Usa Pathology Exam 3

Front 1

Diseases Causing Left Heart Failure

Back 1

-ischemic heart disease
-mitral/aortic valve disease
-hypertension
-non-ischemic myocardial disease

Front 2

Ischemic Heart Disease Definition

Back 2

disease resulting from insufficient blood supply to the myocardium
AKA: coronary artery disease,
coronary heart disease

Front 3

Causes of Myocardial Ischemia

Back 3

-reduced/obstructed coronary artery blood flow*
-hypertrophy
-shock
-hypoxemia from resp. problem
-extreme rapid heart rate

Front 4

Consequences of Myocardial Ischemia

Back 4

-reduced nutrient supply
-dec. removal of metabolites
-dec. oxygen supply
-dec. ATP production

Front 5

Causes of Coronary Obstruction

Back 5

-Mainly atherosclerosis, then other changes in plaque such as:
-cracking, hemorrhaging, embolism, platelet aggregation, thrombosis, vasospasm

Front 6

Structural Damage Resulting from IHD

Back 6

Myocardial Necrosis in ventricles
(myocardial infarction)

Front 7

Myocardial Infarction Determinants of Damage

Back 7

-location (site of occlusion, CA anatomy) affects subendocardial region 1st b/c poor perfusion
-size
-progression of necrosis; begins in 20-30 min, max at 3-6 hrs

Front 8

Clinical Manifestations of IHD

Back 8

-angina pectoris
-acute MI
-sudden cardiac death
-chronic ischemic heart disease w/ CHF

Front 9

Typical Angina Pectoris

Back 9

-reversible
-stress induced, relieved by rest or nitroglycerine
-chest crush feeling, radiating px down left arm

Front 10

Variant Angina

Back 10

-at rest or awakens pt asleep
-coronary artery spasm near atherosclerotic plaque
-relieved by nitroglycerine

Front 11

Unstable Angina

Back 11

-inc anginal pain
-more intense, longer than stable
-harbinger of serious IHD
-"pre-infarction angina"

Front 12

Infarction Angina

Back 12

-irreversible
-chest crush, radiating px to neck, jaw, epigastrium, shldr or left arm
-long lasting pain not relieved by rest or vasodilators

Front 13

Myocardial Infarction

Back 13

-critical stenosis (75%)
-15% pts asymptomatic
-usually left ventricle, LCA
-causes inflammatory response

Front 14

MI Symptoms

Back 14

-chest crush sensation w/ referred pain for 30 min to hrs
-may show: pallor, weak rapid pulse, diaphoresis, dyspnea

Front 15

MI Diagnostic Test

Back 15

EKG: change to Q wave, ST segment and T inversion, shows arrhythmias
Blood Tests: CK-MB, lactate dehydrogenase, troponin I and T all increase

Front 16

MI Complications

Back 16

-contractile dysfxn
-arrhythmias
-myocardial rupture
-pericarditis
-thromboembolism

Front 17

Myocarditis

Back 17

Myocyte damage from inflamm by:
-coxsackieviruses A & B
-parasites (chaga's disease)
-bact infection (lyme disease)
-bact toxin (diptheria)
-allograft rejection
-drug allergy

Front 18

Dilated Cardiomyopathy

Back 18

-90% of cardiomyopathy
-may be caused by viral infection, poorly controlled diabetes or thyroid disease
-most common cause is CAD

Front 19

Hypertrophic Cardiomyopathy

Back 19

-abnormal diastolic filling reducing ventricular space and dec SV
-outflow obstruction by excessive contraction
-extremely rapid contraction causing dec SV

Front 20

Restrictive Cardiomyopathy

Back 20

-ventricular expansion prevented by endomyocardial fibrosis, dec SV
-less common

Front 21

Hypertensive Heart Disease

Back 21

hypertension causes inc afterload, causing inc demand of myocardium, resulting in hypertrophy
=>hypertrophy results in myocardial ischemic injury

