• Depends on how much you release, and how responsive your vasculature is to the factors • Autoregulation ○ Occurs in \_\_\_\_ to a fine degree ○ Vessels use the pressures in \_\_\_\_ systems to maintain the BP where they want it § Constrict and dilate at a rate \_\_\_\_ of other factors § Keeps brain functioning § Can also be bad - constant constricting of vessels > \_\_\_\_ of the vessels and will be less responsive
hyperperfusion brain closed independent thickening
• CO
○ ____
§ Targeted most readily
○ Cardiac factors
• PR ○ \_\_\_\_ pathway ○ Prostaglandins & kinins § These pathways keep peripheral resistance maintained ○ Autoregulation § Plays a \_\_\_\_ role ○ Neural factors § \_\_\_\_ § Major biologic underpinnings of mindfulness are these [???] □ Can control the systems by keeping yourselves in a \_\_\_\_ state
sodium renin/angiotensin local exercise mindfulness mindful
Role of kidney
• Affects both ____
• Renin/Angiotensin system
– ____
– ____ induces Na+ retention
• Antihypertensive source
– ____, Kallikrien/kinin, ____, NO
• Glomerular Filtration depends on ____
• ____ (i.e. ANF) inhibit Na+ reabsorption
• Vasoconstrictors and dilators is released by kidney • RAT ○ Leads to increased \_\_\_\_, and changes in CO § Affects both parts of equation • Antihypertensives ○ When kidney is dysfunctional, can increase BP and won't secrete antihypertensives § For long-term hypertensives this is bad! • Kidney function dependent on GMF ○ Glomeruli filter blood, excrete toxins and keep reagents; secrete sodium, keep water ○ Controls BP ○ If problem > affect RAT, AHS, and changes \_\_\_\_ (i.e. ANF)
CO and PR vasoconstriction aldosterone prostaglandins PAF BP natriuretic factors
PR
contractility
Role of Vessel Wall
• Peripheral Resistance
– ____
– Constriction
– ____
dilation
autoregulation
Potential Causes of Essential Hypertension
• Genetic
– ____/polygenic
– Continuous variation
– Rare single mutation (i.e. ____ syndrome)
– ____ in renin/angiotensin (accounts for racial differences)
– 107 hypertension related loci
• Environmental
– Stress, obesity, smoking, sedentary lifestyle
– High salt augments mechanism
GENETIC
• Multifactorial genes
○ 107 genes
§ Regulate systolic pressure, diastolic pressure, or pulse rate
○ Personalized and precision-based medicine
• Liddle syndrome
○ Causes change in ____ resorption
○ Single mutation
• Polymorphism in promoter for renin gene
○ Higher incidence in ethnic group
ENVIRONMENTAL
• Aging
• Things that put at risk for hypertension also put you at risk for atherosclerosis
multifactorial
Liddle
polymorphism
Na+
Proposed Mechanisms
- ____ Retention
- ____ and Vascular hypertrophy• Renal retention
○ Holds in salt, holds in water, which increases BP and increases CO > increases ____ [???]
