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Advanced Patho Exam 3 > Exam 3: CAD/HTN > Flashcards

Exam 3: CAD/HTN Flashcards

1
Q

what are the comprehensive risk factor profile for coronary artery disease? (5)

A
  • dyslipidemia
  • genetic factors
  • traditional modifiable risk factors
  • non-modifiable risk factors
  • novel risk factors
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2
Q

what is dyslipidemia? give examples (4)

A

o Abnormal amount of lipids in the blood
 Triglycerides, phospholipids, cholesterol, lipids

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3
Q

what are lipids?

A

fats transported in plasma in form of lipoproteins

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4
Q

what are lipoproteins?

A
  • particles made of protein and fats (lipids). They carry cholesterol through your bloodstream to your cells
  • a molecule consistent with water soluble molecules with a core of cholesterol and triglycerides covered by phospholipids
  • it varies their contribution in atherosclerotic risks
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5
Q

VLDL

A

primarily triglycerides and protein

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6
Q

LDL

A

mostly cholesterol and protein
- contains 70% of cholesterol in circulation
- metabolic byproduct/end product of VLDL

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7
Q

HDL

A

mainly phospholipids and protein
- each 1 mg/dL increase in HDL–estimated to decrease CAD risk by 2% in men and 3% in women

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8
Q

Chylomicron

A

what we put in our mouth, the least dense of lipoproteins, primarily contain triglycerides

  • not thought to be atherosclerotic but the remanence of the breakdown of their lipolysis are atherogenic
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9
Q

how does HDL lower CAD risk?

A

because of reverse cholesterol transport

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10
Q

CAD risk factors: dyslipidemia (3)

A
  • elevated LDL-C
  • low HDL-C
  • hypertriglyceridemia
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11
Q

how does elevated LDL-C cause CAD?

A

 Can penetrate arterial wall, promote atherosclerosis
 Increased concentration of LDL is an indicator for coronary risk; however, the risk depends of the presence of other risk factors such as;
* Age, diabetes, CKD

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12
Q

how does low HDL cause CAD

A

 HDL picks up cholesterol and brings to liver where it can be further processed; need to move oxidized LDL out of macrophages and bring to liver
* “reverse cholesterol transport”

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13
Q

CAD risk factors: genetic factors

A

o Heterozygous vs Homozygous
 Homozygous familial hypercholesterolemia harder for body to remove LDL from blood
o Blacks > white

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14
Q

what is familial hypercholesteremia?

A
  • these individuals have fewer or defective LDL receptors
  • significant atherosclerosis and premature CAD in the absence of other risk factors unless the hypercholesteremia is treated with medication or aphaeresis at a very early age.
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15
Q

what is the function of LDL receptors on the liver?

A

the receptors are responsible for clearing and removing cholesterol from circulation

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16
Q

modifiable risk factors for CAD (5)

A
  • smoking
    -HTN
  • physical inactivity
    -DM
  • Obesity
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17
Q

How does smoking contribute to CAD

A

lowers HDL further, reduces coronary blood flow, decreases endothelial fxn, increase vasospasm, increase plt aggregation

**leading cause of preventable death

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18
Q

what is the most prevalent CAD?

A

-HTN

**theres a relationship between BP elevation and incidence of CAD and stroke

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19
Q

how does DM play a role in CAD?

A

-increases plt aggregation
- hyperinsulinemia–>occurs in T2DM promotes smooth muscle proliferation and cholesterol accumulation in arterial wall

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20
Q

what are non-modifiable risk factors for CAD? (3)

A
  • FAMILY HISTORY
    **first degree family with CAD and at young age
    **risk factor for having MI is inversely r/t at the age the MI occurred in the parents
    **risk is greater if your father had an MI at 40 compared to him having an MI at 75

-AGE
**risk for having CAD or MI increases with age
**about 4/5 of fatal MI occurs in ppl >65
-GENDER
**the onset of symptomatic CAD is 10 years earlier in men compared to women
**the risk evens out when women reaches menopause

