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Pathophysiology: Cardivascular and Pulmonary Disorders

Lipoprotein Structure
1. cholesterol and triglycerides, in varying amounts, surrounded by lipoprotein structure (phopholipids), and apoproteins that control metabolic fate of lipoprotein - hydrophillic.
2. cholesterol and triglycerides are hydrophobic.
1. largest and made in small intestine
2. moves dietary (exogenous) cholesterol and triglycerides digested in GI tract to skeletal muscle for breakdown (energy production) and adipose tissue for storage.
3. Remaining cholesterol is transported to liver to made VLDL and HDL.
VLDL (Very Low Density Lipoprotein)
1. contains small amounts of cholesterol and large amounts of triglycerides
2. transports endogenous triglycerides and cholesterol to skeletal muscle and adipose tissue.
3. Once triglycerides are removed VLDLs are enriched with cholesterol and become IDLs
IDL (Intermediate Density Lipoprotein)
1. contains larger amounts of cholesterol and smaller amounts of triglycerides.
2. they move into BV for transport
LDL (Low Density Lipoprotein)
1. converts IDL to LDL in the blood vessels
2. they can accumulate in the blood stream or move back to the liver to be recycled into VLDL.
3. considered the bad cholesterol because they can build up in the blood stream and develop into atherosclerotic lesions.
2 Pathways for LDL transport
1. receptor dependent pathway - hepatocytes ingest LDLs via phagocytosis and then digests the outer core and releases cholesterol and triglycerides into the cytoplasm.
2. non-LDL receptor pathway - monocytes and macrophages phagocytize LDLs which can result in the build up of cholesterol esters - foam cells in arterial walls, which can develop into atherosclerosis.
HDL (High Density Lipoprotein)
1. made in the liver
2. low in cholesterol and high in phospholipids
3. carries cholesterol from the peripheral tissues back to the liver.
4. removes atheroscleratic plagues from aterial walls.
5. good cholesterol
Major cause of 2° Hyperlipidemia
1. obesity and high calorie intake - ↑ VLDL production→↑LDL and triglycerides, excess dietary cholesterol reduce LDL receptor formation.
2. diabetes mellitus - predispose to dyslipidemia and ↑ triglycerides, low HDL, and minimal LDL
1. hardening of arteries, especially coronary arteries, by accumulation of fatty lesions.
2. Three types of lesions
Fatty streaks
1. thin, flat, yellow intimal discolorations that progressively enlarge as they grow in length.
2. common in young children
3. may or may not be associated with atherosclerotic formation
Fibrous atheromatous plaque
1. basic lesion of atherosclerosis
2. consists of accumulation of lipids, proliferation of smooth muscle cells, and scar tissue
3. begins as a gray or pearly white, thickening of tunica intima with core of lipids covered by fibrous cap of ct. and smooth muscle.
4. occludes vessels and predisposes to thrombus formation - slows blood flow
Complicated Lesions
1. characterized by hemorrhage, ulceration,and scar tissue deposits
2. thrombus formation is biggest complication of atherosclerosis - caused by slow turbulent blood flow in the region of plaque and ulceration.
Constitutional Risk Factors of Heart Disease
1. age
2. gender
3. family predisposition
Lifestyle Risk Factors for Heart Disease
1. smoking
2. obesity
3. hypertension
4. hyperlipidemia
5. Diabetes (type II)
CRP (C-reactive Protein)
1. serum marker for systemic inflammation
2. binds to invading microorganisms that mark them for destruction
Raynaud Phenomenon
1. discoloration of the digits due to vasospasm (excessive vasoconstriction) in arteries and arterioles
2. associated with previous vessel injury, frostbite, occupational trauma associated with the use of heavy vibrating tools, collagen disease, neurologic disorders, and exposure to alternating hot and cold temps.
3. first symptom of collagen diseases
4. occurs in people with lupus and scleroderma
5. Changes in skin color (from pale to blue), numbness and tingling, intense redness, throbbing pain, brittle nails, thick skin over fingers, arthritis, ulceration and gangrene.