• Vasoconstriction/vascular hypertrophy
○ Lifetime of ____
○ Vessels have wear and tear > become thicker > increases to ____, heart has to beat harder to get blood through
• Both comes from ____, evidence of both from patients
renal vasoconstriction PR autoregulation peripheral resistance pathology
Renal retention
- ____ is primary cause of HT
- Initiating event is increase ____ retention
- Increased H2O retention → increased ____
- Increased Cardiac output → autoregulation (vasocontriction) → ____
- Now Na+ can be excreted setting stable blood pressure at ____ level• More Na+ > increased H2O > increased CO > continues to increase, then PR is increased > now Na+ can be excreted, which will occur at new higher BP
○ Renal retention hypothesis
Na+ homeostasis Na+ CO PR higher
Some Evidence for Renal Retention
- Increase in Na+ intake increases ____
- Reducing Na+, reduces blood pressure
- Large increased Na+ loads → HT in normotensive individuals
- Genetically predisposed animals fed Na+ exhibit increased blood pressure• Normotensive people who eat more sodium > their BP will ____
○ People with high BP, reduce sodium > it goes down
• Animal studies match closely what is seen in people
○ Suggest it’s a good therapeutic target, but it’s insufficient
§ Doesn’t explain those who don’t eat salt and have ____; and vice-versa
BP
increase
hypertension
Vasocontriction/Vascular Hypertrophy
- Peripheral Resistance Primary cause
- Initiating events:
– Induce functional vasoconstriction
• ____ factors
• Vasocontricting agents
• Increased sensitivity of ____ to vasocontricting agents
– Induce structural changes in vessel wall
• ____ induces SMC proliferation
• SMC defect leading to chronic vasocontriction
• PR ○ Wear and tear; high BP increases with aging • Have constricting agents that are released as part of normal life ○ Neurogenic/vasoconstrictors > BV constrict • SMC may be more sensitive to constriction ○ May have \_\_\_\_ underpinnings • When those happens > structural changes > evidence seen pathologically: ○ \_\_\_\_ of vessel wall ○ Angiotensin II (secreted during hypertension): cause SMC to proliferate (may lead to \_\_\_\_ arteriosclerosis) ○ Some SMC may chronically vasoconstrict when they shouldn't
behavioral/neurogenic smooth muscle cells angiotensin II genetic thickening hyperplastic
Causes of Hypertension • Altered \_\_\_\_ Na+ retention • Levels of \_\_\_\_ substances (angiotensin II) • \_\_\_\_ of SMC to Pressor agents • Smooth Muscle Cell Growth
• Altered levels of substance that lead to vasoconstriction
renal
pressor
sensitivity
Actual mechanism
Elements of both altered ____ and ____ participate in idiopathic hypertension.
renal regulation
vasoconstriction/vascular hypertrophy
Malignant Hypertension
• Extremely high pressure (> ____) with steep rise
• Associated with more than 1 risk factor
– ____, age, ____, renal issues, essential hypertension
• Progress more ____ to pathologic consequences
– More ____ arteriolosclerosis
– Presence of ____
• New value is 190/100 • Unknown reason as to why BP spikes • Have more of the two types of \_\_\_\_ (hyaline and hyperplastic) • Will have inflammation of vessel wall that leads to death of that wall ○ Necrotizing arteriolitis ○ Death and collapse
220/120 race smoking quickly hyperplastic necrotizing arteriolitis arteriosclerosis
Clinical presentation: Malignant Hypertension
• Early symptoms include:
– ____, nausea, ____, visual impairments, ____ (spots before the eyes)
• Early signs
– ____, hematuria
• If untreated die of ____, cerebral damage, etc
• Symptoms do not imply malignant hypertension when first become apparent • Can also experience nosebleeds • Hematuria ○ May notice red urine; but \_\_\_\_ may mask it ○ Urine test • Proteinuria ○ Urine test ○ \_\_\_\_ (the only sign)
headaches vomitting scotomas proteinuria renal failure vitamins bubbly
Consequences of Hypertension
• ____
* Most important consequence that leads to MI * \_\_\_\_, lipid core, \_\_\_\_, dysfunctional endothelium, oxidized \_\_\_\_
atherogenesis
fibrous cap
macrophages
LDL
Consequences of Hypertension
- Atherogenesis
- Small Vessel Disease (arteriolosclerosis)
– Hyaline arteriolosclerosis
• Extravasation of ____ proteins • Increased ____ deposition
– Hyperplastic arteriolosclerosis • Reduplication of \_\_\_\_ • \_\_\_\_ proliferation • \_\_\_\_-skinning • More with \_\_\_\_ hypertension
• Small vessel disease ○ Hyaline § Extravasation of fibrin, albumin; forms on outside of vessel > smooth, \_\_\_\_ appearance (formation of a corona) § Less \_\_\_\_ - seen more in regular hypertension (some hyperplastic, but mostly hyaline) ○ Hyperplastic § More severe hypertension § In addition to plasma proteins > induce SMC to proliferate and put down another set of BM □ Multiple layers of \_\_\_\_ in these small vessels □ Looks like an onion (onion-skinning phenotype)
plasma ECM basement membrane smooth muscle cell onion malignant eosinophilic dangerous SMC
