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UTA PATHOPHYSIOLOGY EXAM
3 QUESTIONS WITH VERIFIED
ANSWERS.
Arteriosclerosis --Answer-- Thick and Hardened artery HTN | Smoking | Diabetes Intima is damaged and walls stiffen. Elasticity and compliance decreases. Atherosclerosis --Answer-- Fatty Deposits Plaques form | tissue inflamed | High amount of LDL's (low-density lipoproteins=more fat than protein) Hypertension --Answer-- the force of the blood against the artery walls is too high. Pre - Stage I - Stage II Preload --Answer-- Volume of blood returning from the heart. Normal volume = 4-6ml Afterload --Answer-- Amount of blood ejected from the heart Contractility --Answer-- How effectively the heart works to eject blood "toned" Arterial Insufficiency --Answer-- Muscle tone and the state of the lumen are compromised. Aneurysms --Answer-- A ballooning and weakened area in an artery.
Venous Disorders --Answer-- Chronic Venous Insufficiency (CVI) Deep Vein Thrombosis (DVT) Valvular Disorders --Answer-- Gravity Winning - not necessarily pathogenic Valve Incompetence - pathology invlolved Cardiogenic Shock --Answer-- Heart suddenly can't pump enough blood to meet your body's needs What side of the heart is the Arterial side? --Answer-- The LEFT. OXYGENATED blood is going "out" via aorta to all arteries and tissues What side of the heart is the Venous side? --Answer-- The RIGHT. DEOXYGENATED blood if flowing "in" from all the veins and tissues. Inotropic --Answer-- POSITIVELY or NEGATIVELY modifying the force or speed of contraction of muscles. pos- pumps faster neg- pumps less Systemic Vasodilation --Answer-- from anaphalaxis or Sepsis Analyphalyaxis --Answer-- severe, potentially life-threatening allergic reaction. It can occur within seconds or minutes of exposure to something you're allergic to. Low blood pressure (hypotension) A weak and rapid pulse In a case of HIGH preload --Answer-- Volume too LARGE- heart is working too hard. CAUSES: Fluid Excess States
- heart failure
- iatrogenic fluid overload
- hormonal imbalances (SIADH) In a case of LOW preload --Answer-- Volume too SMALL - not enough to sustain good perfusion
Venous Congestion Issues --Answer-- Gravity winning, being on feet too long, Valve Incompetence (venous insufficiency) Chronic Venous Insufficiency --Answer-- Leg vein valves wearing out "floppy" valves not closing properly during diastole causing back flow. Pool of nonmoving blood is called VENOUS STASIS. results in increased hydrostatic pressure. pressure pushes fluid into the tissues causing EDEMA (dry, tight, brownish skin) Further engorgement leads to tissue breakdown and VENOUS STASIS ULCERS- back flow can go further into the surface veins, twisting and distorting them causing VARICOSE VEINS (local back flow) Name a few causes of Edema --Answer-- HTN right-sided heart failure venous problems kidney disease injury lymphatic problems hypoosmolar problems Deep Vein Thrombisis --Answer-- A clot the develops ON THE WALL of the vein (deep veins of calves and thighs) THROMBOPHLEBITIS vein becomes inflamed or swollen Virchows Triad --Answer-- the three broad categories of factors that are thought to contribute to thrombosis. STASIS HYPERCOAGULABILITY INJURY Dangerous Sequela of DVT --Answer-- DVT > IVC > RA > RV > PA part of thrombus breaks free and gets stuck in pulmonary arteries. PULMINARY EMBOLUS S&S- SOB > Shock > Hemoptysis (blood in sputum) > Death Treatment for Venous Problems --Answer-- Encourage mobility Encourage hydration
Elevate feet Blood thinners (Heparin, Coumadin) Asprin- prevents clotting Blood Pressure (Systolic and Diastolic) --Answer-- Blood Pressure- simply the fluid pressure in the arterial system Desired range: 110/60 - 115/ Systolic- pressure in the arteries exerted when the heart is contracting and ejecting blood OUT Diastolic- pressure of fluids existing in the arteries when the heart is between contractions Prehypertension --Answer-- SYSTOLIC - 120- DIASTOLIC - 80- Stage I Hypertension --Answer-- SYSTOLIC - 140- DIASTOLIC - 90- Stage II Hypertension --Answer-- SYSTOLIC - 160-above DIASTOLIC - 100-above S&S of decreased perfusion and ischemia --Answer-- Ischemic pain- increases with exertion and diminishes with rest. (Exertion=more O2 demand) this pain is in the tissue distal to the plaque or narrowing. (femoral arteries affected, pain in the calves) Diminished pulses, delayed CRT, skin pale/cool, sometimes blue , delayed healing, delayed Cardiac Output, altered consciousness, Stroke, diminished urine output. Risk Factors of arterial narrowing --Answer-- NON-MODIFIABLE = family history, advancing age MODIFIABLE = Diet, obesity, alcohol, sedentary lifestyle, cigarette smoking Lipodystrophy --Answer-- a disorder in which the body is unable to produce fat. characterized with DM2- increased circulating LDL's
