Hypertension Flashcards by J L

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

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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

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Regulators of Hypertension

BP = ____ x ____

cardiac output

peripheral resistane

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Cardiac Output
• Blood volume
– ____ homeostasis

• Cardiac factors 
– \_\_\_\_
– \_\_\_\_
○ Neurologic
○Renal

Na+
heart rate
contractility

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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

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• CO
○ ____
§ Targeted most readily
○ Cardiac factors

• PR
	○ \_\_\_\_ pathway
	○ Prostaglandins &amp; 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

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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

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Role of Vessel Wall

• Peripheral Resistance
– ____
– Constriction
– ____

dilation

autoregulation

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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+

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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

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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

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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

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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

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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

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Actual mechanism

Elements of both altered ____ and ____ participate in idiopathic hypertension.

renal regulation

vasoconstriction/vascular hypertrophy

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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

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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

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Consequences of Hypertension
• ____

* Most important consequence that leads to MI
* \_\_\_\_, lipid core, \_\_\_\_, dysfunctional endothelium, oxidized \_\_\_\_

atherogenesis
fibrous cap
macrophages
LDL

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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

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Consequences of Hypertension

• Vascular wall changes
– Aortic dissection
• Blood flowing into wall > ____ of vessel
• Combination of ____, and the ____ through the area > shearing of wall and blood going into it

– Cerebrovascular hemorrhage
	• Stroke (fresh)
		○ Bursting of vessel > hemorrhage > if an \_\_\_\_ bursts (fast) and blood expands brain > fixed amount of space > pushed out \_\_\_\_ and crush cerebral tonsils
	• Fixed
	• \_\_\_\_ becomes much larger

occlusion
atherosclerosis
BP

arteriole
foramen magnum

hemispheres

Consequences of Hypertension

• Hypertensive Heart Disease
– Systemic (____) HHD
– Pulmonary (____) HHD

	• Both depend on hypertension
	• Systemic (left sided heart disease)
		○ High hypertension
	• Pulmonary (right sided heart disease)
		○ Can be secondary to systemic

left sided

right sided

Systemic Hypertensive Heart Disease

Systemic Hypertensive Heart Disease
• Left Ventricular hypertrophy
– Absence of other ____
– ____ hypertrophy

Left ____ dilation
____ (evidence) of hypertension – Even mild (ie 140/90 mmHg)
Ventricle wall > ____cm in diameter
Larger cells require more ____• BP is so high in ____ > now need to pump blood harder > left ventricle becomes thickened (now more than 2x the side of the RV)
• Without any other pathology (ischemia, etc.) > hypertension (thickened LV)
○ Walls become less ____ > do not pump blood as well > blood pools in ventricle > becomes dilated
• Blood cannot move forward > move back to lungs:
○ ____: difficulty breathing
○ Response to blood > alveolar macrophages try to clear blood in lungs > digest away RBC that enter alveoli > take in a lot of iron and heme > can break down heme somewhat > deformation of body pigments > ____ > ____ cells
• Larger cells requires more O2
○ Have hypertension, need to lower BP, but now you need more ____ to supply the heart that is working harder

cardiopathology
concentric
atrial
history
2
O2

periphery
elastic
congestion
hemosiderin
HF cells
O2

Consequences of Left Ventricle Hypertrophy

• Myocardial dysfunction (less elastic)
• Ventricular and atrial \_\_\_\_ (accommodate increased blood in ventricle)
• Congestive Heart Failure
– \_\_\_\_ congestion
– Reduced \_\_\_\_ perfusion 
• Water \_\_\_\_
• If severe, \_\_\_\_
• Sudden Death

• Atrial dilation > pulling back from the lungs
• Pulmonary congestion > begins backing up in system > secondary RH failure
	○ Because cannot get enough blood into system > kidney hypoperfused > release renin > activate \_\_\_\_ > retain H2O to raise the BP
		§ Lifetime of high BP > now signaling to kidney that you need even higher BP in order for heart to work properly
		§ A point to where it can revert to RSHF > \_\_\_\_ accumulating in your kidney

