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Pathology 3 > quiz 1- CV 1-3 > Flashcards

quiz 1- CV 1-3 Flashcards

1
Q

• What is atherosclerosis?

A

chronic inflammatory response in walls of arteries, mostly dt deposition of lipoproteins (plasma proteins that carry cholesterol and TGs).
• hallmark is formation of multiple plaques within arteries.

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2
Q

• What are the multiple cellular elements involved in development of atherosclerosis?

A

• Endothelial cells, smooth muscle cells, plts, WBCs, many chemotactic and inflammatory mediators.

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3
Q

• What is atherogenesis?

A
  • result of complex and incompletely understood interactions bw the cellular elements and other biologic processes; lead to signs of atherosclerosis
  • Contributors: Vasomotor function, thrombogenicity of vessel wall, state of activation of coagulation cascade, fibrinolytic system, smooth muscle cell migration and proliferation and adrenergic stimulus
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4
Q

• What is the “response to injury” theory?

A
  • Help explain atherogenesis; endothelial injury is main factor initiating it
  • Vascular injury (mechanical, immune complexes, viruses, homocysteine, etc)
  • Trap LDL in arterial wall
  • Oxidize LDL (oxLDL)
  • monocytes/T-cells adhere/migrate into subendothelium
  • Monocytes/M0s ingest lipid = “foam cells”
  • Foam cell, T-cells, and smooth muscle “fatty streak”
  • Continued cell influx and smooth muscle proliferation “fibrous plaque”
  • plaque fissure/rupture w activation of platelets and thrombogenesis
  • Occlusive thrombi and ischeimic event
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5
Q

• What may contribute to endothelial injury?

A
  • HTN and cell wall damage from sheer force of blood flow
  • ↑ oxLDL, hyperglycemia, hyperhomocystinemia
  • infectious agents
  • chemical toxins, particularly cigarette smoke.
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6
Q

• What do monocytes do?

A
  • Circulate, infiltrate intima
  • differentiate into M0s, ingest oxLDL
  • slowly turn into large “foam cells“
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7
Q

• what are foam cells?

A
  • Many cytoplasmic vesicles of high lipid content.

* eventually die, further propagate inflammatory process.

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8
Q

• What happens to smooth muscle in atherogenesis?

A
  • Proliferate in intima, induced by PDGF, cytokines, NO

* Makes of large part of fatty streak

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9
Q

• How do platelets play role in atherosclerosis?

A
  • Release factors to promote proliferation of SM
  • Part of clotting= yields thrombus
  • Extrinsic: activated by blood and vascular elements
  • Intrinsic: vascular only (skin, muscle, CT)
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10
Q

• What is the fatty streak?

A
  • earliest grossly visible pathologic lesion of atherosclerosis
  • dt focal accumulation of serum lipoproteins in intima.
  • Micro: foam, T, smooth mm cells in varying proportions.
  • Seen in aorta and coronary arteries of most individuals by 20 years of age.
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11
Q

• What can a fatty streak progress to?

A
  • fibrous plaque dt lipid accumulation and migration and proliferation of SM
  • SM cells responsible for deposition of ECM CT
  • = fibrous cap over foam cells, EC lipid, necrotic cellular debris
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12
Q

• Are atherosclerotic plaques random?

A
  • lesions of atherosclerosis don’t occur in random fashion.
  • Hemodynamic factors interact with the activated vascular endothelium.
  • blood shear stresses generated by blood flow modulate genes in endothelium activity of occur in branching, curves, where blood has sudden changes in velocity and direction of flow.
  • shear stress and turbulence promotes atherogenesis at important sites in coronary arteries, major branches of TA and AA, large vessels of lower extremities.
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13
Q

• What does growth of the fibrous plaque cause?

A

• vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, compromised O2 supply to target organ.

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14
Q

• What is ischemia?

A

• imbalance bw supply and demand of blood (O2, nutrients, waste removal) to a tissue

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15
Q

• what is Coronary artery disease (CAD)?

A

• describes a reduction in blood flow to cardiac muscle.

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16
Q

• What is Ischemic heart disease (IHD)?