Abdominal Aortic Aneurysm
1.abnormal dilation of blood below renal artery at the biforcation of aorta and common iliac arteries
2. major cause: atherosclerosis
3. common in men with hypertension, smoking, and genetic predispositions
4. usually saccular or fusiform
5. classic signs: mild to severe abdominal and back pain by compression of spinal nerves
Clinical definition of Hypertension
1. hypertension in adults 18 years or older with BP readings of 140 SBP/ 90 DSP or higher
2. two stages 140-159/90-99 and 160/100 or greater.
Renin Angiotensin Aldosterone Mechanism
1. kidney releases renin in response to ↓BP, low ECF, and low Na⁺
2. renin enters circulation , activates angiotensinogen to angiotensin I
3. Angiotensin I moves to lungs and converts to Angiotensin II
4. angiotensin II is a vasocontrictor which ↑ peripheral vascular resistance and is a stimulus for aldosterone production in adrenal glands
5. Aldosterone ↑ tubular reabsorption of Na⁺ and H₂O.
6. Angiotensin II also stimulates the release of ADH in response to ↓bp and blood volume (vasocontricts and retains H₂O)
What contributes most to the long term regulation of BP?
1. kidneys play a long term role in the regulation of ECF.
2. renal control mechanisms alter equilibrium of bp by the retainment and release of Na⁺ and H₂O
Effects of Diuretics on BP
1. decrease vascular volume via suppression of Na⁺ reabsorption and ↑ sodium and water excretion
2.↓ COand eventually peripheral resistance
B-Andrenergic Blockers (Beta Blockers)
1. ↓ HR
2. ↓ CO
3. ↓ renin release by kidneys
ACE Inhibitors (Angiotensin converting enzymes)
1. inhibit conversion of angiotensin I to II
2. ↓ vasocontriction
3. ↓aldosterone
4. ↓ renal blood flow and glomerular filtation rate
Ca²⁺ Channel Blockers
1. ↓ peripheral vascular resistance
2. blocks Ca²⁺ channels
3. ↓ smooth muscle contraction
a₂-Andrenergic agonists
1. block a₁ receptors on vascular smooth muscle
2. ↓peripheral resistance by relaxing smooth muscle contraction thus ↑ vasodilation
1. hypertension during pregnancy with BP greater than 140/90
2. primarily occur during 1st pregnancies, subsequent pregnancies with multiple fetuses, diabetes mellitus, or coexisting renal disease.
3. associated with hydatidiform mole - abnormal pregnancy caused by pathologic ovum, resulting in masses of cysts.
4. ↓ placental blood flow, release of toxic mediators that damage endothelium
5. results in intravascular clotting, hypoperfusion, DIC, cerebral hemmorhage, hepatic failure, and acute renal failure
6. Thrombocytopenia is most common symptom
7. may lead to convulsions which is indicator of ecclampsia and death.
Orthostatic Hypotension
1. aka postural hypotension
2. abnormal drop in BP in change of posture to standing
3. drop of 20mmHg or more (systolic) or drop of 10mmHg (diastolic)
Chronic Stable Angina
1. paroxysmal chest pain or pressure associated with fixed coronary obstruction (stable athersclerotic plaque) that produces a disparity between coronary blood flow and metabolic demands of the myocardium.
2. initial manifestation of Ischemic Heart Disease
3. provoked by exertion or emotional stress and can be relieved by nitroglycerin
4. suffocating pain that occurs in substernal area that radiates to left arm, shoulder, and jaw
Myocardial Ischemia
1. imbalance between blood supply and demands of the heart
2. Limitations of coronary blood flow are associated with atherosclerosis, vasospasm, and thrombosis
3. Symptoms: angina (chest pain), pain in left arm and jaw, migraines, raynaud phenomenon, and arrhythmias
Cardiac Tamponade
1. rapid accumulation of exudate or blood in pericardium that compresses the heart, life threatening
2. results from trauma, cardiac surgery, cancer, uremia, or cardiac rupture from myocardial infarction
3. causes ↑ intracardiac pressure, ↓ ventricular diastolic filling, ↓ SV and CO
4. depends on rate of accumulation and amount of fluid that can lead to jugular distention, ↑ venous pressure, ↓ venous return, ↑ HR
5. leads to circulatory shock
Acute Myocardial Infarction
1. heart attack
2. ischemic death of myocardial tissue determined by coronary artery that is affected.
3. typically severe crushing pain in chest, described as suffocating and constricting - prolonged
4. sudden death can be attributed to arrhythmia - sudden cardiac death.