* Thickness of the LV
* \_\_\_\_ muscles are also hypertrophied

dilation
pulmonary
kidney
retention
azotemia

RAT
hyperemia
papillary

• Using ____

○ Macrophages filled with hemosiderin in the ____

PAS

alveoli

Pulmonary Hypertension • Secondary to increased ____ in pulmonary vasculature – i.e. Atheromas in pulmonary vasculature, ____, bronchiectasis, ____, emphysema, ____ • Right ventricular hypertrophy if ____ • ____, Spleen and Liver congestion • ____(legs/ankles) • ____ (pure right sided heart failure) • Right sided heart failure ○ Secondary to high BP in the lung • Not caused by hypertension, but specifically in the lung ○ Lung BP is quite lower than ____; but still has range where it has to be maintained • Normal left ventricles > right ventricles will hypertrophy ○ Not as impressive as LV; but it will almost be as large as ____ § Not normal • Blood pools in periphery > hyperemia in kidney spleen and liver ○ And peripheral edema > classic feature of ____ > more of an indication of ____ because of peripheral accumulation • Cor pulmonale ○ Anything pure RSHF ○ Blood isn't being pumped into lungs at high rate, chronic, ____ accumulation § Chronic pulmonale ○ Anything that leads to acute blockage of blood into lungs § ____ of leg trauma moving into heart and blockage of flow before lungs □ ____ cor pulmonae

``` resistance cystic fibrosis pulmonary thromboemboli COPD chronic kidney peripheral edema cor pulmonale ``` systemic LV CHF RHF peripheral embolus acute

Chronic Cor Pulmonale • ____ dilation and hypertrophy • Right ventricle is almost as thick of left ventricle ○ LV is normal • ____ is dilated bcause blood is pooling backwards into system

right ventricle | right atria

• Something that may cause pulmonary hypertension • If you have ____ in legs > leg veins are ____ > travel through heart and enter lungs and dissolve; but when they don't > can embed and recanalize, eventually one can embolize > reduce ability of blood to flow through the lungs ○ Reduces lumen size

thrombi | large

Arteriolosclerosis • Will see because will have hypertension in pulmonary system ○ Can also occur in the ____ ○ ____ (onion-skinning)

lung | hyperplastic

Liver Hyperemia • ____ liver • Backing up of blood • Hyperemia in ____ Centri-lobular Congestion • Central lobular congestion • Normal ____; congestion around the ____

nutmeg portal tracts hepatocytes veins

Consequences of Hypertension • Other Organs – Eyes – Kidneys Retinopathy • Fundoscopy ○ Left is normal retina § Nice edges on optic nerve; arterioles are even and smooth, can see the lumen in some of them ○ Right is hypertensive retina § Image below the one on the right § Pale areas > ____ spots > micro-infarcts > damage to underlying tissue § ____ > hemorrhages > the BV is a lot thicker § Arteriole-venous thickening □ ____ then thick, and so on □ Not even arterioles § Blurring of the optic disk > ____ > impair vision □ ____

``` cotton-mole flame spots thin papilloedema scotomas ```

Kidneys ``` • Benign Nephrosclerosis – ____ due to narrowed vessels – ____Thickening – ____ Arteriolosclerosis – Rarely ____ (mild ____) ``` ``` • Benign and malignant NS • BN ○ Hyalinzed arteriosclerosis > arterioles ____ > hypoperfusion > ischemic areas ○ Thickening of the ____ • Kidneys look ____ ○ Areas of microinfarctation ○ Otherwise, kidney is fairly normal ```

``` focal ischemia medial hyaline symptomatic proteinuria smaller media leathery ```

Kidneys ``` • Malignant Nephrosclerosis – ____ Arteriolosclerosis – ____ arteriolosclerosis – ____ – Ischemia – Kidney damage • (i.e. long standing ____ hypertension, arteritis, ____) • Activation of renin:angiotensin – Initially ____ and hematuria, but progresses to ____ failure ``` • Both hyaline and hyperplastic arteriosclerosis • Complete destruction of the vessel: necrotizing arteriolitis ○ ____ necrosis • Damage to vessel > ischemia and kidney damage ○ Kidney will interpret as hypoperfusion > activate RAT > risk for malignant hypertension (rising BP)

``` hyaline hyperplastic necrotizing arteriolitis benign coagulopathy proteinuria renal ``` fibrinoid

