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Patho 1016- Test 2 Review Study Guide, Study Guides, Projects, Research of Pathology

Virginia State University (VSU)Pathology

Patho 1016- Test 2 Review Study Guide

Typology: Study Guides, Projects, Research

2023/2024

Available from 07/17/2024

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Patho 1016- Test 2 Review Study Guide
1.tunica intima: smooth inner layer; composed of simple squamous
epithelium
2.tunica media: middle layer; composed of elastic connective tissues
and smooth muscle
3.tunica externa: outer layer, composed of collagen connective tissues.
4.endothelium cells: plays an important role in controlling vascular
function, me- tabolism of hormones and regulate immune and
inflammatory reactions.
5.endothelium cells: controls the transfers of molecules, regulating blood
flow and vascular resistance, and control platelet adhesion and blood
clotting.
6.angiogenesis: formation of new blood vessels
7.Endothelium cells controls:: Oxygen, Na,K Cl
8.Endothelium cells regulates vascular resistance by:: signalling outer
muscu- lar layer to relax- Nitrous Oxide.
9.Endothelium cells: Adhesion and blood clotting: they are slick like
silicon to let blood flow.
10.Endothelium cells: Metabolism: Insulin production signalling when
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Patho 1016- Test 2 Review Study Guide

  1. tunica intima: smooth inner layer; composed of simple squamous epithelium
  2. tunica media: middle layer; composed of elastic connective tissues and smooth muscle
  3. tunica externa: outer layer, composed of collagen connective tissues.
  4. endothelium cells: plays an important role in controlling vascular function, me- tabolism of hormones and regulate immune and inflammatory reactions.
  5. endothelium cells: controls the transfers of molecules, regulating blood flow and vascular resistance, and control platelet adhesion and blood clotting.
  6. angiogenesis: formation of new blood vessels
  7. Endothelium cells controls:: Oxygen, Na,K Cl
  8. Endothelium cells regulates vascular resistance by:: signalling outer muscu- lar layer to relax- Nitrous Oxide.
  9. Endothelium cells: Adhesion and blood clotting: they are slick like silicon to let blood flow.
  10. Endothelium cells: Metabolism: Insulin production signalling when

2 / 25 increasing glucose levels.

  1. Exogenous lipid pathway: absorption of fats from the digestive tract into the circulation
  2. Endogenous lipid pathway: transportation of fats synthesized in the liver b/w the liver and the peripheral tissues
  3. Hyperlipidemia: excessive amounts of lipids in the blood
  4. High-density lipoprotein (HDL): good cholesterol synthesized by the liver and transports cholesterol back to the liver from the periphery.
  5. low-density lipoprotein (LDL): "bad cholesterol" in the blood, which raises the risk of cardiovascular disease, and atherosclerotic lesions
  6. hypercholesteremia: increased levels of cholesterol in the blood.
  7. management of hyperlipidemia: reduce LDL; Pt will need to increase con- sumption of unsaturated fats that increases HDL's, pt can exercise and they can take medications and supplements such as statins, niacin, bile acid resins, fibrates and omega 3 fish oil.
  8. Major risk for CAD include:: smoking, hypertension, Diabetes and family h/x
  9. atherosclerosis: affects vascular system and the means formation of fibro-fatty lesions in the intimal lining of large and medium sized

4 / 25 migrate b/w the endothelial cells to stay in the intimal, and transforms into macrophages and engulf LDLS

  1. lipid accumulation and smooth muscle proliferation: activates macrophages release toxic oxygen species that oxidize LDLs
  2. clinical manifestation of atherosclerosis: depends on vessel involved and the extent of vessel occlusion and cerebral vascular versus cardiac disorder
  3. stable plaque: Thick fibrous caps, partially block vessels, doesn't usually form emboli
  4. unstable plaque: Thin fibrous caps that can rupture and become emboli, may completely block the artery
  5. neural mechanism of blood pressure regulation: located in the medulla and pons; it is the intrinsic and extrinsic reflexes.
  6. hormonal mechanism of blood pressure regulation: Renin-angiotensin- al- dosterone( RAA) system from the kidneys, and ADH, that is released by the posterior pituitary.
  7. hypertension: an elevation in systolic or diastolic BP, it is most common in young male of all health problems leading factors for CV disorders.