Front 22

Hypertenion Mechanism of Myocardial Ischemic Injury

Back 22

regurgitation of blood into pulmonary circulation->inc hydrostatic pressure->inc edema->inc resp membrane thickness->dec oxygen perfusion

Front 23

Valve Stenosis vs. Insuffieiency

Back 23

stenosis- failure to open completely impeding fwd flow
insuffiencey- failure to close completely allowing reverse blood flow

Front 24

Causes of Valve Disease

Back 24

-mitral stenosis
-aortic stenosis
-mitral regurgitation
-aortic regurgitation

Front 25

Mitral Stenosis

Back 25

-postinflammatory scarring resulting from rheumatic fever induced by GROUP A STREPTOCOCCI

Front 26

Aortic Stenosis

Back 26

-senile calcific aortic stenosis
-post inflamm scarring
-degeneration caused by calcification
-results in pressure overload and consequent left vent hypertrophy
-angina and syncope symptoms

Front 27

Mitral Regurgitation

Back 27

-mitral valve prolapse (loose)
-most common in industrial world
-postinflamm scarring
-infective endocarditis
-results in dec SV = dec CO
-asymptomatic, auscultation reveals MIDSYSTOLIC CLICK

Front 28

Aortic Regurgitation

Back 28

-post inflamm scarring from rheumatic disease
-infective endocarditis
-Marfan Syndrome loss of fibrillin

Front 29

Causes of Right Heart Failure

Back 29

-left heart failure
-valve disease
-Cor Pulmonale

Front 30

Cor Pulmonale

Back 30

right heart disease caused by pulmonary hypertension result of lung or pulmonary vascular disease

Front 31

Acute Cor Pulmonale

Back 31

-caused by pulmonary embolism: >50% vascular bed obstructed-> inc burden-> r vent dilation and failure

Front 32

Chronic Cor Pulmonale

Back 32

-chronic obstructive lung disease: pulm hypertension -> r heart hypertrophy -> dilation and failure

Front 33

Cor Pulmonale Clinical Manifestation

Back 33

venous congestion leading to: -soft tissue edema
-distended neck veins
-tender liver
-DVT

Front 34

Congenital Heart Disease Facts

Back 34

-8:1000 births
-most common cause of child heart disease in world
-unknown cause, likely genetic and environmental factors
=> L to R shunts, R to L shunts, obstruction of blood flow

Front 35

L to R Shunt Congenital Defects

Back 35

-atrial septal defect
-ventricular septal defect
-persistent ductus arteriosus

Front 36

R to L Shunt Congenital Defects

Back 36

CYANOSIS
-tetralogy of Fallot: VSD, ASD, great artery transposition
-isolated artery transposition

Front 37

Congenital Blood Flow Obstruction

Back 37

abnormal narrowing of the aorta

Front 38

Red Blood Cell Disorders

Back 38

Anemia: dec RBC concentration 2* to hemorrhage, inc destruction or dec production
Polycythemia: inc RBC concentration

Front 39

Conditions Inducing Increased RBC Destruction

Back 39

-hereditary spherocytosis
-sickle cell
-thalassemia
-G6PDH deficiency
-mechanical trauma to RBC
-malaria
-narrowing of vessels

Front 40

Conditions Causing Decreased RBC Production

Back 40

-nutritional deficiency (megaloblastic anemia)
-multipotent stem cell suppression (aplastic anemia)
-marrow replacement via tumor (myelophistic anemia)
-chronic disease

Front 41

Blood Loss Anemia

Back 41

result of hemorrhage, can occur acutely from trauma (volume loss, then shock and death) or chronic if rate of loss exceeds rate of production

Front 42

Mechanical Trauma to RBC

Back 42

-RBC membrane shredding in circulation, destroyed locally
-result of TURBULENT FLOW as in valve prosthesis or vascular graft or MICROCIRCULATION DMG

Front 43

Hereditary Spherocytosis

Back 43

-hereditary RBC membrane defects result in sphere shape, and dec deformation
-weak spectrin, ankyrin, band 4.2 and band 3
-result SPLENIC HEMOLYSIS