A
  • Aka: myocardial ischemia
  • inadequate supply:demand ratio by heart muscle.
  • more a clinical rather than pathological term
  • > 90% cases: reduction in coronary blood flow dt atherosclerotic coronary arterial obstruction.
  • 10% involves coronary artery spasm or embolism.
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17
Q

• What are the 4 major syndromes of clinical manifestation of IHD?

A
  • Myocardial infarction (MI): duration/severity causes death of heart muscle.
  • Angina pectoris: less severe, doesn’t cause death of cardiac muscle. 3 main types: stable, variant, unstable (may lead to MI)
  • Chronic IHD w HF
  • Sudden cardiac death.
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18
Q

• Is CAD always symptomatic? IHD?

A
  • CAD: In most cases, there is a long period (usually decades) of silent, slowly progressive, coronary atherosclerosis before becomes symptomatic.
  • IHD: clinical presentations and syndromes are only the late manifestations of coronary atherosclerosis that usually begins during childhood or adolescence.
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19
Q

• Why is CAD complex?

A

• dynamic interaction, many processes like fixed atherosclerotic narrowing of coronary arteries, intraluminal thrombosis over disrupted atherosclerotic plaque, resultant platelet aggregation, and vasospasm.

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20
Q

• What is the human reaction to plaque formation?

A
  • coronary arteries enlarge

* luminal stenosis may only occur once plaque occupies > 40% area bound by internal elastic lamina.

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21
Q

• How does lesion progress prior to MI or acute syndromes?

A
  • not necessarily a severely stenotic and hemodynamically significant lesion prior to its acute change.
  • plaques that undergo abrupt disruption leading to coronary occlusion usu previously produced only mild to moderate luminal stenosis.
  • ~2/3 plaques that rupture w total/near-total occlusive thrombosis have < 50% luminal occlusion before rupture
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22
Q

• What is the process of a plaque leading up to rupture?

A
  • As fibrous cap succumbs to sheer forces or vasospasm, inflammatory cells localize, cause weakening until plaque ruptures.
  • Disruption of endothelium exposes thrombogenic contents of core of plaque to circulating blood.
  • Rupture of plaque exposes thrombogenic core
  • Leads to thrombus formation, partially or completely occlude blood flow
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23
Q

• What are the sxs of CAD?

A
  • highly variable.
  • mild atherosclerosis may have severe angina, MI or sudden cardiac death as their first sx of
  • anatomically advanced disease may have few if any sxs, no functional impairment
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24
Q

• what are the main sxs of angina and MI?

A
  • Chest pain, usu across anterior precordium, tightness, pain, weight
  • Pain may radiate to jaw, neck, arms, back, epigastrium.
  • Dyspnea indicates poor ventricular compliance w acute ischemia.
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25
Q

• What are some additional sxs of angina and MI?

A
  • Diaphoresis
  • Anxiety
  • Lightheadedness and syncope
  • Cough/ wheezing
  • N/V or abdominal pain, usu w infarcts of posterior or inferior walls of heart.
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26
Q

• What is angina pectoris?

A

• Paroxysmal usu recurrent attacks of chest discomfort (constricting, squeezing, choking, knifelike) caused by transient (15 sec -15 min) myocardial ischemia wo cellular necrosis of MI

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27
Q

• What is stable angina pectoris?

A
  • cardiac ischemia usu dt fixed lesion in coronary artery.

* Sxs occur only on exertion, generally relieved by rest/medications which dilate arteries, such as nitrates.

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28
Q

• What is variant angina?

A
  • Aka Prinzmetal angina.
  • exact pathophysiology unknown
  • intermittent vasospasm mb key to sx devt
  • Pain usu at rest, mmbay be well controlled by vasodilators such as calcium channel blockers.
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29
Q

• What is unstable angina pectoris?

A
  • pattern of inc frequency/intensity of chest pain, usu at rest
  • prolonged episode may cause MI
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30
Q

• what are the ssx of MI?