5. Diagnosed by presence of serum markers and elevated ST segment
Valvular Stenosis
1. valve will not properly open due to build up of collagen on leaflets
2. ↑ resistance to blood flow
3. ↑ volume and work of chamber to empty
4. ↑ work demands on the heart
Valvular Regurgitation
1. valve will not properly close; causing back flow.
2. ↑ work demands on the heart
Mitral Stenosis
1. incomplete opening of mitral valve due to fibrous replacement of tissue becomes stiff and fused.
2. chordai tendinae cannot contract to all the valve to open due to increased diastolic ventricular pressure
Mitral Valve Regurgitation
1. improper closing of mitral valve causing back flow of blood in to the left atrium during systole of left ventricle.
2. can also result from rupture of chordae tendinae or papillary muscles
3. common caused by mitral valve prolapse
Aortic Valve Regurgitation
1. improper closing of aortic valve causing back flow of blood into the left ventricle during diastole
2. requires an ↑ SV to allow for back flow.
3. causes ↓ in coronary perfusion due to↓ in diastolic pressure.
Aortic Valve Stenosis
1. improper opening of aortic valve due to fibrous replacement of valve tissue.
2. requires ↑ resistance to eject blood and increase systolic pressure of left ventricle.
3. left ventricle works harder to eject blood
4. SV is ↓
Mitral Valve Prolapse
1. condition in which the valve leaflets are floppy and do not close properly.
2. leads to mitral regurgitation.
Acute Coronary syndrome
1. spectrum of coronary heart disease from unstable angina through myocardial infarction.
Classification of of ACS as high or low risk for AMI
1. ECG variables
2. serum cardiac markers
3. time of presentation
EKG Changes related to ASC
1. T-wave inversion - alteration of myocardial repolarization (diastole)
2. ST-segment Depression or elevation
3. Abnormal Q wave - no depolarization, indication of infarction
Serum Cardiac Markers for ASC
1. release of these markers are indicators of AMI
2. Creatine Kinase - enzyme in muscle cells
3. Myoglobin - O₂ carrying cells of muscle
4. Troponin I and T - regulate actin-myosin contractility
5. Troponin Assays - primary biomarker for MI
Unstable Angina
1. myocardial ischemia ranging from stable angina to MI.
2. results from unstable atherosclerotic plaque, platelet aggregation, 2° hemostasis, and coronary vasoconstriction
3. may occur as 1°, 2° due to non-coronary conditions, post infarction angina after AMI
4. cocaine can induce myocardial ischemia
5. Symptoms: severe and frank pain and in a pattern that is prolonged and frequent.
6. Diagnosis: no serum markers, T wave inversion, ST segment Elevation
Dilated Cardiomyopathy
1. progressive hypertrophy and dilation (expansion) of ventricles.
2. impairs pumping of all 4 chambers
3. contractility ↓
4. caused by myocarditis, toxic agents, metabolic influences, neuromuscular diseases, and immunologic disorders.
5. can also be genetic: auto domin. or X-linked
6. related to HF or is an indication of heart transplant.
Rheumatic Heart Disease
1. rheumatic fever is acute immune mediated disease that affects the heart.
2. caused by gas infection
3. manifests in three stages
4. causes inflammation of pericardial and myocardial layers of the heart, valvular disorders, migratory polyarthritis of large joints, erythema marginatum (large lesions), subcutaneous nodules (hard painless nodules on extremity joints), and Syndenham chorea (CNS complication)
5. commonly affects school age children
Effects of Rheumatic Disease on valvular disorders
1. commonly associated with Mitral and aortic Stenosis, though affects all valves.
2. causes redness and swelling of valves
3. leads to development of vegetative lesions on leaflets - which constantly release bacteria and grow damaging leaflets
4. acute inflamm. response causes fibrous tissue to develop shortening chordae tendinae
5. causes fusion of commisures during healing
Left to Right shunting
1. blood moves from left to right (arterial to venous)
2. normally occurs in a fetus via foramen ovale but not common in adulthood unless there is a problem with the fusion of the foramen.