Front 44

Thalassemia

Back 44

-alpha and beta forms
-result in altered Hb formation reducing oxygen carrying capacity
-altered RBC structure causing lysis

Front 45

Sickle Cell Anemia

Back 45

-amino acid GAG alteration to GTG coding for Valine resulting in sickle Hb
-O2 binds to RBC, then de-O2-> RBC shape change occurs and cells cause clotting->hypoxia->necrosis, especially in large jts

Front 46

Immune Hemolytic Disorders

Back 46

-increase in RBC destruction because of antibodies directed at antigens on RBC surface
-can occur with transfusion reactions or newborn disease as in erythroblastosus fetalis

Front 47

Impaired RBC Production

Back 47

-nutritional deficiency
-dec erythropoietin (kidney disease)
-stem cell suppression
-tumor replacing marrow

Front 48

Nutritional Deficiency Anemia

Back 48

-iron
-folate
-vitamin B12 and intrinsic factor (related to gastric bypass or stapling)

Front 49

Suppression of Multipotent Stem Cell

Back 49

-stem cell injury resulting from chemotherapy and radiation
-aplastic anemia which alters production of RBC and WBC

Front 50

Marrow Replacement by Tumor

Back 50

metastatic cancer deposited in marrow or granulomatous disease alters production; immature precursors may be released into blood

Front 51

Symptoms of Anemia

Back 51

-weakness
-malaise
-fatigue
-dyspnea w/ mild exertion
-headache
-dim vision
-feel faint

Front 52

Signs of Anemia

Back 52

-splenomegaly
-jaundice due to inc bilirubin
-tacchycardia
-tacchypnea
-angina w/ preexisting heart probs

Front 53

Anemia Complications

Back 53

-marrow expansion in skull
-inc iron absorption
-tissue anoxia changes
-liver, heart, kidney fatty change

Front 54

Coagulation Disorders

Back 54

result in excess bleeding
congenital or acquired
dec production
ineffective production
inc destruction (antibodies or sequestration in spleen)
THROMBOCYTOPENIA

Front 55

Coagulation Factor Deficiencies

Back 55

Inherited= von Willebrand disease, hemophilia A and B
Acquired= vitamin K deficiency, liver disease, DIC

Front 56

Upper Respiratory Tract Acute Infections

Back 56

-common cold; rhinovirus 60%
-acute pharyngitis
-acute bacterial epiglottis
-acute laryngitis

Front 57

4 Major Diffuse Obstructive Lung Disorders

Back 57

Emphysema (indirect)
chronic bronchitis
bronchiectasis
asthma

Front 58

Obstructive Lung Disease General Mechanism and Clinical Determination

Back 58

-occurs two ways: airway narrowing and loss of elastic recoil
TEST: FEV1

Front 59

COPD Diseases and Commonalities

Back 59

-emphysema
-chronic bronchitis
-chronic asthma
-bronchiectasis
=>all show DYSPNEA and CHRONIC AIRFLOW LIMITATION

Front 60

Allergic Asthma

Back 60

-most common, childhood, commonly hereditary
-triggered by allergens
-attacks preceded by rhinitis, urticaria, eczema

Front 61

Nonreaginic Asthma

Back 61

-not hereditary, no assoc. allergies, usually triggered by resp. tract infection such as viruses
-hyperirritability of the bronchial tree, viral inflammation, air pollutants

Front 62

Drug Induced Asthma

Back 62

-aspirin sensitive to small doses
-cyclooxygenase pathway inhibited, unaffected leukotrienes cause vasoconstriction

Front 63

Occupational Asthma

Back 63

-minute quantities of fumes trigger attack occurring after repeated exposure
-type I hypersensitivity, bronchoconstrictor liberation, uknown hypersensitivity

Front 64

Asthma Structural Changes

Back 64

-hyperplastic mucus glands
-hypertrophied bronchiole smooth muscle
-inflammatory infiltrate (thick mucus plugs bronchioles)

