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Patho Exam 3
Week 6 Hepatobiliary Disorders Ch. 36 pg 981-
1. Liver - Hepatic Portal Triad Hepatic Portal Vein: digestive tract and major abdominal organs Hepatic Veins: valveless veins that empty into the IVC Hepatic Artery 2. Functions of Liver - Produce bile salts - Eliminate bilirubin - Metabolize Steroid hormones Drugs Carbohydrates Protein and fat - Store minerals and vitamins - Filtrate blood and removal of bacteria Functions of the Liver and Manifestations of Altered Function
Function Manifestations of Altered Function Production of bile salts Malabsorption of fat and fat-soluble vitamins Elimination of bilirubin Elevation in serum bilirubin and jaundice Metabolism of Steroid Hormones Sex hormones (^) Disturbances in gonadal function, including Glucocorticoids gynecomastia in the male Aldosterone Signs of increased cortisol levels ( i.e. , Cushing syndrome) Metabolism of drugs Signs of hyperaldosteronism ( e.g. , sodium retention and hypokalemia) Decreased drug metabolism Decreased plasma binding of drugs owing to a decrease in albumin production Carbohydrate metabolism Hypoglycemia may develop when glycogenolysis and gluconeogenesis are impaired Stores glycogen and synthesizes glucose from amino acids, lactic acid, and glycerol Abnormal glucose tolerance curve may occur because of impaired uptake and release of glucose by the liver Fat Metabolism Formation of lipoproteins Impaired synthesis of lipoproteins Conversion of carbohydrates and proteins to fat Synthesis, recycling, and elimination of cholesterol Altered cholesterol levels Formation of ketones from fatty acid Protein Metabolism Deamination of proteins Formation of urea from ammonia Elevated blood ammonia levels Synthesis of plasma proteins Decreased levels of plasma proteins, particularly albumin, which contributes to edema formation Synthesis of clotting factors (fibrinogen, prothrombin, factors V, VII, IX, and X) Bleeding tendency Storage of minerals and vitamins Signs of deficiency of fat-soluble and other vitamins that are stored in the liver Filtration of blood and removal of bacteria and particulate matter by Kupffer cells Increased exposure of the body to colonic bacteria and other foreign matter
3. Clinical Manifestations
- End-stage chronic liver disease
- Predisposed to portal hypertension
- Functional liver tissue replaced by fibrous tissue
- Sign & Symptoms Weight loss Weakness Anorexia Hepatomegaly Splenomegaly 5. Jaundice
- Yellow discoloration of skin and tissues
- Abnormal high levels of bilirubin (>2.0)
- Causes Excessive destruction of RBC Impaired uptake of bilirubin Decreased conjugation of bilirubin Obstruction of bile flow
- Categories Prehepatic Excessive hemolysis of RBC Unconjugated bilirubin Intrahepatic Caused by disorders that directly affect the ability of the liver to remove bilirubin Conjugated bilirubin Posthepatic Bile flow is obstructed Conjugated bilirubin 6. Acute Pancreatitis
- Risk Factors & Etiology Acute inflammation Possible reversible damage Alcohol-induced
- Pathophysiologic changes Damage to acinar cells Premature activation of pancreatic enzymes
- Clinical manifestations Mild to severe abd. Pain Fever Tachycardia Hypotension Resp. distress Abd. Distension
- Lab & Diagnostic Elevated C-reactive protein Hypocalcemia Elevated amylase and lipase serum
↑ WBC and bilirubin
- Complications SIRS ARDS Organ failure Pancreatic pseudocyst 7. Cholecystitis
- Risk Factors & Etiology Diffuse inflammation of the gallbladder 2 nd^ to obstructive gallbladder outlet Gallstones Sepsis, severe trauma, infection
- Pathophysiologic changes 85-90% are associated w/the presence of gallstones
- Clinical manifestations RUQ or epigastric pain Mild Fever N/V Sudden onset
- Lab & Diagnostic ↑ WBC and bilirubin ↑ AST, ALT, AP US CT Nuclear scan
- Complications Removal of gallbladder 8. Hepatitis
- Acute or chronic inflammation of the liver
- Viral hepatitis (hepatotropic viruses)
- Varying factors, mode of transmission, mechanism, and ability to evolve