3. results in ↓ blood to the body and ↑ blood to lungs
4. causes pulmonary edema, pulmonary hypertension
Right to Left Shunting
1. blood move from right to left (venous to arterial)
2. De-oxygenated blood moves into the body and less blood travels to the lungs.
3. causes tachycardia, ↑ clotting, ↑ viscosity, hyperventilation
Silent Myocardial Ischemia
1. characterized by no pain or angina but still experiences ischemia
2. occurs in people with previous cases of MI
3. associated with defects in pain transmission- neuropathy
4. common in people with diabetes mellitus and the elderly
Variant or Vasoplastic Angina
1. caused by spasms of coronary arteries due to coronary stenosis
2. occurs during rest and sleeping
3. result from sympathetic NS responses
4. causes arrhythmia
Chronic Ischemic Heart Disease
1. imbalance of blood supply from coronary arteries and the heart's demand for O₂
2. imbalance of blood caused by atherosclerosis, vasospasm, and thrombosis
3. higher O₂ demand caused by stress, exercise, and cold
4. ranges from Chronic Stable Angina, Silent Myocardial Ischemia, and Variant Angina
Stable Plaques
1. fibrous atherosclerotic plaques
2. thick fibrous caps
3. partially blocked vessels
4. do not tend to form clots or emboli
Unstable Plaques
1. thin fibrous caps that can rupture and form larger caps (combo of clot and lipids)
2. results in total occlusion which causes infarcts and embolisms
3. resistant to traditional therapies
4. dislodged where mechanical stress is greatest - biforcations of vessels
Determinants of Plaque Rupture
1. size of lipid rich core and thickness of cap
2. presence of inflammation with plaque degradation
3. lack of smooth muscle cells with impaired healing
Types of thrombi that develop due to plaque rupture
1. white thrombi - grayish white and platelet rich, commonly found in unstable angina
2. red thrombi - rich in fibrin and rbc, and stasis of blood flow, commonly found in vessel occlusion of AMI.
Coronary Heart Disease
1. caused by atherosclerotic lesions in 1 or all 3 of coronary arteries (lft anter. descending, lft circumflex, and rt. coronary artery)
2. stable and unstable lesions obstruct blood flow, rupture, and cause platelet adhesion and thrombus.
3. includes chronic ischemic Heart disease and Acute Coronary syndrome
4. coronary artery bypass graft is used for treatment to ↑ blood flow to arteries.
Hypertrophic Cardiomyopathy
1. abnormality that is characterized by excessive ventricular hypertrophy
2. results in abnormal diastolic filling, ↓ SV with worsen sympathetic activity
3. associated with arrhythmias
4. most common cause of death in young athletes
5. can be an autosomal dominant inherited disorder
Treatment for Rheumatic Fever in Children
1. priorities include: eliminate infection, reduce inflammation, prevent cardiac complications and recurrence of disease
2. antibiotics and anti-inflammatories (corticosteriods) are used for GAS infection and inflammation
3. surgical procedures may be done to repair damaged heart valves
4. life-long therapies such as antibiotic therapy till young adulthood or life.
Compensatory mechanisms for stenosis.
as flow resistance ↑, leads to...
↑ volume of chamber
dilation of chamber (lft atrium, lft ventricle)
↑ pressure in volume
↑ workload of chamber
Cardiac Output
amount of blood ejected by each ventricle in 1 min.
Compensatory Mechanisms for ↑ Heart workload
1. Frank Starling Mechanism
2. Sympathetic NS Activity
3. Renin-Angiotensin Aldosterone Mechanism
4. Natriuretic Peptides
5. Endothelin
6. Myocardial Hypertrophy and remodeling
Frank Starling Mechanism
1. activation of neuro-humoral influences
2. ↑ EDV (preload) thru stretch and contraction→ ↑SV
3. ↑ diastolic filling, dilates myocardium
4. ↑ force of contraction → ↑CO
5. chronic elevation of lft. ventricular end diastolic pressure - which eventually leads to pulmonary congestion
Sympathetic NS Activity
1. affects vascular tone, HR, and contractility
2. causes vasoconstriction to other organs and vasodilation of heart and skeleton
3. ↑ BP
4. can lead to ↑ vascular resistance, ↓ blood flow to other parts of the body, promotion of arrhythmias that can lead to death.
