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exam 3 study guide for patho, Study Guides, Projects, Research of Pathophysiology

University of Central Florida (UCF)Pathophysiology

exam 3 study guide for pathophysiology

Typology: Study Guides, Projects, Research

2020/2021

Uploaded on 06/02/2023

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Concept Clarification: Patho Exam 3 (Respiratory, Vascular, Hepatobiliary)
Respiratory
1. Pathophysiology and pathogenesis for asthma and COPD
Asthma
- Risk Factors & Etiology
Genetic disposition for development of IgE mediated response
Family history
Antenatal exposure to tobacco smoke
- Pathophysiologic changes
Chronic disorder of airways
- Clinical manifestations
Airways narrow due to bronchospasms
Edema of bronchial mucosa
Mucous plugging
FEV1 -> decreased
- Lab & Diagnostic
Careful history and physical exam
Pulmonary function studies
Labs
Spirometry
Inhalation challenge tests
COPD: Emphysema
- Risk Factors & Etiology
Loss of lung elasticity and abnormal enlargement of the airspaces distal to the
terminal bronchioles
- Pathophysiologic changes
Enlargement of airspaces and destruction of lung tissues
- Clinical manifestations
Lack of cyanosis
Use of accessory muscles
Pursed-lip breathing
Airways collapse during expiration
Trapping in alveoli and lungs (Barrel Chest)
- Lab & Diagnostic
Careful history and physical exam
Pulmonary function studies
Chest radiographs
Lab tests
COPD: Chronic Bronchitis
- Risk Factors & Etiology
Airway obstruction of the small and major airways
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Concept Clarification: Patho Exam 3 (Respiratory, Vascular, Hepatobiliary)

Respiratory

  1. Pathophysiology and pathogenesis for asthma and COPD Asthma
  • Risk Factors & Etiology  Genetic disposition for development of IgE mediated response  Family history  Antenatal exposure to tobacco smoke
  • Pathophysiologic changes  Chronic disorder of airways
  • Clinical manifestations  Airways narrow due to bronchospasms  Edema of bronchial mucosa  Mucous plugging  FEV 1 -> decreased
  • Lab & Diagnostic  Careful history and physical exam  Pulmonary function studies  Labs  Spirometry  Inhalation challenge tests COPD: Emphysema
  • Risk Factors & Etiology  Loss of lung elasticity and abnormal enlargement of the airspaces distal to the terminal bronchioles
  • Pathophysiologic changes  Enlargement of airspaces and destruction of lung tissues
  • Clinical manifestations  Lack of cyanosis  Use of accessory muscles  Pursed-lip breathing  Airways collapse during expiration  Trapping in alveoli and lungs (Barrel Chest)
  • Lab & Diagnostic  Careful history and physical exam  Pulmonary function studies  Chest radiographs  Lab tests COPD: Chronic Bronchitis
  • Risk Factors & Etiology  Airway obstruction of the small and major airways

 Most commonly seen is middle-aged men

  • Pathophysiologic changes  Increased mucous bronchitis  Obstruction of small airways  Chronic productive cough
  • Clinical manifestations  Cyanosis  Fluid retention associated with right-sided heart failure
  • Lab & Diagnostic  Careful history and physical exam  Pulmonary function studies  Chest radiographs  Lab tests
  1. Asthma symptoms: What sets off an asthma attack? ● Allergy or environment trigger
  2. What is asthma? What happens in the airway when someone has an asthma attack, why do we hear wheezes?
  3. What is it called when u have a bad asthma attack that we are having trouble getting it reversed?

● assess for hypoxemia

  1. Know difference between community and hospital acquired pneumonia Community : infections from organisms found in the community rather than in the hospital. May be either bacterial or viral. Antibiotic therapy. Most common causes influenza virus, RSV, adenovirus, and parainfluenza virus Hospital acquired : lower respiratory infection that was not present or incubating on admission. Most are bacterial. Main different they have antibiotic resistance.
  2. Know difference between types of pneumonia ● Broncho pneumonia : more widespread ● Lobar pneumonia : in a specific lobe, not affecting all of the lungs ● Immunocompromised pts: any type of infectious pneumonia like pseudomonas pneumonia, candida, and fungi and opportunistic infections , would get a more widespread pneumonia ● Pneumococcal pneumonia is common in elderly and immunocompromised
  3. ARDS : acute and the lungs airways are becoming thick and fibrotic , so not much air coming in, not much perfusion, happens in alveoli too, there is inflammation and swelling in lungs that prevent getting well oxygenated or getting co2 out **Atherosclerosis
  4. Inflammation always begins in which part of the vessel? Endothelium** of vessel
  5. Explain the pathogenesis of atherosclerosis plaque: ● When there is too much high cholesterol, high triglycerides in the body, u can’t use them all, so they get deposited fatty cholesterol plaques deposited in the wall of the arteries ● So, endothelium is triggered inflammation begins to try to wall it off from the rest of the body plaque continues to be deposited there and fat continues to attach and aggregate there, create more inflammation ● Finally the plaque is covered by fibrin: Fibrin cap over the plaque
  6. Where are atherosclerotic plaques deposited in the wall of the arteries? ● between endothelium and the smooth muscle layer underneath
  1. What happens if fibrin cap breaks off from that plaque or gets loose due to some injury or high blood pressure? ● Release of all that lipid into bloodstream causes immediate inflammation u get a big blood clot and closes or obstructs the artery
  2. What are the two ways an artery can become blocked due to atherosclerotic plaque?
  3. The plaque itself getting bigger and narrows the space of the vessel
  4. The fibrin cap from the plaque breaking open and causes a blood clot that blocks the vessel
  5. What is the difference between atherosclerosis and arterial disease? ● Fatty deposits/plaque in the wall of the artery, but not yet blocking the artery: atherosclerosis ● Once the artery is blocked called arterial disease − can lead to coronary artery disease or peripheral arterial disease
  6. The Risk of that plaque breaking loose and causing blood clot that blocks up that artery vessel depends on what factors? how quickly the plaque accumulated and whether the fibrin cap is very thin or very thick
  7. what causes progression of atherosclerosis and how does it lead to arterial disease where the blood clot blocks up artery or vessels? (Hint: it is NOT vasoconstriction) the atherosclerotic plaque causes lumen of artery to decrease , to get smaller = less blood flow through narrow space
  8. modifiable and non-modifiable risk factors for atherosclerosis Venous and Arterial Disease
  9. know difference between peripheral venous disease and peripheral arterial disease Peripheral Venous Disease : Varicose Veins. Torturous veins in lower extremity. Prolonged standing increases venous pressure. Peripheral Arterial Disease: atherosclerotic occlusive disease. Commonly seen with advanced age, risk factors cigarette smoking, diabetes.
  10. symptoms of peripheral venous disease : ● swelling, redness (rubor)...if there is a lot of edema, pulse may be hard to palpate but it’s probably still there
  11. Symptoms of peripheral arterial disease : not enough blood flow