- Viruses Hep A (HAV) Hep B (HBV) Hep B- associated delta virus (HDV) Hep C (HCV) Hep E (HEV)
- Causes Autoimmune disorders Reactions to drugs or toxins Infectious disorders (malaria, salmonellosis, amoebiasis) Primarily affect liver cells
Euphoria Combative/agitated Hyperventilation Cyanosis
- Lab & Diagnostic ABG (arterial blood gas) Pulse oximetry 3. Hypercapnia
- Risk Factors & Etiology Alteration in carbon dioxide production Disturbance in the gas exchange function of the lungs
- Pathophysiologic changes Increased carbon dioxide level in arterial blood
- Clinical manifestations Respiratory acidosis (decreased pH, ↑ PCO 2 ) Vasodilation of blood vessels CNS depression
- Lab & Diagnostic Physiologic manifestations Arterial pH ABG levels Obstructive Airway Disorders 1. 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 2. 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 3. 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
CT Scan/MRI PET
2. Non-Small Cell Lung Cancer (NSCLC): Squamous Cell Carcinoma - Risk Factors & Etiology Found most in men Associated with a history of smoking - Pathophysiologic changes Associated with paraneoplastic syndrome that produce hypercalcemia - Clinical manifestations Weight loss Anorexia Chronic cough SOB Hemoptysis Pain - Lab & Diagnostic History and Physical Chest X-ray Bronchoscopy Cytological studies CT Scan/MRI PET 3. Non-Small Cell Lung Cancer (NSCLC): Adenocarcinoma - Risk Factors & Etiology Most common lung cancer in North America Associated with cigarette smoking, but weaker than squamous cell carcinoma Most common in women and nonsmokers - Pathophysiologic changes Origin in either bronchiolar or alveolar tissue Areas of scarring Poorer stage-for-stage prognosis - Clinical manifestations Weight loss Anorexia Chronic cough SOB Hemoptysis Pain - Lab & Diagnostic History and Physical Chest X-ray Bronchoscopy Cytological studies CT Scan/MRI PET 4. Non-Small Cell Lung Cancer (NSCLC): Large Cell Carcinoma
- Risk Factors & Etiology Poor prognosis Tendency to spread to distal sites early in their course
- Pathophysiologic changes Large polygonal cells Periphery of the lung
- Clinical manifestations Weight loss Anorexia Chronic cough SOB Hemoptysis Pain
- Lab & Diagnostic History and Physical Chest X-ray Bronchoscopy Cytological studies CT Scan/MRI PET Pneumonia 1. Etiology Inflammation of parenchymal structures of the lung, in the lower respiratory tract 6 th^ leading cause of dead in the US 2. Classification According to setting Community or hospital-acquired According to type of agent causing infection Typical or atypical According to distribution of infection Lobar or bronchopneumonia 3. Lobar pneumonia VS bronchopneumonia
- Lobar pneumonia Consolidation of a part or all the lung lobe
- Bronchopneumonia Signifies a patchy consolidation involving more than one lobe 4. Community-Acquired VS Hospital-acquired
- Community-Acquired Infections from organisms found in the community rather than in the hospital May be either bacterial or viral Common viral causes include influenza virus, RSV, adenovirus, and parainfluenza virus Treatment involves appropriate antibiotic therapy
- Hospital-Acquired Lower respiratory infection that was not present or incubating on admission to the hospital
Fat embolism Chest trauma Disseminated Intravascular Coagulation Multiple blood transfusions
- (^) This list is not intended to be inclusive.
- Clinical Manifestations of ALI/ARDS Rapid onset of respiratory distress usually within 12-18 hours of initiating event Increase respiratory rate Signs of respiratory failure
- Increased permeability The increased permeability permits fluid, plasma proteins, and blood cells to move out of the vascular compartment into the interstitium and alveoli of the lung. Diffuse alveolar cell damage leads to accumulation of fluid, surfactant inactivation, and formation of a hyaline membrane that is impervious to gas exchange. As the disease progresses, the WOB becomes greatly increased as the lung stiffens and becomes more difficult to inflate.