Natriuretic Peptides
1. release of peptides
2. atrial Natriuretic Peptide (ANP) - (released by atrial cells) acts as antagonist to Angiotensin II and inhibits release of epinephrine and norepinephrine (affects HR)
3. Brain Natriuretic Peptide (BNP) - ↑ ventricular filling pressures
1. released by endothelial cells
2. potent vasoconstrictor
3. ↑ vascular smooth muscle prolif. and myocyte hypertrophy
Myocardial Hypertrophy and Remodeling
1. may improve work performance but ↑ risk of mortality
2. inapproriate hypertrophy and remodeling may cause changes in structure and function
3. can cause pump dysfunction and hemodynamic overload.
Left Sided HF
1. impaired pumping of blood from pulmonary circulation to systemic circulation.
2. causes ↓ CO, ↑ Left atrial and left ventricular end diastolic pressure
3. leads to pulmonary edema due to pulmonary cap. filtration pressure > capillary osmotic pressure
4. caused by AMI, cardiomyopathies, mitral and aortic valve disorders
Right Sided HF
1. impairs the ability to move De-O₂ blood from systemic circulation to pulmonary circulation.
2. causes ↑ in rt atrial and rt ventricular end diastolic pressure, and systemic venous pressures.
3. leads to peripheral edema - evidenced in lower extremities when standing, on the lower back in supine, and in weight gain.
4. caused by Lft sided HF, acute or chronic pulmonary diseases, tricuspid and pulmonary valve disorders, Rt. vent. infarcts, and cardiomyopathies
Hypovolemic Shock
1. hemorrhaging shock - rapid ↓ blood volume
2. leads to a + feedback cycle that can cause death
3. results from trauma, aneurysms, internal GI tract bleeding, and rupture of ectopic pregnancy
4. causes vasoconstriction in skin, muscles, kidneys, and liver; lactic acid buildup
5. Symptoms: anxiety, cyanosis, low or no urine output, profuse sweating, shallow breathing, dizziness, chest pain, confusion, loss of consciousness, tachycardia, and weak pulse.
6. treatment is aimed at replenishing fluids such as blood transfusion and medications to promote pumping
Anaphylactic Shock
1. caused by anaphylaxis - severe systemic allergic reaction
2. results from release of histamine which vasodilates arterioles and venules to ↑ cap. permeability
3. causes life threatening laryngeal edema and bronchospasm, circulatory collapse, contraction of GI and uterine smooth muscle, urticaria (Hives), and angioderma (swelling of skin)
4. caused by allergic reactions such as penicillin, foods, insect venoms, bee stings, and latex
Acute Respiratory Distress Syndrome (ARDS)
1. respiratory failure that follows severe shock
2. ↑ respiratory rate and breathing effort
3. profound hypoxemia and hypercapnia caused by impaired matching of ventilation and perfusion, poor gas diffusion, and thickened alveoli
4. accumulation of neutrophils in pulmonary vasculature - causes fluid to leak into interstitium and alveolar spaces - impairs gas exchange, stiffens lung making it more difficult to inflate, and alveolar collapse
Health Problems associated with Diastolic Dysfunction
1. Pulmonary edema in left ventricular diastolic dysfunction
2. peripheral edema in rt ventricular diastolic dysfunction.
Cardiogenic Shock
1. inability of the heart to pump blood to other organs of the body
2. caused by MI, embolism, valve disorders, endothelial rupture, ventricular fibrillation
3. causes confusion, anxiety, sweating and cold in extremities
Obstructive Shock
1. occurs with obstruction of blood flow through central circulation
2. caused by dissecting aortic aneurysm, cardiac tamponade, pneumothorax, pulmonary embolism
3. causes elevated rt heart pressure, impaired venous return, elevation of central venous pressure, jugular venous distention
Distributive Shock
1. BV dilate, blood flow↓, and not enough blood returned to heart and distributed to other organs
2. loss of BV tone, enlargement of vascular compartment, displacement of vascular volume away from heart and central circulation.