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  1. pathophysiology of hypertension: caused by increased in cardiac output and peripheral resistance that caused and increase in HR
  2. primary hypertension: The chronic elevation in blood pressure that occurs without evidence of other disease
  3. secondary hypertension: high blood pressure caused by the effects of another disease
  4. Hypertension manifestations: "silent killer", fatigue, headache, malaise, and dizziness; frequently asymptomatic until it becomes severe at target organs
  5. hypertension target organ damage in the heart: atherosclerosis and an in- crease work load, and left ventricular hypertrophy.
  6. hypertension target organ damage in the brain: TIA/ Storke and dementia
  7. hypertension target organ damage in the kidneys: neprosclerosis
  8. hypertension target organ damage in the eyes: retinopathy
  9. Hypertension complications: systolic of 180 and a diastolic BP of 120, and if pt has severe headache, dyspnea, arterial spasm of cerebral arteries and if pt has cerebral edema.
  10. Hypertension during pregnancy: preclampsia/ eclampsia

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  1. Aldosterone: "salt-retaining hormone" which promotes the retention of Na+ by the kidneys. na+ retention promotes water retention, which promotes a higher blood volume and pressure
  2. Beta Blockers: decrease heart rate and dilate arteries by blocking beta recep- tors
  3. Diuretics: Drugs that elevate the rate of bodily urine excretion
  4. ACE inhibitors: renal damage
  5. right sided heart failure: causes swelling in extremities
  6. Left sided heart failure: affects pulmonary
  7. coronary heart disease: heart disease caused by atherosclerosis in the arter- ies that supply blood to the heart muscle, and an occlusion of blood flow to the coronary arteries.
  8. pathogenesis of CAD: lesions tend to be located at the first several centimetres of the left anterior descending and left circumflex and the entire length of the righty coronary artery.
  9. acute coronary syndrome (ACS): caused by acute plaque distribution and range from unstable angina to MI
  10. Chronic Ischemic Heart Disease: caused by atherosclerotic or vasospastic obstruction of coronary arteries ( stable angina)

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  1. pathophysiology CAD: occlusion of arteries, contractility stops after several mins depriving the myocardial cells of glucose for aerobic metabolism and lactic acid accumulation that irritate myocardial fibres.
  2. stable angina: Pain when heart's oxygen demand increases
  3. variantangina: pain when coronary arteries spasm
  4. silent myocardial ischemia: myocardial ischemia without pain
  5. chronic stable angina: angina pectoris is a sudden attack of chest pain or pressure due to transient myocardial ischemia
  6. chronic stable angina: Associated with a fixed coronary obstruction that pro- duces a disparity between coronary blood flow and metabolic demands of the myocardium; often associated with atherosclerosis
  7. chronic stable angina: Triggered by increased work demands of the heart, physical exertion, cold, or emotional stress
  8. chronic stable angina; primary manifestations of pain.: Steady pattern and Constricting, squeezing or suffocating sensation
  9. chronic stable angina; primary manifestations of pain in the substernal area: may radiate to the left shoulder, jaw, arm or other areas of chest

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  1. ECG T wave: ventricular repolarization
  2. Troponin: regulatory protein that binds to actin, tropomyosin, and calcium
  3. CK-MB: an isoenzyme highly specific for injury to myocardial tissue and be- comes elevated within 4-8hrs after injury and will return to normal in 2-3 days
  4. unstable angina: pain at rest/new onset of pain in last month/more frequent pain and no serum biomarker changes
  5. stable angina: sufficient myocardial damage to release detachable quantities of troponin
  6. Treatment for unstable angina: • ASA
  • Beta-blockers
  • ACE inhibitors
  • Nitrates
  1. Treatment for Unstable Angina: Percutaneous coronary intervention (PCI) and or Coronary artery bypass grafting (CABG)
  2. ST Elevation Myocardial Infarction (STEMI): ischemic death of myocardial tissue
  3. ST Elevation Myocardial Infarction (STEMI):Size and pattern of infarct

11 / 25 depends: location and extent of occlusion, the amount of heart tissue supplied by the vessel and metabolic needs of the affected tissue and also the extent of collateral circulation and HR, BP and cardiac rhythm.

  1. Reperfusion: Reestablish blood flow using fibrinolytic therapy or revasculariza- tion procedures.
  2. Early Reperfusion benefits: prevent necrosis, improve myocardial perfusion in the infarct zone and may also prevent microvascular injury.
  3. Clinical Manifestations of MI: Chest pain characteristics:: severe and crush- ing, and usually substernal, radiating to left arm, neck or jaw.
  4. MI manifestations: angina, fatigue, nausea, SOB, diaphoresis, indigestion -can be silent MI
  5. AMI:arrhythmia: Abnormal heart rhythm
  6. AMI: Mechanical complications: pump failure
  7. Treatment of AMI; For persons with ECG evidence of STEMI: • Fibrinolytic therapy
  • Percutaneous coronary intervention (PCI)
  • Coronary artery bypass grafting (CABG)
  1. Fibrinolytic Drugs :Tenectaplase (TNKase): Interact with plasminogen

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  • Dilated cardiomyopathy
  • Valvular heart disease
  1. Heart:Right side: of heart accepts deoxygenated blood from the venous sys- tem and pumps to the lungs (pulmonary artery)
  2. Heart: Left side: of heart accepts oxygenated blood (pulmonary veins) from the lungs and pumps it to the body
  3. Heart: Systole: The ventricles contract forcefully expelling blood into the outflow vessels
  4. Heart: Diastole: The ventricles relax and fill with blood from the atria
  5. Cardiac Output: CO = SV x HR: Efficiency of the heart is determined by the amount of blood that it ejects each minute, the heart is regulated by balance b/w SNS and PNS
  6. Cardiac Output: CO = SV x HR :Persons with heart failure use their cardiac reserve at rest: Cardiac reserve is the ability of the heart to increase its output during increased activity eg athlete swimmers can increase their cardiac output by 5 to 6 times, that is their cardiac reserve
  7. Heart as a pump: Preload: The volume of the ventricle during of

