What does the circulatory system do?
Delivers oxygen & nutrients needed for metabolic processes to the tissues, carries waste products away from cellular metabolism to kidneys and other excretory organs for elimination, and circulates electrolytes & hormones needed to regulate body functions
What are the 2 parts of the circulatory system?
Pulmonary Circulation (AKA central circulation)
Systemic circulation (AKA peripheral circulation)
What does the pulmonary circulation consist of?
Right side of heart, the pulmonary arteries, the pulmonary capillaries, and the pulmonary veins
(Moves blood thru the lungs and creates a link for gas exchange)
What does the systemic circulation of?
The left side of the heart, the aorta, and its branches, the capillaries that supply the brain and peripheral tissues, and the systemic venous system and vena cava.
(moves blood throughout all other tissues of the body)
What are the 3 factors that affect blood flow thru vessels?
Pressure, resistance, flow/velocity.
Outer cover of heart.
Visceral pericardium- faces the organ
parietal pericardium - faces away from organ.
What is the cardiac conduction system?
The SA Node : functions as the pacemaker of the heart
The AV Node: connects the atrial and ventricular conductive systems
What is the cardiac cycle?
The ryhthmic pumping action of the heart. Divided into 2 parts: Systole & Diastole
Period when ventricles are contracting
blood pushes against AV valves & they shut
Blood pushes thru semilunar valves into aorta and pulmonary trunk
Period when ventricles are relaxed and filling with blood
Blood enters atria
blood flows thru AV Valves into ventricles
Semilunar valves are closed.
What is stroke volume?
EDV - ESV (End Diastolic volume - end systolic volume)
the amount of blood the heart pumps out in a single beat.
What is cardiac Output
Stroke Volume X heart rate
Amount of blood pumped out of heart per minute
What is formula for blood pressure?
Cardiac Output X Peripheral resistance
Helps to understand blood pressure: if Peripheral resistance is high, then BP is high & vice versa
what is the formula for Ejection Fraction?
Stroke volume/ End diastolic volume
The percent of blood pumped out
Elevated levels of lipids or fats in the blood.
Cholesterol and triglycerides are insoluble in plasma and are encapsulated by special fat carrying proteins called lipoproteins for transport in blood
LDL is main carrier of cholesterol
Dietary lipids absorbed from intestines as chylomicrons, which adipose & muscle cells take up, but chylomicrons remnants are intermediate-density lipoproteins.
IDLs become LDL's and delivers fat to the liver and other tissues
Form of Hyperlipidemia: Primary Hypercholesterolemia
Independent of other causes, no known cause
Form of hyperlipidemia: Secondary Hypercholesterolemia
Associated with other health conditions
- Diabetes mellitus
- sedentary lifestyle, etc
Treatment for hyperlipidemia
Dietary, Therapeutic, medication ( decrease cholesterol production or absorption, remove cholesterol from blood stream)
Are blood vessels that carry oxygen and nutrients from your heart to the rest of your body, but when there is too much pressure the arteries become thick and harden, which can restrict flow
a type of arteriosclerosis, refers to build up of fats in and on artery walls (plaques) which can cause vessel stenosis and restrict blood flow.
It is considered a heart problem, but it can occur anywhere.
Lipids get into vascular endothelium (proportional to LDL Levels)
Macrophage tries to clear them away, then macrophage turns into a foam cell.
WBS & vascular endothelium release growth factors that promote plaque formation
Plaques block the arteries.
What are the lesions associated with atherosclerosis?
The fibrous atheromatous plaque
The complicated lesion
the earliest lesion, which is present in children, lesions result from collections of macrophage that phagocytize and accumulate fat within their cytoplasm (Foam Cells)
Fibrous Atheromatous plaque
basic lesion of clinical atherosclerosis; characterized by accumulation of intracellular and extracellular lipids, proliferation of vascular smooth muscle cells, formation of scar tissue and calcification.
what are the clinical manisfestations of atherosclerosis (depends on extent and vessels involved
1. Stenosis of the vessel (Narrowing) and ischemia.
2. sudden vessel obstruction due to plaque hemorrhage or rupture
3. Thrombosis and formation of emboli resulting from damage to the vessel endothelium.
4. Aneurysm formation due to weakening of vessel wall.
The most important complication of atherosclerosis bc it causes acute blockage of arteries. It is caused by slow and turbulent blood flow in the region of the plaque and ulceration of the plaque.