A
  • PE mb normal, mb asx
  • Anxious, agitated, pale, diaphoretic
  • HTN- may cause MI, or may be st catecholamines of anxiety and stress
  • Hypotension- mb large infarct, often if RV
  • Dysrythmias
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31
Q

• What are the risks for MI?

A
  • PMHx or FHx of MI (M45
  • Younger age, females=outlier, may go undiagnosed
  • Cocaine, insulin-dependent, hi cholesterol, FHx CAD
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32
Q

• What are the stats on MI deaths?

A
  • > 50% occur in pre-hospital setting
  • 10% are in-hospital
  • 10% of MI occur in first post-infarction year
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33
Q

• What are the major types of MI?

A
  • Transmural infarction, usu dt acute coronary thrombosis
  • Subendothelial (non-transmural): Coronaries narrowed but patent, Thrombotic occlusion → thrombolysis, short period of ↑ O2 demand/dec O2 delivery
  • Hypotension/HTN
  • Anemia
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34
Q

• What are lab findings with MI?

A
  • ECG may show progression from ischemia to infarction.
  • Specific EKG abnormalities can reflect location
  • MI dt total coronary occlusion has more homogeneous tissue damage, shown by Q-wave MI pattern on EKG.
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35
Q

• How does acute anterolateral MI appear on ECG? Causes? Risks?

A
  • ST elevation in leads over anterior and lateral surfaces
  • the more significant the ST elevation , the more severe the infarction.
  • loss of general R wave progression across precordial leads
  • mb symmetric T wave inversion
  • frequently caused by occlusion of proximal left LAD CA, or combined w R CA or LCx.
  • Hi risk arrhythmias: LBBB, hemo-blocks, type II second degree AV conduction blocks.
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36
Q

• What are the labs reflective of acute MI?

A

↑ WBC, LDH, cardiac enzymes:
↑ Creatine phosphokinase (MB band )
↑ Troponin (esp. Troponins I and T)

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37
Q

• what is CAD?

A
  • Progressive luminal narrowing of CA dt expansion of fibrous plaque, usu dec flow
  • > 50-70% of lumen diameter is obstructed.
  • Sxs: inadequate blood to target organ if inc metabolic activity, or w superimposed coronary spasm
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38
Q

• What is AMI?

A
  • myocardial necrosis dt prolonged critical imbalance bw supply and demand of O2 for myocardium
  • commonly dt plaque rupture in coronary artery.
  • subendothelial area exposed, platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into plaque, varying degrees of vasospasm.
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39
Q

• What are other common causes of AMI?

A
  • Emboli to coronary arteries, mb dt cholesterol or infection.
  • Coronary artery vasospasm: if prolonged, w underlying atherosclerotic dz, or poorly functioning heart muscle
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40
Q

• What are some additional causes of MI?

A
  • Coronary anomalies: irregular or absent CAs, aneurysms CAs
  • Hypoxia dt pulmonary dz, CO poisoning, or other inhaled toxins.
  • Arteritis
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41
Q

• What is the physiology behind MI?

A
  • Dec O2 to myocardium → anaerobic instead of aerobic metabolism.
  • ATP synth dec in 1-2 min; reduced to 50% by 10 mins
  • dec ATP disrupts Na+/K+ ATPase = inc membrane permeability of cardiac muscle
  • myocytes swell, cellular function declines
  • Cal influx activates degradative enzymes, disrupts all cellular function.
  • Irreversible cell death in ~15-20 min from onset of injury
  • reperfusion in 1-6 hrs may save most of the affected myocardium, dramatic reduction of morbidity and mortality.
  • MI may → lethal effects in minutes, aka sudden cardiac death.
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42
Q

• What are the gross and histo-pathology changes after MI in the first day?

A
  • 0-0.5 hrs; none; none
  • 0.5-4 hrs; none; Glycogen Depletion, seen w PAS Stain and poss. waviness of myocardial fibers at borders
  • 4-12 hrs; slight mottling; Initiation of coagulation necrosis, edema, hemorrhage
  • 12-24 hrs; dark mottling; Ongoing coagulation necrosis, hypereosinophilia, contraction band necrosis in margins, beginning of neutrophil infiltration
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43
Q

• What are the gross and histo-pathology changes after MI at 1-10 days?