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21
Q

Novel RF (non-traditional, newer) of CAD (5)

A

o elevated lipoprotein (a)
**we all have lipoprotein (a) but if it is elevated, it can be a risk factor- looks like LDL and clotting factor (plasminogen) but meds don’t reduce it or lifestyle changes
**elevated levels have shown to be an important risk factor for coronary atherosclerosis, especially in woman
o elevated high sensitivity- CRP
**inflammatory factor, when elevated increases CAD
o elevated fibrinogen
o elevated LDL particle number
**this is the total #
o small, dense LDL

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22
Q

describe atherosclerosis

A

o a thickening and hardening of the vessel that are caused by the accumulation of lipid-laden macrophages within the arterial wall, which leads to the formation of a lesion called a “plaque”.
 Lesions are likely to develop following endothelial injury
o Atherosclerosis is not a single disease but rather a pathologic process that can affect vascular systems throughout the body- multi-process

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23
Q

what is atherosclerosis the leading cause of?

A

CAD and cerebrovascular disease

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24
Q

the earliest manifestation of atherosclerosis

A

endothelial dysfunction

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25
Q

define CAD

A

o Narrowing or blockage of the coronary arteries, usually caused by atherosclerosis
o CAD can dimmish blood supply until deprivation impairs myocardial metabolism enough to cause ischemia

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26
Q

progressive process of atherosclerosis

A

normal–>fatty streak–>fibrous plaque–>occlusive atherosclerotic plaque <–>plaque rupture/fissure and thrombosis

which can lead to:
-unstable angina
-MI
-coronary death
-stroke
-critical leg ischemia

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27
Q

fatty streak

A

o First lesion of atherosclerosis- was first found in children when they would die suddenly
o They are consisted of lipid laden macrophages (“foam cell”), when significant amounts accumulate, they form a legion called “fatty streak”
o focal thickening of the intima
 intima- first layer of the artery
 media- muscle layer of the artery
o increase in smooth muscle cells and extracellular matrix.
o Smooth cells migrate and proliferate into the intima
 Smooth muscle cell migrates into where the atherosclerotic lesion begins, which enlarges the lesion
o lipid deposits accumulate
o macrophages and T-lymphocytes (early damage to vessel wall).
o Aggregation of lipid thick foam cells in intima. When LDL oxidized, taken into macrophages

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28
Q

fibrous plaque

A

o The second phase
o evolves from fatty streak and increase accumulation of connective tissue.
o Increased number of smooth muscle cells laden with lipids.
o Deeper extracellular lipid pool.
o  Results in further endothelial cell dysfunction, necrosis of underlying vessel tissue, and narrowing of the lumen as the lesion protrudes out from the vessel wall

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29
Q

Advanced (Complicated) Lesion

A

o Last phase
o Smooth muscle cells, numerous macrophages, T-cells, often associated with lipid core and necrotic material.
o Covered in fibrous cap (smooth muscle cells surrounded by connective tissue matrix).
o White in appearance, usually elevated and protrudes into lumen of artery
o Can compromise blood flow but often does not
o Unstable lesion is prone to rupture (type 1 MI caused by plaque rupture)
 Plaque that have ruptured are called “complicated”
* Once rupture occurs, exposure to the underlying tissue results in platelet adhesion, initiation of the clotting cascade, rapid thrombus formation that may suddenly occlude the affected vessel.

  • the fourth stage is the end stage of atherosclerosis, in which the artery becomes completely blocked and blood flow is severely reduced or completely blocked. This stage can be life-threatening and often requires surgery to restore blood flow, such as coronary artery bypass surgery or a heart transplant.
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30
Q

Compare and contrast stable and unstable atheromatous lesions.