3. caused by ↓ in sympathetic control of vasomotor tone, presence of vasodilator substances, vessel damage from hypovolemia
4. 3 stages - neurogenic shock, anaphylactic shock, and septic shock
Neurogenic Shock
1. caused by ↓ sympathetic control of BV tone due to defects in vasomotor center of brain
2. due to brain injury, depressant drugs, general anesthesia, hypoxia, lack of glucose, fainting, and spinal cord injury
Septic Shock
1. associated with severe infection (sepsis) and release of inflammatory mediators
2. endotoxins damage tissues and cause activation of coagulation factors and complement cascades, and release of vasodilators
3. lead to major complications such as: pulmonary insufficiency, DIC, and multiple organ dysfunction
1. viral infection affecting URT and LRT
2. 3 types: Influenza A, B, C
3. spread via aerosol or direct contact
4. 3 types of infections: uncomplicated URT, viral pneumonia, and respiratory viral infection
5. viruses kills ciliated epithelial cells, and sheds bronchial and alveolar cells
6. promote bacterial adhesion
7. cause pneumonia
8. symptoms: fever, tachycardia, tachypnea, cyasnosis, hypotension, and severe cases hypoxemia and death.
9. 2° complications: sinusitis, otis media, bronchitis, bacterial pneumonia
Common cause of bacterial pneumonia
1. influenza
2. bacteria involved are S. pneumoniae, S. aureus, H. influenzae, M. catarhalis
How are cold viruses spread?
either by children or fingers and hands
1. inflammation of the alveoli and bronchioles of the lungs
2. 2 types: affects entire lobe of lung, and patchy distribution over more than 1 lobe.
3. Manifestation: infection, inflammation, exudate leaking into air spaces, and congestive productive cough
4. symptoms of inflammation: malaise, fever, and chills
Pathogenesis of TB
1. Bacteria passes down bronchiole tree into alveoli
2. macrophages engulf bacteria and initiate cell mediated response
(3 to 6 weeks for positive TB test)
3. brings in T lymphocytes that cause macrophages to release lytic enzymes that kill bacteria and surrounding tissue
4. ghon focus develop
Ghon Focus
1. gray white granulomatous lesions that contain bacteria, macrophages, and other immune cells
2. enventually becomes necrotic - soft and caseous
3. can travel through lymph system
1° TB
1. initiated by inhaling droplet nuclei that contain the tubercle bacillus - first time offenders, latent infections where disease is usually contained and not contagious
2. most go on to damage multiple sites of lungs
3. symptoms are insidious and non-specific: fever, weightloss, fatigue, night sweats, pleuritis, and lymphadenitis
4. rare cases, bacteria can travel to BV that give rise to hematogenic dissemination
Upper Respiratory Infection
1. includes sinuses, nasal passages, pharynx, and larynx
2. common infections: cold, sinusitis, laryngotracheitis, tracheitis
3. symptoms: runny nose, cough, sore throat, difficulty breathing, and lethargy
4. influenza passes from URT to LRT
Lower Respiratory Infection
1. include lower airways and lungs
2. common infections: penumonia, TB, bronchitis
3. Symptoms: productive cough, difficulty breathing, fever, malaise
4. infleunza can move to lower airways and cause 2° complications
1. upper airway infection in infants
2. acute laryngotracheobronchitis
3. caused by viral infection
4. manifests to stridor (high pitched wheezing) and slight dyspnea - recovery when exposed to moist air
5. as obstruction ↑, stridor is continuous, there is nasal flaring, and chest retration
1. upper airway infection
2. inflammation of the epiglottis and pharynx
3. acute condition that can be fatal
4. there is airway contriction and asphyxia
5. syptoms: pale, toxic, and lethargic, must assume sitting up position, lead to severe respiratory distress and complete obstruction causes death
6. most life threatening
Acute Bronchiolitis
1. lower airway infection
2. inflammation and obstruction small airways and necrosis of cell lining
4. symptoms: fever, diminished appetite, respiratory distress
5. severe cases: hypoxemia, hypercapnia, cyanosis, pallor, listlessness, absence of breath
Respiratory Distress Syndrome
1. hyaline membrane disease
2. pulmonary immaturity and surfactant deficiency lead to alveolar collapse
3. causes infants to work harder with each breathe - alveoli cannot work equally
4. results in stiff con-compliant lungs
5. produces a hyaline fibrin membrane around alveol - impairs gas exchange
6. leads to hypoxemia, CO₂ retention, cyanosis, breathing problems, and chest wall retraction
7. treatment: supportive care and incubation
Small Cell Lung Cancer
1. characterized by small round shapes
2. grow in clusters, highly malignant, early metastasis
3. brain metastasis is most common
5. Bronchogenic carcinoma - most common type
6. tendency to release bioactive products and produce paraneoplastic syndromes
Non-small cell Lung Cancer
1. squamous cell carcinoma, adrenocarcinomas, and large cell carcinomas
Symptoms and complications of Lung Cancer
1. chronic cough
2. dysnpea
3. wheezing
4. hemptysis (bloody sputum)
5. chest pain
6. hoarseness - larynx compression
7. superior vena cava syndrome - compression of vena cava which interrupts blood flow
8. pleural effusion
1. incomplete expansion of lung or portion of lung
2. caused by airway obstruction, lung compression, ↑ recoil of lung cause by ↓ surfactant
Tension pneumothorax
1. air enters pleural cavity through the wound during inhalation but does not leave on exhalation.