Front 65

Asthma Manifestations

Back 65

-severe dyspnea
-coughing
-wheezing
-bronchospasm
=>dec FEV1

Front 66

Chronic Bronchitis Definition

Back 66

chronic inflammation of the large bronchi, productive cough for 3 mos 2 consecutive years

Front 67

Chronic Bronchitis Causes

Back 67

-SMOKING, pollutants, grain, cotton, silicon dust
-bacterial and viral infections trigger attack

Front 68

Chronic Bronchitis Structural Changes

Back 68

-hypertrophy of submucosal glands in trachea and bronchi
-large airway hypersecretion of mucus

Front 69

Chronic Bronchitis Pathogenesis

Back 69

-neutrophil proteases (elastase & cathepsin) and matrix metalloproteinases stimulate mucus hypersecretion
-persistence leads to small airway goblet cell inc producing more mucus

Front 70

Cigarette Smoke Influences on Infection

Back 70

-impairs ciliary action
-may cause direct epithelial dmg
-inhibits bacterial clearing by leukocytes

Front 71

Chronic Bronchitis Functional Deficit

Back 71

DECREASED AIRFLOW
-inc mucus->thick sputum + lrg # of mucus secreting cells in bronchial epithelium->airway obstruction

Front 72

Chronic Bronchitis Symptoms

Back 72

CHRONIC COUGH AND SPUTUM
-worse in morning/night
-may exist without evolving to obstructive lung disease

Front 73

Obstructive Lung Disease Common Symptoms

Back 73

-shortness of breath
-prolonged expiration
-fever/malaise w/ infection
-wheezing
-hypoxemia & mild cyanosis
-dec exercise tolerance
-hypercapnia (inc blood CO2)

Front 74

Chronic Bronchitis Tests

Back 74

-FEV1
-Blood CO2 inc and O2 levels dec
-hypoxemia leads to polycythemia

Front 75

Emphysema Definition

Back 75

Abnormal permanent enlargement of airspace distal to terminal bronchiole, airspace wall distruction without obvious fibrosis
-DOES NOT APPEAR UNTIL 1/3 OF LUNG TISSUE INCAPACITATED

Front 76

Emphysema Pathogenesis

Back 76

SMOKING IRRITATES LUNGS CAUSING INFLAMMATION
-leukocytes release elastase damaging alveolar wall reducing elasticity
-hereditary deficiency of AAT + free radical inhibition of AAT leads to dec control of elastase = MORE TISSUE DMG

Front 77

Emphysema Structural Deficit

Back 77

enlargement of distal airspaces and decrease in gas exchange surface area

Front 78

Emphysema Functional Deficit

Back 78

-dec gas exchange capability
-loss of elasticity causes dec recoil of lungs and impaired expiration

Front 79

Emphysema Symptoms

Back 79

-1ST IS INSIDIOUS ONSET DYSPNEA
-cough/wheezing

Front 80

Emphysema Signs

Back 80

-OBVIOUS PROLONGED EXPIRATION
-weight loss (careful of tumor)
-barrel chest
-pt sits hunched
-breathes w/ pursed lips
-overventilation=> inc O2 "pink puffers"

Front 81

Emphysema Tests

Back 81

FEV1!!

Front 82

Emphysema Complications

Back 82

-COPD death result of resp acidosis and coma
-right heart failure

Front 83

Bronchiectasis Definition

Back 83

permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic tissue due to chronic necrotizing infections

Front 84

Bronchiectasis Causes

Back 84

-develops with other obstructive and infectious diseases
-uncommon due to antibiotic rx

Front 85

Bronchiectasis Symptoms

Back 85

-severe productive cough with foul smelling purulent sputum
-fever
-finger clubbing
-dyspnea/orthopnea if severe

Front 86

General Conditions Leading to Restrictive Lung Defect

Back 86

-Extrapulmonary disorders (chest wall probs: polio, obesity, pleural disease)
-Acute or chronic interstitial infiltrative disease
RESULT IN DEC TLC AND FVC