A
  • When lesions/plaque is covered by a cap and it is stable and dense it is considered to be “protective”
    o Thick cap provides stability to the lesion
    o Gradually increase in size and may partially occlude the vessel lumina
  • thin, no-uniform cap, macrophage-rich makes an unstable lesion, prone to rupture  leads to thrombosis, hemorrhage, and/or calcification
    o plaque rupture occurs because of inflammatory activation of proteinases, apoptosis of cells within the plaque and bleeding within the lesion
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31
Q

how does myocardial ischemia develop?

A

Develops if coronary blood flow or the oxygen content of coronary blood is insufficient to meet the metabolic demands of myocardial cells

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32
Q

How long does it take myocardial cells to become ischemic?

A
  • Myocardial cells become ischemic within 10 seconds of coronary occlusion, after a few mins the heart loses the ability to contract, cardiac output decreases
    o Cardiac cells remain viable for ~20min, under ischemic conditions > can be restored
    o >20min  MI
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33
Q

causes of MI

A

o Reduced blood supply and O2 to the myocardium-
 Coronary spasms, hypotension, dysrhythmias, decreased O2-carrying capacity of the blood- anemias/hypoxemia, valvular disease
* hemodynamic factors (increased coronary vessel resistance, hypotension, decreased blood volume)
* cardiac factors (decrease diastolic filling time, increased HR),
* hematologic factors (O2 content in blood),
* systemic disorders that reduce blood flow of availability of O2 (shock)
o Increase in myocardial O2 (MVO2) demand-
 Tachycardia, SBP htn, hypertrophy (left ventricular hypertrophy caused from htn or aortic stenosis), valvular disease
 Increase force of myocardial contraction (exercise)

34
Q

hemodynamic consequences of MI

A

o The severity of functional impairment depends on the size of the lesion and the site of infarction. Changes can include-
 Decreased cardiac contractility with abnormal wall motion
 Altered left ventricular compliance
 Reductions in SV, CO, and EF
 Increased left ventricular end-diastolic pressure and volume (LVEDV)
 Increased resistance to ventricular filling (stiffness of heart)
* Sinoatrial node malfunction
 If the coronary obstruction involves the perfusion to the left ventricle, pulmonary venous congestion ensues (LHF); if the right ventricle is ischemic, increases in systemic venous pressures occur (RHF)

35
Q

Effects of ischemia on myocardial metabolism

A

o Decline in production of high energy phosphates (ATP, CP) and decline in tissue stores
o ATP> 60% baseline control: tissue is reversibly injured by ischemia
o ATP< 20% control: cells can’t regenerate high energy phosphate or maintain physiologic ionic gradients
o Ventricular tachydysrhythmias caused by enhanced automaticity, reentry, or triggered activity
 Cell membrane and function changes
 Normal resting membrane potential -90, ischemic membrane potential -70
 Tachydysrhythmias more common in irreversible injury
o Reduction in ATP stores interferes with Na-K exchange
o Intracellular Na and Ca elevate
o Reduction of Ca uptake by SR and extrusion of Ca from cells
o Increased intracellular Ca causes mitochondrial Ca overload, decreasing ATP production further

36
Q

what is reperfusion injury?

A

o Blood flow restored.
o After reperfusion, myocardial cells show structural changes, indicative of cell injury and/or death
o Causes dysrhythmias, further ischemic injury, and contribute to myocardial stunning

37
Q

what is myocardial stunning

A

“myocardial dysfunction”
* A temporary loss of contractile function that persist for hours to days after perfusion has been restored
o After MI or post cardiac surgery
* following a brief episode of severe ischemia, prolonged myocardial dysfunction occurs, then a gradual return of contractile activity.