Kidneys • Tiny microhemorrhages > the vessels are becoming no longer intact ○ ____ presentation § Attacked by a swarm of flees

fleebin

Fibrinoid necrosis • ____ of vessel • Cannot see the ____ anymore, completely obliterated

destruction | vessel wall

Renal dysfunction • Ischemia induced activation of ____ – Na+ – Vasocontriction * No longer secrete ____ * Inability to secrete ____ * ____, hematuria, proteinuria • ____ neproschlerosi > renal dysfunction ○ Activate RAT § Na+ retention § Vasoconstriction ○ BP being raised, and removal of breaks (anti's) ○ Azotemia § ____-based compounds remaining in your blood § High level of ____ (nitrogen-urea based compounds)

``` renin-angiotensin antihypertensives Na+ azotemia malignant nitrogen BUN ```

Consequences of Hypertension (ALL OF THEM) • ____ • ____ – Hyaline arteriolosclerosis – Hyperplastic arteriolosclerosis • ____ – Aortic dissection – Cerebrovascular hemorrhage • ____ – Systemic (left sided) HHD – Pulmonary (right sided) HHD • ____ – Eyes – Kidneys

``` atherogenesis small vessel disease (arteriolosclerosis) vascular wall changes hypertensive heart disease other organs ```

Valvular diseases ``` • Consequences: – Stenosis • Failure to ____, obstruction of forward flow – Insufficiency • Failure to close, ____ ``` ``` • Affects ____ valve most often • May occur singly or ____ • Produce murmurs • Outcome – Degree of impairment – Speed of development, – Compensatory mechanisms ``` • Stenosis ○ Do not open - blood doesn't go forward • Regurgitation ○ Blood falling ____ ○ Does put heart at risk of ____, when you do procedure that may lead to bacteremia? • Whether to prophylactically treat patients with antibiotics prior to dental procedures ○ No prophylaxis with antibiotics • More than one valve can become affected • Speed of development ○ If born and adjustment as developing § Can be okay ○ Damaged to valve if heart isn't ready to deal with § More dangerous

``` open regurgitation mitral simultaneously back infection ```

``` Degenerative valve disease • Calcific Aortic Stenosis – ____ valves – Associated with ____, atherosclerosis – Affects ____ valve – ____ hypertrophy – Patients develop ____, CHF, syncope ``` • Calicified valves ○ Can occur on the ____, at place of annulus, along on the leaflet (anywhere in between) ○ Will affect valve function; heart will have to compensate > beat harder ○ Common consequence > ____ of compartment behind § Mitral > ventricle will be hypertrophy [???] • CHF ○ Secondary to the valve itself ○ Same mechanism as in ventricular hypertrophy, insufficiency to push blood to the system

``` calcified aging aortic left ventircular angina cusps hypertrophy ```

* (A) Calcium deposits on leaflet > the valve has difficulty ____ > blood flows back * (B) Two fused leaflets ____ > oopening based on the calcification > congenital > predisposed to calcium > difficult closing * © on ____ * (D) calcium extending into ____; extends down below the valve itself * All lead to regurgitiation effects in the valve

closing congenitally annulus myocardium

Degenerative Valve ``` • Myxomatous Mitral Valve – Affects 3-5% of adults – Genetic linkage to ____ disorders – 7X more likely in ____ – Floppy ____ valve leaflets – Most are ____ – ____ click by auscultation – 3% go on to develop ____ – Risk for ____? ``` ``` • Congenital disorder • Floppy mitral valve ○ Looks like a parachute ○ A little extra tissue that's extended [???] • Asymptomatic ○ But can hear with stethoscope • Would treat with prophylaxis? ○ Right now: ____ ``` • Ballooning up of the mitral valve • Hypertrophy of the LV and the papillary muscles ○ No other ____

``` connective tissue women mitral asymptomatic mid systolic CHF infective endocarditis no ``` pathologies