● so u are still breathing ok, u are getting air in there, but u are not getting gas exchange because no blood is going through to that part of the lung ● Symptoms of low o2 o2 sat falls, pt can feel very dyspnea (short of breath), pt feels alarmed and afraid can cause sudden death Hypertension

  1. Modifiable and non-modifiable risk factors for hypertension
  2. know potential complications of Hypertension (HTN) ● stroke in brain ● bursting of aneurysm ● kidney disease ● damage to endothelium ● plaque can break loss and cause blood clot ● heart disease: left ventricle must push against that high pressure in hypertension, and left ventricle can hypertrophy
  3. Levels of blood pressure for prehypertension stage 1 and 2 ● Pre hypertensive up to stage 1: normal 120/<80 elevated 120-129/< ● Stage 1: 130-139/80- ● Stage 2: >140/>=
  4. Pathophysiology of blood pressure ● All about fluid balance ● RAAS, ADH where they come from, how they are monitored in the body, which organs involved ● Is blood pressure high enough for kidneys to be well perfused? If it’s not, there are humeral (endocrine) interventions to increase blood pressure (save sodium and water to increase fluid in body)
  5. Primary (essential) vs secondary hypertension

● Primary: no known cause, 90% of ppl with HTN have this type ● Secondary: due to some known cause

  1. Baroreceptors: sensory nerve endings monitoring pressure of blood vessels, sends messages to CNS about blood pressure is too high or too low or if its adequate, especially if its too low (life threatening) **Liver
  2. Liver failure** ● Not enough protein in body: not enough albumin = decreased osmotic colloid pressure in the vessels peripheral edema ● Hematologic: Less clotting factors: risk of bleeding out ● Liver can’t make bile = No bile = can’t digest fats, can’t absorb fat soluble vitamins − Bile salts (digest fats and make it easy to absorb) and bilirubin are all used to synthesize bile ● Can’t conjugate or break down bilirubin: excess bilirubin in the blood , poison to CNS and deposited in the skin, eyes, and mucus membranes Jaundice/icterus-yellow discoloration ● More ammonia in the blood − Liver normally excretes nitrogenous waste from protein metabolism (converts ammonia to urea) and urea is excreted through kidneys. In liver failure, since ammonia is not eliminated BUN and creatinine levels increase − Ammonia increase hepatic encephalopathy ● Hepato renal syndrome is rare, usually at end stage of liver failure, no questions on this exam
  3. Signs of end stage liver failure ● Jaundice ● Bleeding ● Change in level of consciousness and going into a coma due to hepatic encephalopathy
  4. Anything causing swelling or fibrosis in liver will lead to portal hypertension. How does it happen? ● If liver is stiff from inflammation/edema or scarred/fibrosed from cirrhosis, u don’t have easy or good blood flow through the congested liver
  1. Hepatitis : know the differences between Hep A, B, C, D, E ● Vaccines for which ones? − Hep A and B Which ones evolve into a carrier state? − Hep B, C, D ● Which hepatitis are chronic? − Hep B, C, D ● Highest mortality rate? − Hep E, advances quickly ● Transmitted fecal-oral − A, E ● Transmitted by blood and serum − B, C, D Gallbladder
  2. Anatomy, Know difference between cystic duct and common bile duct
  3. Cholecystitis : inflammation of gallbladder

● Happens in the gallbladder and the cystic duct − Where is cystic duct? It joins the gallbladder to the common hepatic duct ● Symptoms: ● Location of pain if acute cholecystitis: Right upper quadrant , under ribcage, on the side, behind liver

  1. Cholelithiasis : gallbladder stones , created in the gallbladder , move through the common bile duct ● Bile duct can get obstructed with stone Pancreas
  2. Pancreatitis ● Location of pain: epigastric to the umbilical area, can go to the back too ● Main risk factor: alcoholism ● Chronic is irreversible and acute can be reversible ex. if it’s an infection ● Inappropriate activation of pancreatic enzymes causes the pain can cause autodigestion of pancreas (eats itself), or if it ruptures, it can leak into the abdomen and start digesting everything
  3. What can cause worsening symptoms in a patient with pancreatitis? So anything that would cause u to excrete or secrete pancreatic enzymes into digestive system, can worsen the pain − Ex. If patient smells food, or give food to a patient, it wakes up digestive enzymes causes further damage of pancreas and pain