38
Q

mechanism for myocardial stunning

A

-transient calcium overload of myocyte immediately after re-perfusion
-generation of o2 derived free radicals

39
Q

list the acute coronary syndromes

A

o Unstable angina
o Myocardial Infarction
 STEMI
 Non-STEMI

  • Caused by persistent ischemia or the complete occlusion of coronary artery
40
Q

describe unstable angina

A

o Form of acute coronary syndrome that results in reversible myocardial ischemia
o Signals that an atherosclerotic plaque has become a complicated lesion (ruptured) and MI might soon follow
 Emergent situation
o Small fissuring or disruption of atherosclerotic plaque
o Labile thrombus at site of plaque injury
o Transient episodes of occlusion of thrombotic vessel (no more than 10-20 minutes) with return of perfusion before significant myocardial necrosis occurs
o Release of vasoactive substances by platelets, endothelial vasodilator dysfunction

41
Q

the classifications/severity of unstable angina

A

 Class 1: new onset, severe or accelerated angina
 Class 2: angina at rest, subacute (within preceding month but none within last 48 hours)
 Class 3: at rest and within last 48 hours
* This one is “currently” happening

42
Q

clinical features of unstable angina

A

 Changes ECG- ST segment depression, T wave inversion, often resolves with relief of pain
 No troponin or CPK bump

43
Q

findings on physical exam of unstable angina

A

o Transient 3rd and 4th heart sounds
**indicates increase in ventricular filling as well as S4 sounds ->the very end of diastole, when atrial contraction against a stiff ventricle is responsible for the 4th heart sounds
->when theres a reduction of filling b/c of stiff ventricle–creates 4th heart sounds
->third heart sound: more commonly occurred as an increase filling phase (sound often heard with HF)

o Transient systolic murmur or mitral regurgitation
->b/c the ischemia may have effected the mitral valve apparatus

44
Q

describe the pathophysiology of NSTEMI

A

o Thrombus breaks up before complete distal tissue necrosis has occurred, the infarction will involve only the myocardium directly beneath the endocardium
o more severe plaque damage, more persistent thrombotic occlusion (up to 1 hour), plaque rupture

  • NSTEMI usually results from severe coronary artery narrowing, transient occlusion, or microembolization of thrombus and/or atheromatous material
  • a type of heart attack caused by the complete blockage of a minor coronary artery or partial blockage of a major coronary artery
45
Q

clinical features of NSTEMI

A

 Initial EKG does not show elevated ST;
 Present with ST depression and/or inverted T waves
 Early peak CK level

46
Q

pathophysiology of STEMI

A

o Thrombus lodges permanently in the vessel, the infarction will extend through the myocardium all the way from endocardium to epicardium
o lager plaque fissures, fixed and persistent thrombus, cessation of myocardial perfusion of > 1 hour, transmural necrosis of involved myocardium

47
Q

clinical features of STEMI

A

 May have prodromal symptoms
* unstable angina, malaise, exhaustion
 Pain variable, more severe
 Pain lasts longer than in angina, unrelieved by rest and nitroglycerine
 May present as symptoms of acute LV failure, weakness, or syncope (in the elderly)
 Labs- elevation of CK, CK-MB, myoglobin, LDH1, troponin (begin to rise at 3 hrs from onset)
 ECG changes- ST elevation T wave inversion, Q waves (deep wide Q waves if intervention not done quickly)

48
Q

findings on physical exam of STEMI (6)

A
  • anxious and restless
  • cold perspiration and skin pallor
  • variable HR and BP responses
  • fourth heart sound (reduction in LV compliance)
  • third heart sound (with severe LV dysfunction)
  • systolic murmur (mitral regurgitation)
    ** ischemia could affect mitral valve apparatus, but can also affect the conduction system, affect SA/AV node, can present with bradycardia or heat block
49
Q

classification of STEMI type 1

A

 Type 1:
* caused by atherothrombotic CAD precipitated by plaque disruption (rupture or erosion)
o detection of rise/fall of trop with at least 1 value above the 99th percentile and with at least one of the following-
 ss of acute MI
 new ischemic ECG changes
 development of pathological Q waves
 imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with ischemic etiology
 identification of coronary thrombus by angio including intracoronary imaging or by autopsy