Rheumatic Heart Disease • Sequelae of ____ Infection • Inflammation of myocardial tissues – Myocardium –____ – Pericarditis (____ exudate) – ____ necrosis of the valves, ____ formation • Stenosis and regurgitation – ____ treatment of Strep reduces sequelae • Fibrinoid necrosis of valves ○ Growths on valves > cannot connect > valve regurgitiation • Can be prevented by treating strep infections with antibiotics > reduces sequelae ○ Can cause other secondary effects

``` strep aschoff bodies fibrinous fibrinoid verrucae antibiotic ```

• Valve doesn't close • Aschoff bodies ○ Form in accumulations of ____ aggregates within normal myocardia

inflamed

Infective Endocarditis • Serious Infection requiring prompt diagnosis and intervention • Composed of ____, thrombus and organisms • Acute – ____, bulky and destructive vegetations • ____, inflammatory cells and ____ • Subacute – Low ____ infection overlying previously damaged valves • Inflammation due to infection • Bland vegetations that aren't infectious, but can also have infectious ○ Active bacteria growing > treatment • Unlike calcifications > these vegetations are ____ and grow on top ○ Largely made up of fibrin, inflam cells • Subacute ○ Infection laying on top of previous-exisitng damage ○ Will not know until ____ symptoms (dysfunction of valve, or if it becomes acute)

necrotic debris friable fibrin microorganisms virulent loose severe

Congenital diseases ``` • Non-cyanotic – Left to right shunts • ____ defects • ____ defects • ____ ``` – May become cyanotic if pulmonary hypertension develops leading to ____ syndrome • reversing shunt flow from right to left. • Forcing ____ blood into the system • Lead to ____ hypertrophy (depending on valve affected), and whether or not to treat with antibiotics CONGENITAL DISEASES • Aren't genetically defined - have to do with an aberration during development ○ Allow child to be born and live; no ____ • Non-cyanotic ○ Whether this defect allows oxy blood to go into system (inefficient circulation - non-cyanotic) ○ [???] ○ Can become cyanotic > eisenmeger syndrome § ____ develops in system > reversal of flow; blood leading from blood shunting from left to right atria > can switch and go the other direction; unoxygenated blood going out into the periphery • Cyanotic ○ Unoxy blood shunted into oxy blood flow > unoxy blood entering the system

``` atrial septal ventricular septal patent ductus arteriosis eisenmenger unoxygenated ventricular ``` still-births hypertension

• Atrial septal defect ○ Communication btween ____; oxy being shunted to right • Vent septal defect ○ Oxy blood back and ____ • PDA defect ○ Aorta in communication with pulmonary vessel > oxy blood into the ____ system • All are left-to-right shunt

LA to RA reoxygenated pulmonary

Congenital malformations • Cyanotic ``` – Tetralogy of Fallot • ____ septal defect • Right ventricular outflow obstruction (____) • Overriding the VSD by the ____ • ____ hypertrophy ``` – ____ of the great arteries – Both require surgical correction, are associated with ____, osteoarthropathy, and ____ • Tetralogy of Fallot ○ Combination of congenital defects > cyanotic fomraiton § Induced Eisenweger ○ Two ventricles talking to each other ○ Obstruction of flow out of ____ ○ Aorta coming near the VSD > ____ blood into the aorta ○ RVH ○ VSD normally has blood going other direction, obstructing outflow, and aorta in right location > uxoxy blood is going into RV instead of other direction • Transpoisiton of great arteries ○ Aorta and pulmonary ____ switch • Paradoxical emobolism ○ Normally emboli are in venous system; don't end up arteries ○ In this case, because you get crosstalk bt oxy and unoxy > emboli occur in ____ system

``` ventricular subpulmonic stenosis aorta right ventricular transposition polycythemia paradoxical embolism RV unoxy trunk arterial ```

• (A) > blocking flow to ____ system; backflow that makes difficult to go pulmonary ○ Aorta is close to septal defect > unoxy blood entering into the system • (B) tranpsoition of vessels ○ ____ off RV ○ ____ of LV ○ Can also have the VSD > good coming here, blood oxy switching § Can be compensatory • Both need to be corrected with surgery

pulmonary aorta pulm trunk

Obstructive Lesions ``` • Aortic Coarctation – Narrowing of Aorta • Seen in ____, ____ syndrome – 2x more likely in ____ – Most common ____ abnormality – Clinical manifestations depend upon • ____ of narrowing • Presence or absence of ____ ``` • AC ○ Aorta itself becomes narrowed > more difficult for blood to flow through > LV hypertrophy ○ Most common congenital abrnoamlity in the heart

``` down syndrome turner's males congenital severity PDA ```