* may cause acute vessel occlusion
Where is the most frequent sites of atherosclerosis
Peripheral Arterial Disease
Atherosclerosis changes that result in tissue ischemia (low blood)
Most common in men in 60s & 70s
Risk factors include: Smoking, diabetes
Ischemic Symptoms of Peripheral Arterial Disease
Gradual onset of intermittent claudication (pain in calf when walking)
Atrophic changes of the skin (pale bc skin is not getting oxygen)
Rest pain, only if severe, ulceration, and gangrene can develop (when blood flow no longer meets minimal needs)
Treatment for PAD
avoidance of injury,walking program, reduce risk factors, antiplatelet agents, surgery,
Diagnose by: Inspection, check pulses(DP & PT), ankle brachial index
Functional disorder of arteries & arterioles of the skin - there are intense spasms of arteries & arterioles in the fingers and less often in the toes in response to stimuli. its aggravated by cold or emotional stress.
More common in feet and in middle-aged women
Treatment of Raynauds Phenomenon
avoidance of triggering events, no smoking, use of vasodilator drugs.
An abnormal localized dilation of a blood vessel or wall of the heart., which may rupture or hemmorhage. Most common in abdominal aorta
can occur in arteries or veins
Causes of aneurysm
atherosclerotic plaque formation (most common)
congenital abnormality or arterial wall
locations of Aneurysms
Aorta (most common)
- Abdominal aorta (bw renal arteries & iliac branches)
- Thoracic aorta (ascending, transverse, or descending)
Cerebral artery ( at circle of willis)
Femoral and popliteal arteries
Complications of aneurysms
Rupture - risk increases with increasing size
pressure on adjacent structures
* involving large vessels in critical locations
what are the four forms of aneurysms
Dissecting ( most common in ascending aorta)
Abdominal Aortic Aneurysms
can go undetected for long periods of time bc they are asymptomatic. A pulsating mass found on routine abdominal examination may be first evidence.
Develop in Men after 50
90% occur below renal artery
ultra sound, echocardiography, CT, MRI, surgical repair
an abrupt presence of excrutiating pain, described as tearing or ripping, high mortality rate.
Arterial Blood Pressure
the rythmic ejection of blood from the left ventricle into the aorta. It rises as left ventricle contracts and falls as it relaxes.
The highest pressure is systolic and the lowest is Diastolic
Normal blood pressure
Systolic <120/ Diastolic <80
Stage 1 Hypertension
Stage 2 Hypertension
most common of all health problems in adults and leading risk factor for cardiovascular disorders and is usually asymptomatic. When symptons do occur its usually related to long-term afects on the organ systems.
90% of hyepertenssive patients
More frequent in Males, Black, Poor, Older, Obese
10% of hypertensive patients
Cause is known- most common cause is Renal Disease
Risk Factors of Hypertension
- family history, race, sex
- high sodium diet, excessive calories, excessive alcohol, physical inactivity, oral contraceptives, sleep apnea
- NOT stress (acute only), NOT High fat diets,
- Smoking unknown
Most common sites of HT organ damage
Kidney- Renal Failure
Brain- Cerebral Vascular accident (stroke) CVA, TIA0 transient ischemic accident (a smaller stroke)
Heart - chest pain (angina), LVH (left ventricle hypertrophy), CAD, CHF
Eyes - retinopathy
blood vessels - peripheral vascular disease(PVD), arteriosclerosis
you treat patients to live longer, not feel better. Must take repeated BP measurements to be diagnosed with HT
AKA postural Hypotension, an abnormal drop in BP upon standing.
Symptoms: Dizziness & Syncope (fainting)
Causes: Reduce blood volume, Drug induced, aging, immobility
Diagnosis & treatment for Orthostatic Hypotension
Diagnosis: sitting and standing BP measurements
Treatment: alleviate the cause(ie if it is due to dehydradtion, then rehydrate), education, adjusting meds, support hose
The venous system
Low-pressure system, pumped by skeletal muscles to return blood to hear
and has venous valves to prevent retrograde flow
2 components: Deep Veins ( these return blood to the heart) & Superficial Veins
What are the Disorders of Venous Circulation
Dilated, tortuous veins, engorged with blood resulting from improper venous valve function.