50
Q

classification of STEMI type 2

A
  • ischemia in context of oxygen supply and demand mismatch (not atherothrombosis)
    o i.e. acute GI bleed, sustained tachyarrhythmia, severe HTN
    o oxygen demands are HIGH
    o detection of rise/fall of trop with at least 1 value above the 99th percentile and evidence of an imbalance between myocardial oxygen supply and demand unrelated to acute coronary atherosclerosis, requiring at least one of the following-
     ss of acute MI
     new ischemic ECG changes
     development of pathological Q waves
     imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with ischemic etiology
51
Q

examples of type 2 MI

A

o MI with non-obstructive coronary arteries (MINOCA)
 More common in woman
 STEMI more common
 Ischemic mechanism
 Causes may be plaque disruption and thrombosis, spasm (clamping down on artery), SCAD
o Spontaneous Coronary Artery Dissection (SCAD)
 Epicardial coronary artery dissection not associated with atherosclerosis or trauma
 Mechanism of myocardial injury is coronary artery obstruction caused by formation of an intramural hematoma (IMH) or intimal disruption
 More common in young women, especially pregnancy-associated MIs

52
Q

described stable angina

A

o chest pain caused by MI.
o Caused by gradual luminal narrowing and hardening of the arterial walls, so that affected vessels cannot dilate in response to increased myocardial demand associated with physical exertion or emotional stress
o With rest, blood flow is restored and no necrosis of myocardial cells results
 Associated with disturbance in myocardial fxn but without necrosis. Begins gradually, reaches maximal intensity within minutes. Relieved by rest and/or NTG.
 Related to atherosclerosis where there is a STABLE plaque

53
Q

findings on physical exam for stable angina

A

 Typically experienced as transient substernal chest discomfort, sensation of heaviness/pressure to moderately severe pain
* pain is caused by the buildup of lactic acid or abnormal stretching of the ischemic myocardium that irritates myocardial nerve fibers.
o Pain can radiate to the neck or down the right arm, pallor, diaphoresis, dyspnea may be associated with the pain
 rise in BP and HR during angina
 have physical indicators of peripheral vascular disease
 S3 and pulmonary crackles indicate transient LV dysfunction

54
Q

biggest risk factors for stable angina (2)

A

smoking and DM

55
Q

pathophysiology for stable angina

A

 imbalance between myocardial O2 requirements and supply.
- MVO2 may be elevated by increases in HR, LV wall stress, and contractility; commonly arises from NE release in response to exertion, emotion, or mental stress

56
Q

what is the most common complication of MI?

A

-dysrhythmias
o Abnormal rate of impulse generation by the SA node or by the abnormal conduction of impulses through the hearts conduction system
 blocks

57
Q

the common complications of MI (7)

A
  • dysrhythmias
  • LV failure
  • RV infarction
  • cardiogenic shock
  • papillary muscle rupture
  • pericarditis
  • LV aneurysm
58
Q

LV failure in MI

A

o Many MI result in some degree of HF
o Pulmonary HF

59
Q

RV infarction

A

inferior wall MI

60
Q

what is cardiogenic shock

A

o cardiac output is insufficient to maintain normal arterial pressure and to perfuse kidneys and other organs adequately

61
Q

what causes papillary muscle rupture

A

o tissue necrosis in or around the papillary muscles can cause rupture of these muscles or of the chordae tendineae

62
Q

what is pericarditis

A

o inflammation of the pericardium, rub is often noted 2-3 days after MI

63
Q

LV aneurysm

A

o Weakening of the wall of the infarcted ventricle
o Late complication of MI, occurs months to years after acute event
o Ventricle bulges with systole, resulting in impaired pump function and sign risk for dysrhythmias

64
Q

impact of MI on LV

A

o zone of myocardium loses ability to shorten and perform contractile work. Remaining normal myocardium becomes hyperkinetic (reduction of shortening) as a result of compensatory mechanisms
o Paradoxical contraction (systolic bulging) can lead to aneurysm formation
o Ventricular remodeling