Risk factors: high sodium intake, water retention, high pressure in circulatory system Overactivity of the SNS --Answer-- due to sustained stressors, genes, Epinephrine overstimulates Beta receptors and over-increases HR and contractility. this in turn leads to a greater cardiac output and sustained increased BP Overactivity of RAAS --Answer-- normally RAAS is compensatory in a drop in BP causing vasoconstriction and increased blood volume. in this case it is chronically overactive thus blood volume and pressure is high. HTN affects the vasculature in what 3 systems? --Answer-- Neurological- brain and eyes Renal - hematuria or proteinuria cardiovascular - workload of heart Aneurysms --Answer-- localized dilation or out-pouching or arterial vessel wall. weakened walls from HTN or atherosclerosis create bulging. can happen in the brain, aorta, abdominal aortic, thoracic aortic. HDL value --Answer-- should be at least 40mg/dl Medical approaches to combat arterial problems. --Answer-- Overactivity of the SNS - beta blockers Overactivity of RAAS - ACE inhibitors Coumadin or Heparin to combat clots. Stroke Volume --Answer-- amount of blood ejected per contraction ~ 70ml/beat P wave --Answer-- Atrial depolarization QRS complex --Answer-- ventricular depolarization T wave --Answer-- ventricular repolarization ST wave --Answer-- time interval between end of ventricular depolarization (S) and repolarization (T)
Hear rate --Answer-- the rate of impulses generated by the SA node. Normal is 60- Three factors of healthy arteries --Answer-- Good Perfusion Good vasomotor tone Patent Lumen Inotroipc --Answer-- describes the effect in different factors of contractility. Positive = enhances contractility Negative = decreases contractility Pulmonary Vacsular Resistance --Answer-- Normal RV afterload Normal Systemic Restiance --Answer-- Normal LV afterload Some possible causes of Tachycardia --Answer-- Neurohormonal - sympathetic = epinephrine - binds to BETA receptors electrolyte changes - hypokalemia - causes hyperpolerization - ischemia from RCA glitches in the SA or AV node Some possible causes of Bradycardia --Answer-- Neurohormonal = parasympathetic vages nerve secretes acetylcholine hypokalemia - causes hyperpolerization - ischemia from RCA glitches in the SA or AV node Dysrhythmia --Answer-- aka- Arrhythmia ischemic or infarct tissue interferes with normal conduction. electrolyte imbalances. age related wear and tear. Atrial Fibrillation --Answer-- chaotic impulses in the atria. diminished CO due to no "atrial kick" blood can coagulate. Thrombi in the left atrium can cause --Answer-- emboli out to the body- it can go to the brain and cause a stroke Thrombi in the right atrium can cause --Answer-- emboli out to the lungs
Angina --Answer-- a painful constriction or tightness- chest pain - painful ischemia to the heart. Characteristics of classic angina --Answer-- patient often will describe it as tightness, heaviness ("elephant sitting on me"); sometimes burning, indigestion-like; will sometimes place clenched fist over sternum Pathophysiology of Angina Perception --Answer-- a) buildup of lactic acid and abnormal stretching of ischemic myocardium irritate myocardial nerve fibers b) the afferent sensory nerve fibers in the area transmit the pain impulses to areas of the spinal tract that include C3 to T c) the variety of nerve root areas causes the variation in pain each individual has explains why some patients may have radiation of pain into classic areas such as left arm, jaw, & back Stable Angina --Answer-- pain pattern is very predictable and well-controlled by lifestyle changes. nitroglycerin or aspirin (reduces inflammation- leakiness and swelling, and, inflammation debris) can relieve/treat it A slow development of plaque forms - small and subtle ischemia to tissues stimulates Arteriogenesis --Answer-- a type of angiogenesis (general word for "new blood vessel creation") End result of this is the establishment of COLLATERAL CIRCULATION composed of new branches of the coronaries that develop and can "feed" tissue beyond an occluded or nearly-occluded vessel. The better the collateral circulation, the more stable the CAD. Acute Coronary Syndrome (ACS) --Answer-- one of several possible coronary- artery-flow-blocking situations occurs
- sudden clot development.