A
  • 1-3 d: Infarct center turns yellow-tan; Continued coagulation necrosis, Loss of myocardial cell nuclei and striations, inc neutrophils to interstitium
  • 3-7 d: Hyperemia at border with softening yellow-tan center; Begin dead muscle fiber disintegration, neutrophil necrosis, M0 removal of dead cells at border
  • 7-10 d: Maximally soft lesion w yellow to red-tan margins; Inc phagocytosis of dead cells at border, begin granulation tissue formation at margins
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44
Q

• What are the gross and histo-pathology changes after MI at 10 d- 2 months?

A
  • 10-30 days: Red-gray w depressed borders; Mature granulation tissue w type I collagen
  • 2-8 weeks: Gray-white granulation tissue; Inc collagen deposition, dec cellularity
  • > 2 months: Completed scarring; Dense collagenous scar formed
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45
Q

• What does a 1-day old infarct histo look like?

A

o coagulative necrosis w wavy fibers (elongated and narrow), compared w adjacent normal fibers (at right). Wide space bw dead fibers contain edema fluid and scattered neutrophils.
o 24 hours post-MI. Note the wavy fibers dt edema. Some viable myocytes present. (left: low mag, right: high mag)

46
Q

• What does 2-day post MI histo look like?

A

o pt died 2 days post MI, myocytes are irreversibly damaged by loss of nuclei.

47
Q

• What does 7-10 days post MI histo look like?

A

o Near complete removal of necrotic myocytes by phagocytosis approx

48
Q

• What does 2-month old MI histo look like?

A

o Well healed myocardial infarct w replaced necrotic fibers by dense collagenous scar. Residual cardiac muscle cells present.

49
Q

• What does gross 6/7/9-day post MI look like?

A

o 6: sectioned interventricular septum. dead muscle is tan-yellow w surrounding hyperemic border.
o 7: cross section, large anterior LV wall and septum
o 9: Bw 7-10 d, areas of infarction usu have yellow to reddish-tan borders. at autopsy, tissue is pliable and soft to touch.

50
Q

• What does gross 2-month post MI look like?

A

o previous extensive transmural myocardial infarction of LV. thickness of myocardial wall is normal superiorly, but inferiorly is only a thin fibrous wall.

51
Q

• How long after an MI do cardiac aneurysms most likely occur?

A

o 2-8 wks, dt formation of thin scar tissue

52
Q

• What are some potential cardiac complications following MI?

A

o Abnormal LV function ~ proportional to size of infarct.
o Severe “pump failure” (cardiogenic shock), 10-15% post-MI, usu w large infarct (> 40% LV)
o Arrhythmias, usu cause of sudden death;
o Cardiac rupture dt weak, necrotic, inflamed myocardial muscle; hemopericardium and cardiac tamponade usu fatal.
o Hypotension
o CHF
o Hypoxemia
o Pericarditis
o Repeat MI

53
Q

• What is anterior ventricular wall rupture?

A

o Anterior myocardial rupture 2nd to acute infarction.

54
Q

• What is septal wall rupture?

A

o Rupture of ventricular septum 2nd to acute MI

55
Q

• What is a hemopericardium?

A

o Blood trapped in pericardium → hemopericardium. Such a massive amount of hemorrhage can lead to cardiac tamponade.

56
Q

• What is a papillary muscle rupture?

A

o Complete rupture of necrotic papillary muscle 2nd to acute M.I.

57
Q

• What are potential non-cardiac complications after MI?

A

o Aspiration
o Infection i.e. pneumonia
o Complications from prolonged immobilization (DVT, PE)

58
Q

• How does pericarditis form after MI?

A

o Exudative inflammation
o fibrinous or fibrino-hemorrhagic, develops on 2-4th day after transmural MI, dt inflammatory epicardial response to injury
o usu resolves w/o serious consequence or sequelae.

59
Q

• What does fibrino-hemorrhagic pericarditis look like, gross?