65
Q

what is ventricular remodeling

A

 LV wall thinning and dilation in area of infarctions prior to the formation of a firm fibrotic scar; reduction of myocytes
* When contractility is decreased, stroke volume falls, and left ventricular end-diastolic volume (LVEDV) increases. This causes dilation of the heart and an increase in preload.
* Changes in non-infarcted tissue:
o increase in sarcomere length, greater shortening of fibers
* Neurohumoral activation to compensate for LV dysfunction (hypertrophy): increase in norepi, vasopressin, angiotensin II
 Overall increase in wall tension with LV dilation, wall stress serves as a stimulus for myocyte hypertrophy
* Dilation of the chamber and thickening

Ventricular remodeling refers to changes in left ventricular (LV) geometry, mass, and volume in response to myocardial injury or alterations in load.

66
Q

Compare and contrast gender differences in ischemic heart disease structure, function and symptoms and describe common theories used to explain gender differences.

A
  • Women more likely to have MI with non-obstructive coronary arteries
  • Young women more likely to have coronary artery dissection (especially pregnancy- associated MI’s)
  • Women have more tendency to have inflammatory conditions
  • Women have atypical symptoms at rest
67
Q

Primary- “essential/idiopathic htn”

A

o Approximately 95% of cases of hypertension have no known cause and therefore are diagnosed as primary hypertension

**most common

68
Q

Secondary htn

A

o Secondary hypertension accounts for 5% of cases and is associated with an underlying primary disorder, that raises peripheral vascular resistance or cardiac output
o BP returns to normal if the cause is identified and removed before permanent structural changes occur
 Examples include renal vascular or parenchymal disease, adrenocortical tumors, adrenomedullary tumors (pheochromocytoma), and drugs (oral contraceptives, corticosteroids, antihistamines)

69
Q

Isolated systolic htn

A

o Elevated systolic BP, with normal diastolic bp

70
Q

Discuss hypertension in racial and ethnic minorities.

A
  • higher in blacks and in those with diabetes
  • Lower socioeconomic standing is more prevalent
71
Q

Describe the risk factors for hypertension.

A
  • A combination of genetic and environmental factors is thought to be responsible for the development of primary hypertension
    o Multiple pathophysiologic mechanisms mediate these effects
  • Genetic predisposition
    o polygenic, many genes or gene combos
  • Environmental factors
    o salt, obesity, alcohol, stress, lack of activity, diet, and smoking, with gene predisposition
72
Q

what is HTN cause by?

A

increase in cardiac output, total peripheral resistance, or both.

o Cardiac output is increased by any condition that increases heart rate or stroke volume
 Causes- excess NA intake, renal sodium retention, fluid volume changes, SNS overactivity, stress
o peripheral resistance is increased by any factor that increases blood viscosity or reduces vessel diameter (vasoconstriction)
 Causes- SNS overactivity, increase in renin/angiotensin, cell membrane alterations, hyperinsulinemia, endothelium-derived factors, genetic alteration

73
Q

Explain the primary factors (increased cardiac output and/or peripheral vascular resistance) associated with the pathogenesis of primary hypertension: Renin-Angiotensin System

A

o overactivity of the RAAS contributes to salt and water retention and increased vascular resistance.
o Ang II mediates arteriolar remodeling, which is a structural change in the vessel wall that results in permanent increases in peripheral resistance.
o Ang II is associated with end-organ effects of hypertension, including atherosclerosis, renal disease, and cardiac hypertrophy.

74
Q

Explain the primary factors (increased cardiac output and/or peripheral vascular resistance) associated with the pathogenesis of primary hypertension: inflammation

A

o Endothelial injury and tissue ischemia result in the release of vasoactive inflammatory cytokines.
 Although many of these cytokines (e.g., histamine, prostaglandins) have vasodilatory actions in acute inflammatory injury, chronic inflammation contributes to vascular remodeling and smooth muscle contraction.
o Endothelial injury and dysfunction in primary hypertension are further characterized by decreased production of vasodilators, such as nitric oxide, and increased production of vasoconstrictors, such as endothelin.