- an arterial embolus flows into a narrowed coronary artery
- an existing plaque ruptures & its contents fill up the lumen. Unstable Angina --Answer-- When someone with stable angina develops a change for the worse (usually sudden)
Usually indicates worsening or change in existing coronary plaques - worsening of ischemia
- Substantial change in pain now needs 3 NTG tabs
- EKG shows acute ischemic changes c) patient admitted to the hospital, treatment is still geared towards maximizing coronary patency & perfusion with acute interventions such as IV NTG, IV morphine, possibly angioplasty, heart surgery, etc. Myocardial Infarction --Answer-- Myocardial cells are starting to undergo necrosis S&S usually include 1)severe, unrelenting pain 2)EKG changes = ischemia & certain degree of necrosis
- lab test findings that show increases in: non-specific enzymes released by injured and dying cells = creatine kinase (CK) - troponin. Troponin --Answer-- specific substance only released by injured and dying myocardial cells the higher the serum titer, the more extensive the damage Miscellaneous S&S that often occur in ACS --Answer-- tachycardia - epinephrine "fight or flight" bradycardia, dysrhythmias, large amount of sweating, fatigue, weakness, mental status change, deterioration of responsiveness, hypotension, dyspnea, prolonged CRT, low urine output Cardiomegaly --Answer-- Enlarged heart -- increase in size of cells over time due to cells "working harder" to compensate for less oxygen Heart Valvular Disorders --Answer-- disease processes such as rheumatic fever (post-strep autoantibodies invade & inflame heart valves, joints, and/or kidneys) Problems depend on severity & which valves involved, generally negatively affect CO in one way or another. also caused by bacterial endocarditis, or birth defects Stenosis --Answer-- Valvular narrowing or stiffening
S&S's of fluid back-up into peripheral veins (peripheral venous congestion) -- Answer-- Jugular venous distention (JVD) liver congestion, so enlarged liver ASCITES --the state of extra fluid in the abdominal cavity edema of legs & feet. Cor Pulmonale --Answer-- RHF due to pulmonary vascular resistance (people with bronchitis- mucous in the lungs) treatment of HF using positive inotropic drugs --Answer-- Increases forward flow - digoxin Vasodilators do what in HF --Answer-- decrease resistance. NTG and ACE inhibitors. The Natruietic system --Answer-- causes more sodium to be excreted into the urine water follows thus natriuretic peptides are "natural diuretics" when we need to get rid of fluid. Two Types one secreted from the atria --atrial natriuretic peptide (ANP) one secreted from the ventricles-- b-type natriuretic peptide (BNP) BNP values --Answer-- Normal 50 pg/ml Mild HF = 130 Severe HF = 1000 Normal pH --Answer-- 7.35-7. PO2 --Answer-- pressure of O2 in the blood - gas dissolved in plasma 80 to 100mmHg low O2 = Hypoxemic SO2 --Answer-- Oxygen saturation 97 to 100% PCO2 --Answer-- pressure of CO2 gas in the blood 35 to 45 mm Hg - out of range = respiratory probelm HCO3 --Answer-- 22-26 mEq/l