A

o dark, rough epicardial surface over acute infarct.

o ~17 to 25% of AMI, usu 2-4 days post

60
Q

• What is Dressler’s syndrome?

A

o pericarditis that occurs weeks to months after injury to heart or pericardium.
o Ssx: lo fever, chest pain (usu pleuritic), pericardial friction rub, pericardial effusion.
o AI response to myocardial antigens.

61
Q

• What is optimal blood pressure, by AHA? Pre-HTN? Stage 1 HTN?

A

o systolic <= 80
o P: 121 -139/ 81 -89
o 1: 140-159/90-99

62
Q

• What are the sxs of HTN?

A

o Most asx for decades
o 5% have rapid rise in BP, w/o tx mb death in short time (days- 2 yrs)
o > 180-200/> 120 mb severe HA, retinal hemorrhages, papilledema
o Mb dec level consciousness, sz

63
Q

• When is HTN a medical emergency?

A

o Accelerated, with 1+ sxs

64
Q

• What is primary/essential HTN? Secondary?

A

o P: 90 -95% has unknown cause

o S: other 5-10%. many dt chronic renal failure, renal artery stenosis

65
Q

• What causes renal artery stenosis?

A

o Atherosclerosis primary cause >50; Fibromuscular dysplasia <40
o Other: arteritis, renal artery aneurysm, compression (tumor), neurofibromatosis, fibrous bands

66
Q

• How does renal artery stenosis contribute to HTN? Renal failure?

A

o macula densa senses dec systemic BP dt reduced blood flow thru narrow artery
o =perceived dec BP, activate RAAS (normally counteracts lo BP)
o Causes HTN (high arterial blood pressure).
o RF: dec GFR, w/o tx

67
Q

• What are some causes of 2nd HTN?

A 
o	Many
o	Drugs, NSAIDs
o	Sleep apnea
o	Pheochromocytoma
o	Hyperaldosteronism (Conn's syndrome)
o	Cushing's syndrome 
o	Hyperparathyroidism
o	Acromegaly
o	Hyperthyroidism/ Hypothyroidism
68
Q

• What are some potential MOA for primary HTN?

A

o 1) Abn membrane Na transport dt defect/inhibition of Na-K pump
o 2) Inc cellular permeability to Na = inc intracellular Na, cell more sensitive to sympathetic stimulation.
o 3) Ca follows Na, hi intracellular Ca, not Na, responsible for inc sympathetic

69
Q

• What is the purpose of RAAS?

A

o JGA regulates plasma volume and BP

o Renin, proteolytic enzyme in granules of the JGA cells, catalyzes angiotensinogen to angiotensin I.

70
Q

• What causes chronic renal dz? What does CRD cause?

A

o HTN most common, then DM

o contributes to HTN by incproduction of renin, salt retention, systemic vasoconstriction

71
Q

• What are some complications of HTN?

A

o leading cause of IHD, PVD, cerebrovascular dz, ventricular hypertrophy, CHF

72
Q

• what risks are reduced with reduced HTN?

A

o heart attack, CHF, stroke, kidney failure

73
Q

• what are 3 types of HTN?

A

o labile, benign or accelerated.

74
Q

• What is labile HTN?

A

o inconsistent BP elevations
o “white coat HTN”: pt get nervous/anxious w dr, hi catecholamines; otherwise normotensive
o Pheochromocytoma: events usu dramatic; paroxysmal HAs, sweats, palpitations, HTN, orthostatic hypotension

75
Q

• What is “benign” HTN?

A

o very slow development

o potential sequelae: MI, stroke, RD/RF, PVD, blindness, more

76
Q

• what is an aneurysm?

A

o “ballooning out” of weak vessel wall, mb dt shear force, hi BP
o Mb any vessel, arteries more common
o Greatest morb/mort: aorta, circle of Willia
o AA: Rupture at 6-7 cm, mb felt as mass in abdomen

77
Q

• What is aortic dissection?

A

o life threatening complication of hypertension
o blood penetrates intima and enters media layer.
o can affect ascending, aortic arch, descending, and abdominal aorta

78
Q

• What is gross appearance of an aortic dissection?