2. intrapleural pressure > atmospheric pressure
3. causes chest pressure, atelectasis in unaffected lung, mediastinal shift, vena cava syndrome
4. symptoms: dyspnea, hyperresonnant sound, hoxpoxemia
What occurs as a result of a mediastinal shift?
1. distention of neck veins
2. subcutaneous emphysema
3. clinical signs of shock
Bronchial Asthma
1. chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eiosinophils, T lymphocytes (Th2 cells - respond to allergies), and damage to bronchial epithelial cells.
2. exaggerated inflammatory response
3. causes wheezing, breathlessness, chest tightness and cough.
Intrinsic Asthma
1. inflammation initiated by non-immune mechanisms such as respiratory infections, exercise, hyperventilation, cold air, drugs, chemicals, hormone changes, emotions, air borne pollutants, and gastroesophogeal reflux.
2. can cause mild to severe attacks that lead to respiratory failure
3. symptoms include: chest tightness, slight ↑ in respiratory rate with prolonged expiration, more severe attacks cause loud wheezing, distant breath sounds, moist skin, respiratory failure is indicative by inaudible breath sounds, diminished wheezing, and unproductive cough.
Extrinsic Asthma
1. is initiated by a Type I hypersensitivity reaction to outside stimuli
2. Ig E mediated response that produces pre-sensitized Ig E mast cells
3. exposure to Ag will trigger release of pre-sensitized cells from mucosal surface of airway
4. inflammatory cells flood area and intercellular space open to access Ag
5. there is bronchospasm, mucosal edema, and ↑ mucus secretions
1. loss of lung elasticity and abnormal enlargement of the air spaces distal to the terminal bronchioles with destruction of alveolar wall ans capillary beds.
2. caused by breakdown of elastin and other proteins via proteases
3. smoking in a major cause of emphysema - by inhibition of anti-trypsin, a antiprotease
Centriacinar Emphysema
1. upper lung emphysema
2. affects bronchioles in central lobule
3. predominantly found in male smokers
Panacinar Emphysema
1. lower lung emphysema
2. affects peripheral alveoli and the central bronchioles
3. more common in people with antitrypsin deficiency.
Cystic Fibrosis
1. auto recessive genetic disorder on chrom 7
2. involves mutation of CFTR gene that impairs transport of Cl⁻
3. involves secretion of fluid into exocrine glands of epithelial lining in respiratory tracts
4. causes viscid mucus and impairs mucocilliary clearance and lung infection leading to bronchietasis
Causes of Respiratory Failure
1. Hypoventilation - ↓ volume of air in and out of lungs, caused by depression of respiratory center, diseases of nerves supplying respiratory muscles, disorder of respiratory muscles, or thoracic cage disorders
2. mismatched ventilation and perfusion - COPD,
3. impaired diffusion - impairment of gas exchange between capillary beds and alveoli, caused by interstitial lung diseases, ARDS, pulmonary edema, and pneumonia
Common results of Respiratory Failure
1. Hypoxemia
2. Hypercapnia
1. condition in which there is low PO₂ in blood.
2. caused hypoventilation, mismatched ventilation and perfusion, and impaired gas diffusion commonly found in respiratory failure
3. clinical features: hyperventilation, visual acuity, impaired mental performance, personality changes, convulsions, retinal hemorrhage, brain damage in severe cases.
1. ↑ in CO₂ content in blood
2. can cause respiratory acidosis, dilate BV, and sedates NS.
3. leads to headaches, optic disc swelling, ↑ cerebral spinal fluid pressure, somnolence, disorientation, coma, and death.