Front 87

Acute Interstitial Infiltrative Disease Definition

Back 87

ARDS = FIBROSIS and diffuse alveolar capillary damage resulting in respiratory insufficiency
HISTOLOGY = diffuse alveolar dmg

Front 88

ARDS Predisposing Conditions

Back 88

hospitalization from:
-infection
-injury
-inhaled irritants
-hematologic conditions
-pancreatitis
-hypersensitivity rxns

Front 89

ARDS Structural Deficit

Back 89

CAPILLARY AND ALVEOLAR ENDOTHELIUM DAMAGE:
-inc vascular permeability and alveolar flooding
-loss of diffusion ability
-type II pneumocyte dmg result in surfactant abnormality

Front 90

ARDS Functional Loss

Back 90

-non-homogenous lung stiffness and dec in FVC
-physiogical shunt resulting in hypoxemia

Front 91

ARDS Clinical Manifestation

Back 91

-DYSPNEA AND TACHYPNEA
-respiratory insufficiency, cyanosis, arterial hypoxemia, and respiratory failure

Front 92

ARDS Diagnostics

Back 92

-chest x ray later shows diffuse infiltrates bilaterally
-dec FVC and TLC

Front 93

Chronic Restrictive Lung Disease Definition

Back 93

-chronic inflammation of the interstitium of alveolar walls resulting from particulate accumulation (pneumoconiosis)
-interstitial fibrosis of unknown origin

Front 94

CRLD Susceptible Populations

Back 94

-coal miners
-farmers
-asbestos workers
-sandblasters
ALL PRONE TO PARTICULATE INHALATION

Front 95

CRLD Pathogenesis

Back 95

ALVEOLITIS RESULTING IN LEUKOCYTE ACCUMULATION
->distortion of alveolar structures
->mediator release dmgs lung cells
->results in end-stage fibrotic lung

Front 96

CRLD Clinical Manifestation

Back 96

-dyspnea, tachypnea
-END-INSPIRATORY CRACKLES
-cyanosis w/out wheezing or other evidence of airway obstruction

Front 97

CRLD Tests

Back 97

-FVC decreased
-FEV1/FVC ratio not reduced
-chest xray shows diffuse infiltrates (small nodules, irregular lines or glass shadows)

Front 98

CRLD Complications

Back 98

-pulmonary hypertension
-physiological shunt closes unused blood vessels, increasing right heart workload, cor pulmonale results

Front 99

Atelectasis Definition

Back 99

ALVEOLAR COLLAPSE

Front 100

Compression Atelectasis

Back 100

-fluid accumulation in lung collapses alveoli

Front 101

Resorption Atelectasis

Back 101

-bronchi obstruction collapses alveoli

Front 102

Microatelectasis

Back 102

-surfactant loss collapses alveoli

Front 103

Contraction Atelectasis

Back 103

-increased elastic recoil results in alveolar collapse

Front 104

Atelectasis Functional Loss

Back 104

INADEQUATE AIRSPACE EXPANSION
= loss of lung volume
results in phys. shunt, ventilation-perfusion imbalance and hypoxemia

Front 105

Pleural Effusion and Pleuritis
"Hydrothorax"

Back 105

-exudate or transudate accumulation in pleural space
-exudate via microbe/virus, cancer or pulmonary infarction, results in pleural adhesions
-transudate common from CHF, usually reabsorbed w/out effect

Front 106

Pneumothorax

Back 106

Air accumulation in pleural space most common w/ EMPHYSEMA OR FX RIB, can occur spontaneously in healthy adult

Front 107

Hemothorax

Back 107

blood in pleural cavity, clot presence, usually result of intrathoracic aortic aneurysm

Front 108

Chylothorax

Back 108

milky lymphatic fluid accumulation in pleural space implying lymph duct obstruction by intrathoracic cancer

Front 109

Pulmonary Embolism Susceptibility

Back 109

-cardiac disease or cancer
-immobilization s/p hip fx
-hypercoagulability from factor V, obesity, recent surgery, oral contraceptives or pregnancy
=DVT PRIMARY SOURCE