A

o red-brown thrombus, intimal tear
o “double lumen” effect
o severe atherosclerosis, cystic medial necrosis, hypertension are risk factors

79
Q

• how does aortic dissection present clinically? Classic aortic arch sx?

A

o excruciating pain, mb resistant to large doses of morphine
o mb stroke (carotid dissection), MI (coronary dissection)
o if dt HTN, must immediately control BP, to be surgical candidate and inc likelihood of survival
o arch: pain radiating down back, tearing sensation

80
Q

• What is a carotid artery dissection?

A

o Dissection may occur in carotids

o Mb caused by aortic dissection ascending to carotid

81
Q

• What is Marfan’s syndrome?

A

o AD trait; abn CT, dt production of abn fibrillin-1 protein.
o 5–9% of aortic dissections (often fatal)
o Tall, long extremities, digits

82
Q

• How do vessels abnormalities occur in Marfan?

A

o Aortic aneurysms; usu proximal aortic dissections

o Weak CT, vessels vulnerable to damage

83
Q

• What are the most serious ssx of Marfan?

A

o CV: new onset fatigue, SOB, palpitations, tachycardia, new onset murmur
o Mitral/aortic regurgitation
o Often asx, until cystic medial degeneration causes AA/AD (surgical emergency)

84
Q

• How does histology of cystic medial necrosis look?

A

o mucin stain of aorta wall

o Pink elastic fibers, instead of running in parallel arrays, are disrupted by pools of blue mucinous ground substance.

85
Q

• Which famous person in hx was thought to have Marfan?

A

o Abraham Lincoln, but debated

o more likely had multiple endocrine neoplasia (MEN) type 2B, that caused skeletal features almost identical to Marfan

86
Q

What is CHF?

A
  • heart can’t pump enough blood to get body O2 and nutrients.
  • → inadequate emptying of blood at venous side and inadequate blood delivery to both pulmonary and systemic circulation
  • =heart failure
87
Q

• What does “left” and “right” circulation refer to?

A
  • Right side has de-oxy blood; lowest P veins entering heart; hi P pulmonic arteries
  • Left has oxy-blood; highest P arteries from heart; lo P pulmonic veins
88
Q

• How does heart typically respond to incr demands?

A
  • Inc HR

* Inc contractility of ventricles

89
Q

• When do signs of CHF begin?

A

• As demands on heart outstrip normal range of physiologic compensatory mechanisms

90
Q

• What is contractility?

A
  • =inotropic state
  • ability of muscle to contract or shorten=myocardial muscle fibers
  • stretch in response to inc blood volume during filling of diastole, stretch and shorten when blood is ejected in systole
91
Q

• what happens to contractility of ischemic muscle fibers?

A

• lose their full elastic recoil forcing healthy muscle fibers to work harder to maintain adequate cardiac output

92
Q

• what happens in acute CHF?

A
  • sympathetic NS and RAAS maintain blood flow and pressure to the vital organs.
  • Inc neuro-hormonal activity → inc myocardial contractility, selective peripheral vasoconstriction, salt and fluid retention, BP maintenance.
  • Inc fluid retention 2nd by dec hepatic metabolism of aldosterone dt diminished hepatic perfusion 2nd to systemic venous congestion
  • causes inc blood volume and venous return (preload) to heart.
  • Dec blood to kidneys activates RAAS
  • causes renal arteriolar constriction, dec GFR, inc reabsorption of sodium from proximal and distal tubules.
  • Result is inc fluid retention
93
Q

• What happens in chronic CHF?

A

myocardial cells eventually die → necrosis (or from apoptosis) → fibroblast proliferation, scarring → ↑ ventricular wall thickness, CHF worsens → blood/fluid stasis in lungs → heart failure cells

94
Q

• What is the cycle of chronic CHF?

A

Heart damage → ↓CO → ↓renal perfusion → ↑Na retention, ADH, water reapsorption → fluid overload/edema → heart damage, etc

95
Q

• What are heart failure cells?