what causes non cardiogenic pulmonary edema --Answer-- Smoke, fire. pollutants that disrupt surfactant production in alveoli. Respiratory Opposite --Answer-- PCO2 goes down; pH goes up; PCO2 goes up, pH goes down Metabolic Equal --Answer-- HCO3 goes up, pH goes up; HCO3 goes down, pH goes down Components of inhalation --Answer-- ventilation-- portion of inhalation in which air passes into bronchi & alveoli (lung tissue) - air movement. perfusion-- inhalation in which the blood vessels of the lungs bring CO2 to the alveoli & take away O2 to pass on to the rest of the body. (4 liters or air in and out per min) dyspnea --Answer-- SUBJECTIVE sensation of not being able to get enough air DOE - dyspnea on exertion orthopnea --Answer-- dyspnea upon lying down; usually related to LHF > blood return to heart increases when a person lies down & compromised LV can't pump it forward > back up into lungs paroxysmal nocturnal dyspnea (PND) --Answer-- suddenly awakening at night feeling SOBí same reason as orthopnea Hypoventilation --Answer-- Bradypnea. neuromuscular and/or central nervous system (CNS) problems such as increased pressure on respiratory centers from intracranial bleeding hyperventilation --Answer-- tachypnea "air hunger"-the need for more oxygen by those with a pulmonary problem, or fright/anxiety b) depth-related 3 Depth related breathing patterns --Answer-- hypopnea- shallow breathing. hyperpnea- increased depth (tidal volume) of respirations apnea-no respirations at all
broken rib punctures pleura. Gunshot closed pneumothorax --Answer-- trauma is from the inside air builds up in the thorax enough to put pressure on other lung too. Weakened emphysemic alveoli ruptures pneumonia (community-acquired (CAP), hospital-acquired (nosocomial), & aspiration pneumonia) --Answer-- CAP- sometimes called "walking pneumonia"-don't have to be hospitalized) Gram + Nosocomial- need very strong antibiotics. Gram - Aspiration-nasal drip, food, liquid, foreign body, usually happens in debilitated or other individuals whose gag, swallowing, and/or cough reflexes are depressed or absent dysphagia --Answer-- Cant swallow well atelectasis --Answer-- happens when groups of alveoli cave in due to blockage in the bronchioles (such as collections of mucus from inflammatory changes) air can't get into alveoli so they collapse. consolidation --Answer-- infiltrates + atelectasis areas of lung that become stiff and have diminished function can be either a local area such as a single lobe (lobar pneumonia) OR may be more diffuse (bronchopneumonia) S&S's of any kind of pneumonia --Answer-- fever, chills, malaise, pleural pain, cough, dyspnea upon auscultation: crackles (from fluid in alveoli) or locally diminished breath sounds (consolidated tissue has no air going through it, so no sound) abnormal chest x-ray tx- antibiotics, hydration, pulmonary toilet Noncardiogenic pulmonary edema --Answer-- INJURY TO CAPILLARY endothelium (smoke from a fire) increased capillary permeability and disruption of surfactant production by alveoli LUNG CANCER (AKA bronchogenic carcinoma)- Obstructive pulmonary diseases --Answer-- problems getting air out.
asthma, bronchitis, & emphysema (COPD) asthma --Answer-- chronic inflammatory disorder of the airways due to bronchial hyperresponsiveness to stimuli such as allergens in environment. wheezing sound caused by expiration meds: bronchodilators like ventolin COPD --Answer-- emphysema and/or chronic bronchitis emphysema --Answer-- inspired irritants inability to expel them due to altered cilia (smoking) increased activity of proteolytic enzymes like elastase (an enzyme that breaks down the proteins that make lungs so flexible & "elastic") increased anteroposterior (AP) diameter of chest "pink puffer" "tripod" "pursed lip" chronic bronchitis --Answer-- defined as hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years (inspired irritants) "blue bloaters" "clubbed fingers" cor pulmonale - lots of bloating.