75
Q

Explain the primary factors (increased cardiac output and/or peripheral vascular resistance) associated with the pathogenesis of primary hypertension: Obesity

A

o causes changes in what are called the adipokines (leptin, resistin, and adiponectin) and is associated with increased activity of the SNS and the RAAS.
o Obesity is linked to inflammation, small artery remodeling, endothelial dysfunction, insulin resistance, and an increased risk for cardiovascular complications from hypertension.

76
Q

Explain the primary factors (increased cardiac output and/or peripheral vascular resistance) associated with the pathogenesis of primary hypertension: insulin resistance

A

o associated with endothelial injury and affects renal function, causing renal salt and water retention. Insulin resistance is associated with overactivity of the SNS and the RAAS

77
Q

Explain the primary factors (increased cardiac output and/or peripheral vascular resistance) associated with the pathogenesis of primary hypertension: Sympathetic Nervous System Overactivity

A

o increased production of catecholamines (epinephrine and norepinephrine)
o causes increased heart rate and systemic vasoconstriction, thus raising the blood pressure.
o Efferent sympathetic outflow stimulates renin release, increases tubular sodium reabsorption, and reduces renal blood flow.
* Angiotensin II signals tyrosine kinases -> inflammation, contraction, adhesion, migration, cell growth
* Oxidative stress (increased ROS) -> vascular inflammation, plaque formation, plaque rupture
* Other Associations with HTN
o Obesity
o Metabolic syndrome
o Type 2 DM
o Hyperuricemia: uric acid-mediated activation of RAAS, increase in salt sensitivity
 gout
o Obstructive Sleep Apnea

78
Q

Discuss current theories underlying the development of hypertension: Hypothesis of Autoregulation

A

o intravascular volume contraction and expansion regulated by kidney.
o Initially high CO giving way to a persistently elevated peripheral resistance.
o Blood flow to tissues is more than is required, vessels constrict to reduce supply, PR increases and remains high by structural thickening of arterioles

79
Q

Discuss current theories underlying the development of hypertension: Renal sodium retention

A

o Structural changes in kidney lead to sodium retention.
o In “salt sensitive individuals” with impaired kidney function, a rightward resetting of pressure-sodium excretion curve prevents the return of BP to normal
 You eat something salty; your BP remains high for a couple hours, even when you are on medication
o Inherited defect in renal sodium excretion
 Possible causes-
* Congenital reduction in number of nephrons or in filtration surface (limits Na excretion)
* Nephron heterogeneity- subpopulation of nephrons are ischemic, renin secretion is baseline elevated and interferes with compensatory capacity of normal nephrons to excrete Na
* Excess Sodium Intake
o Causes an increase in fluid volume, increase in vascular reactivity (promote vasoconstriction and elevated BP)

80
Q

what is complicated HTN

A

o chronic hypertension that damages the walls of systemic blood vessels. Within the walls of arteries and arterioles, smooth muscle cells undergo hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called “vascular remodeling”
o Once significant fibrosis has occurred, reduced blood flow and dysfunction of the organs perfused by these affected vessels are inevitable.

81
Q

target organ damage associated with chronic HTN

A

 Kidney, brain, Heart, extremities, eyes

82
Q

Describe the pathophysiologic hallmark of hypertension

A
  • BP= CO x peripheral resistance (the artery’s ability to expand and constrict)
  • development of the disease, of HTN
    o Increased cardiac output
     Increased pre load (filling), increased contractility (pumping)
     It is increased by any condition that increase HR or stroke volume
    o Increased peripheral resistance
     Vasoconstriction- tone function
     Hypertrophy- thickening of smooth muscle cell
     it is increased by any factor that increased blood viscosity or reduces vessel diameter

Advanced Patho Exam 3 (5 decks)

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