A

• hemosiderin containing macrophages in alveoli

96
Q

• what primary heart dos may result in CHF?

A

• CAD, valvular dos, cardiomyopathies

97
Q

• What are precipitating factors of CHF?

A
  • Asx: ssx dt unrelated illness or stress
  • Common: cessation of cardiac drugs, like a diuretic
  • Cardiac pts usu on many drugs, may stop 1 bc: money, poor compliance, side effects, perception of diminished need for medication.
  • Ex: cessation of diuretic, but requires for volume optimization. May → Na and water retention and worse CHF
  • Dysrythmias a
  • Tachycardia: cause dec diastolic filling time , → dec SV
  • Tachycardia may cause angina dt inc myocardial O2 demand
98
Q

• What cardiac conditions is cardiac failure most common?

A

• that result in dec contractility

99
Q

• what are common underlying conditions that can cause impaired myocardial muscle fxn? Systemic that cause CHF?

A
  • inflammatory or degenerative muscle dzs of heart, atherosclerosis, HTN, myocardial ischemia, infarction
  • Systemic: Inc BMR (fever), Anemia/hypoxia dec O2 supply, resp/metabolic acidosis/ electrolyte imbalances (hypocalcemia) dec myocardial contractility → dec CO
100
Q

• How is CHF classified?

A
  • Acute vs. chronic
  • Right vs. left
  • Compensated vs. decompensated
  • Low output vs. high output
101
Q

• What happens w LCHF?

A
  • LV can’t produce adequate SV to overcome resistance → dec CO
  • can → pulmonary congestion dt inc LV end-diastolic P and inc LA
  • usu dt LV infarction, HTN, mitral valve dz
  • Blood overfills ventricle dt damaged heart muscle, overflows back into lungs causing pulmonary complications
102
Q

• What causes LCHF?

A
  • IHD
  • HTN
  • Aortic and mitral valvular dz
  • Non-ischemic myocardial dzs
103
Q

• What is RCHF? Causes?

A
  • Dt ineffective RV contraction
  • most common cause: LCHF
  • Isolated RCHF uncommon
  • Acute conditions such as RV infarction or PE can cause isolated RCHF
104
Q

• What is cor pulmonale? Cause?

A
  • Enlarged RV causs heart failure

* directly dt pulmonary disease: emphysema, chronic bronchitis, PE, PH

105
Q

• what causes pulm htn? And cor pulmonale?

A
  • most commonly dt COPD (emphysema, chronic bronchitis)

* Any dz that causes chronically low blood O2 may lead to PH and CP

106
Q

• What are ssx of L/R CHF?

A
  • Classic: Fatigue, coughing, edema, weight gain
  • Pure LCHF: signs of pulmonary venous congestion
  • pure right: signs of systemic venous congestion.
  • Both L and R can affect the other → combo of both S and P
  • Cough dt fluid in lungs (pulm edema), worse lying
  • Easy exhaustion (not enough blood/O2 to heart)
  • Edema: feet, ankles, legs, belly (fluid backs up from weak heart)= rapid weight gain
107
Q

• What is the so-called nutmeg liver?

A

• Gross appearance of liver congestion dt CHF

108
Q

• What is micro histo appearance of liver congestion dt CHF?

A

• Micrograph of congestive liver demonstrating perisinusoidal fibrosis and centrilobular sinusoidal dilation.

109
Q

• What are high and lo output failure? Sxs?

A
  • Another type of CHF
  • Like pump that is either working too heart or not enough → ineffective
  • High: peripheral vasodilatation and warm extremities
  • Low: vasoconstriction and cool
110
Q

• What causes HO CHF?

A
  • Hyperthyroidism
  • Stimulants: cocaine, meth
  • Anemia: lo O2 carrying capacity, inc HR → failure
  • Paget’s dz: abn bone growth dt inc osteoblast activity → vascularity, needs more blood
111
Q

• What causes LO CHF?

A
  • heart contractibility has weakened: MI, ischemia → ventricular dilation or hypertrophy
  • infections: endocarditis, myocarditis
  • often seen in late stage CHF

Pathology 3 (6 decks)

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