- Intrapulmonary Shunting Increased intrapulmonary shunting of blood, impaired gas exchange, and refractory hypoxemia despite high supplemental oxygen therapy. Gas exchange is further compromised by alveolar collapse resulting from abnormalities in surfactant production. When injury to the alveolar epithelium is severe, disorganized epithelial repair may lead to fibrosis
Week 8 Cardiovascular Disorders Ch. 26 pg. 655-661, 641-648, 646-654 (focus on hypertension, atherosclerosis, and peripheral vascular disease)
Normal <120 And < Elevated 120-129 And < Stage 1 Hypertension 130-139 Or 80- Stage 2 Hypertension >140 Or >=
- Target-Organ Damage Disorders Heart o Angina (due to myocardial ischemia) o Myocardial infarction o Heart failure Brain o Stroke or transient ischemic attack Chronic kidney disease or kidney failure Peripheral artery disease Retinopathy Sexual dysfunction 2. Atherosclerosis
- Hardening of the arteries characterized by the formation of fibrofatty lesions in the intimal lining of large and medium-sized arteries
- Risk factors Hypercholesterolemia Elevations in LDL cholesterol levels
- Development of Atherosclerosis 1. Endothelial Cell Injury The vascular endothelium consists of a single layer of cells with cell-to-cell attachments that protects subendothelial layers from interacting with blood components. Smoking, elevated LDL levels, immune mechanisms, and mechanical stress associated with hypertension share the potential for causing endothelial injury with adhesion of monocytes and platelets 2. Migration of inflammatory cells
Early in the development of atherosclerotic lesions, endothelial cells express selective adhesion molecules that bind monocytes and other inflammatory cells that initiate the atherosclerotic lesions. After monocytes adhere to the endothelium, they migrate between the endothelial cells to localize in the intima of the vascular wall. Monocytes then transform into macrophages, which engulf lipoproteins, particularly LDL. Activated macrophages become foam cells when they release toxic oxygen species that oxidize the engulfed LDL.
3. Lipid accumulation and smooth muscle cell proliferation The recruitment of monocytes and their transformation into foam cells is protective because it removes excess lipids from circulation. However, accumulation of foam cells in the vessel wall eventually leads to lesion progression. Macrophages produce growth factors that contribute to migration and proliferation of SMCs and elaboration of extracellular matrix (ECM) in the vascular wall. Ultimately, foam cell macrophages die, depositing necrotic cellular debris and lipids within the vascular wall. 4. Plaque Structure Atherosclerotic plaques consist of SMCs, macrophages, and other leukocytes; ECM, including collagen and elastic fibers; and intracellular and extracellular lipids. Typically, the superficial fibrous cap is composed of SMCs and dense ECM. Beneath and to the side of the fibrous cap is the “shoulder” consisting of macrophages, SMCs, and lymphocytes. Below the cap is a central core of lipid-laden foam cells and fatty debris. Rupture, ulceration, or erosion of a vulnerable fibrous cap may lead to hemorrhage into the plaque or thrombotic occlusion of the vessel lumen.
Many can be asymptomatic; the lack of signs can be due to the vein not being totally occluded S/S: pain, swelling, deep muscle tenderness Most common site is in the venous sinuses in the soleus muscle and posterior tibial and peroneal veins DVT Diagnosis: Venography, ultrasonography, plasma D-dimer assessment Treatment: anticoagulation drug therapy (ex. Heparin and warfarin) If untreated a DVT can be fatal and travel towards heart
4. Peripheral Vascular Disease Peripheral Arterial Disease
- Risk Factors & Etiology Atherosclerotic occlusive disease Common in lower extremities Commonly seen with advanced age Risk factors: cigarette smoking, diabetes
- Pathophysiologic changes Hardening of the arteries characterized by the formation of fibrofatty lesions in the intimal lining of large and medium-sized arteries
- Clinical manifestations Gradual symptoms Intermitting claudication (pain when walking) Signs of ischemia
- Lab & Diagnostic Inspection of limbs for signs of chronic low-grade ischemia (brittle toenails, hair loss, pallor, coolness, or dependent rubor) MRI CT Peripheral Venous Disease- Varicose Veins
- Risk Factors & Etiology Tortuous veins in the lower extremity Prolonged standing increases venous pressure Prolonged exposure to increased pressure causes venous valves to become incompetent Obesity is a risk factor
- Pathophysiologic changes Primary varicose: originates in the superficial saphenous veins Secondary varicose: result from impaired flow in deep venous channels
- Clinical manifestations Aching in lower extremities Edema
- Lab & Diagnostic Thorough history and examination Doppler ultrasonic flow probe Angiographic studies Peripheral Venous Disease- Venous Insufficiency
- Risk Factors & Etiology Increased venous hydrostatic pressure Incompetent valves DVT Decreased skeletal muscle pump function Effective unidirectional flow and emptying of deep veins cannot occur
- Pathophysiologic changes Persistent venous hypertension on the structure and function of the venous system of the lower extremities
- Clinical manifestations Tissue congestion Edema Eventual impairment of tissue nutrition Stasis dermatitis in advanced cases
- Lab & Diagnostic Thorough history and examination Doppler ultrasonic flow probe Angiographic studies