14 / 25 diastole, The blood pressure in the left ventricle at the end of diastole right before the ventricles contract and the Pressure from the venous system

  1. Heart as a pump: Afterload: The force that the contracting heart muscle must generate to eject blood and Is the resistance that the heart faces during systole
  2. Heart as a pump: Contractility: Ability to contract and Increases cardiac output independent of preload and afterload • Uses energy from ATP and presence Ca ++
  3. High output heart failure: Inability of the heart to supply the body with blood-borne nutrients, despite adequate blood volume and normal or elevated myocardial contractility
  4. Low output heart failure: A type of heart failure where cardiac output is decreased, leading to impaired peripheral circulation and vasoconstriction.
  5. systolic heart failure: heart can't contract and eject
  6. diastolic heart failure: ventricles can't relax and fill
  7. Systolic dysfunction: decreased myocardial contractility that cause a de- crease ejection fraction

16 / 25 vasoconstrictors

  1. Myocardial Hypertrophy and Remodeling: The increase in heart size allows for a larger contractile force and cardiac output. This compensatory method gener- ally takes longer than other methods to develop.
  2. Heart Failure: Manifestations: Fluid retention and edema and Respiratory manifestations.-Dyspnea/exertional dyspnea
  3. Heart Failure: Symtoms: • Cyanosis -Desaturated Hgb
  • Arrythmias -Atrial and ventricular and Sudden cardiac death
  1. acute pulmonary edema: occurs when an excessive amount of fluid collects in the spaces between the alveoli and capillaries, disturbs normal gas exchange
  2. acute pulmonary edema treatments: • Diuretics
  • Digoxin
  • ACE inhibitors
  • Beta-blockers
  1. tissue perfusion: the process of delivery of blood to a

17 / 25 capillary bed in the biological tissue, the meaning to "pour over or through." or Blood flow

  1. aneurysm: an abnormal bulging of an arterial wall " widening", caused by defect or acquired weakness of the arterial wall which worsens over time as blood is pushed against it and bursting is usually life threatening.
  2. ischemia: An abnormally low flow of blood to tissues, "constricting or holding back blood" and Causes damage to the target tissues supplied by the vessels
  3. embolism: A blockage or occlusion that forms when a blood clot or other foreign particle moves through the circulation.
  4. Stroke etiology: Decreased tissue perfusion / Ischemia and Leads to neuro- logical deficits (acute or permanent)
  5. Ischemic (obstructive): reflect infarctions caused by interruption of blood flow
  6. hemorrhage: Excessive or profuse bleeding
  7. Ischemic stroke: a type of stroke that occurs when the flow of blood to the brain is blocked

19 / 25 and posterior cerebral arteries.

  1. Lacunar infarct: Healing lacunar infarcts leave behind lacunae; Lacunae means small cavities or lakes from arteriolar sclerosis.
  2. Transient Ischemic Attack (TIA): a "mini-stroke" caused by the blockage of a blood vessel, which resolves (goes away) within 24 hours
  3. Cardiogenic Embolic Stroke: Caused by a moving blood clot that travels from its origin to the brain and Frequent site is middle cerebral artery.
  4. Acute Stroke Manifestations: sudden in onset;
  • Weakness of the face and arm, sometimes the leg.
  • Unilateral numbness
  • amaurosis fugax
  • Hemianopia
  • Aphasia
  • Dysarthria
  • sudden, unexplained ataxia.
  • Specific stroke signs
  1. Amaurosis fugax: Vision loss in one or both eyes

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  1. Hemianopia: vision loss to one side of the visual field
  2. Aphasia: inability to speak
  3. Dysarthria: slurred speech
  4. Ataxia: lack of muscle coordination
  5. post stroke management: Risk of stroke recurrence is highest in first week after stroke or TIA.
  6. post stroke management (Early implementation): antiplatelet agents and warfarin (anticoagulant) in cardioembolic stroke
  7. Hemorrhagic Stroke: most frequently fatal; it is a rupture of a blood vessels
  8. Hemorrhagic Stroke due to?: compression of the brain tissues due to ex- panding hematoma, and tissue edema compression of brain contents
  9. Hemorrhagic Stroke: Most common: Aneurysmal Subarachnoid Hemor- rhage (SAH)
  10. Hemorrhagic Stroke: Accounts for 15%: Intracerebral Hemorrhage
  11. Risk Factors for Hemorrhagic Stroke:: Advancing age, and hypertension;
  • Aneurysm