Front 110

Physiological Consequences of Pulmonary Emboli

Back 110

-respiratory compromise from poorly perfused blood
-obstruction leads to pulmonary hypertension and R heart failure

Front 111

Pulmonary Emboli Diagnostics

Back 111

-chest xray may show infarct 12-36 hrs after as wedge shaped infiltrate
-pulmonary angiography most definitive but risky

Front 112

Pulmonary Embolism Prevention

Back 112

-early ambulation s/p surgery
-elastic/compression stockings
-preventative anticoagulation drugs

Front 113

Causes of Pneumonia

Back 113

-poor resistance to infection from chronic disease, immune dysfxn, leukopenia
-impaired clearing mechanism

Front 114

Factors Interfering With Lung Clearing Mechanism

Back 114

-loss of cough from coma, anesthesia, NM disorders
-injury to ciliary apparatus
-impaired alveolar macrophages from alcohol, tobacco, anoxia
-pulmonary edema/congestion

Front 115

Community Acquired Acute Pneumonia

Back 115

pneumococcus infection causes inflammatory exudate to fill alveoli and solidifying pulmonary tissue

Front 116

Anatomic Distribution:
Bronchopneumonia

Back 116

-patchy consolidation
-chest xray shows focal opacities

Front 117

Anatomic Distribution:
Lobar Pneumonia

Back 117

-consolidation of a lrg portion or entire lobe
-chest xray radioopaque well defined lobe

Front 118

Nosocomial Pneumonia

Back 118

-acquired during hospital stay
-pts with severe disease, immune suppression, on prolonged antibiotic therapy or mechanical ventilation susceptible
-STAPH AUREUS AND GRAM NEGATIVE RODS MAIN INFECTIONS NOT PNEUMOCOCCI

Front 119

Most Common S/S of Pulmonary Disease

Back 119

-cough 3 types
-dyspnea
-abnormal sputum
-chest px
-hemoptysis
-cyanosis
-altered breathing pattern
-digital clubbing

Front 120

Exocrine Pancreas Disorders

Back 120

-acute pancreatitis
-cystic fibrosis
-pancreatic carcinoma

Front 121

Acute Pancreatitis

Back 121

-inflamm with acinar cell injury
causes:
-ALCOHOLISM OR GALL STONES (CHOLELITHIASIS)
-also blunt trauma, surgery, medication

Front 122

Acute Pancreatitis Pathogenesis

Back 122

AUTODIGESTION
-acinar cell injury leads to activation of trypsinogen, trypsin and proteolytic enzyme activate other enzymes causing autodigestion of pancreas

Front 123

Acute Pancreatitis Pathogenesis
Indirect

Back 123

-duct obstruction from alcoholism or gall stone
-metabolic injury causing impaired intra-acinar proenzyme transport

Front 124

Acute Pancreatitis Pathogenesis
Direct

Back 124

-alcohol, drugs, trauma and virus cause direct release of enzymes and hydrolases that digest pancreatic cells

Front 125

Acute Pancreatitis Manifestation

Back 125

-variable severity of sx
-increasing ab px radiating to upper back or T-L jxn made worse by supine or walking
-nausea, fever, tacchycardia, weakness
PX CAUSED BY EDEMA, IRRITATION FROM ENZYMES, OBSTRUCTED BILIARY TRACT

Front 126

Acute Pancreatitis Complications

Back 126

-peripheral vascular collapse and shock
-ARDS
-renal failure
-hypocalcemia
-pancreatic pseudocyst
-peritonitis

Front 127

Acute Pancreatitis Tests

Back 127

-blood test reveals inc serum amylase in 24 hrs, lipase 72-96 hrs
-urine shows inc amylase
-xray shows pancreatic enlargement

Front 128

Cystic Fibrosis

Back 128

-chromosome 7 abnormality causing defect in Cl- transport affecting all exocrine glands