Most common in legs; edema of calves, leg heaviness, dull aching of lets
- Weakening in valve allows backflow of blood
- Increase pressure in the veins causing walls to stretch
2 types: Primary & Secondary
Complications include: Chronic Venous insufficiency & blood clots secondary to venous stasis
Treatment: Treat underlying cause, anti-embolism socks, exercise, surgical stripping
Primary Varicose Veins
Originates in superficial veins
Secondary Varicose Veins
Result from impaired flow in the deep venous channels
The most common cause is DVT Deep Vein Thrombosis
Chronic Venous Insufficiency
a condition in which the incompetent venous valves result in an ineffective venous pump. THe pump causes tissue congestion and impaired nutrition resulting in atrophy of the skin and fat necrosis. Brown pigmentation occurs bc of hemosiderin deposits resulting from the break down of RBCs
Stasis dermatitis & ulcers
acute development of a blood clot that may cause vessel occlusion or embolization
- causes vessel irritation, which results in inflammation & contributes to occlusion or embolization
- may occur in deep(more serious) or superficial (more common)
- aka thrombophlebitis
The triad that can cause Venous Thrombosis
Venous Stasis: bed rest, immobility, shock, airplane rides, long car rides, AMI (Acute Mycardial infarction)
Hypercoagulability of blood - pregnancy, child birth, BCPs, dehydration, cancer
Vascular Trauma - venous catheters, surgery, massive trauma, hip fracture, orthopedic surgery
Inflammation of the pericardium as a result of systemic or cardiac diseases
- Viral infections (most common)
- Bacterial infection, trauma, radiation, & autoimmune
Associated with fluid collection within the pericardial space ( pericardial effusion)
Pericarditis Pathological changes
when the pericardial becomes inflammed the serous fluid becomes inflammed as well
Pericardial friction run & sharp substernal pain
shallow rapid respirations due to associated pleurisy
mild fever from inflammation
dyspnea, orthopnea, tachycardia
accumulation of fluid in pericardial cavity;
may occur as a result of inflammatory processes, infection, neoplasms, cardiac surgery, trauma. Major threat is compression of the heart chambers with resultant reduction in ventricular filling and cardiac output.
Testing: CXR shows a widened mediastinum & echnocardiogram shows pericardial fluid
Treatment: Pericardiocentesis; Pericardial window; Pericardiectomy
Rapid compression of the heart due to accumulation of fluid, pus, or blood in pericardiarl space. Could be due to infection, inflammation, trauma, or rupture of ventricular wall.
THe compression of the heart results in a decrease in ventricular filling, which ultimately results in a decrease stroke volume & a diminished or absent pulse
a rapid, accurate and widely used method of evaluating pericardial effusion.
Coronary Artery Disease
Impaired Coronary blood flow
- Narrowing of coronary arteries due to atherosclerosis
- Heart disease secondary to mycocardial ishcemia
- strength of myocardial contractions is reduced
- wall motion is abnormal resulting in lower cardiac output
- conduction deficits
- Imbalance in blood supply & the hearts demands for oxygen
- Less blood
- stress, exercise, cold
- Less blood
Acute coronary syndromes
acute ischemic heart diseases
Acute Myocardial Infarction (aka, heart attack)
Intermediate of stable angina and myocardial infarction. Often ischemia is not severe enough to cause permanent myocardial damage
Worst than stable angine, but not quite MI
Due to atherosclerotic plque disruption --> platelet aggregation --> Hemostasis
Acute Myocardial infarction
Occurs when a portion of the myocardium loses its blood supply and the tissue infarcts(dies)
The onset is usually abrupt pain at significant symptom, GI complaints common
The extend depends on location & extent of occlusion, amount of heart tissue supplied by the vessel, duration of the occlusion, metabolic needs of the affected tissue, extent of collateral circulation, & other factors like heart rate.
Ischemic death of myocardial tissue
sudden onset --> pain
reduced blood flow thru one or more coronary arteries causing myocardial ischemia & necrosis
Complications of myocardial infarction
- AMI is most common cause of left HF
rupture of heart
- most common cause of sudden death with AMI
occurs when the ability of the coronary arteries to supply oxygen is inadequate to meet the metabolic demands of the heart.
3 types of chronic ischemic heart disease
Chronic Stable Angina
Pain when hearts oxygen demand increases
Fixed coronary artery obstruction that produces a disparity b/w coronary blood flow and the metabolic demands of the myocardium.
Pain is described as constricting, squeezing, suffocation.
pain relieved by anti-platelet aspirin or nitroglycerin
Pain when coronary arteries spasm
Prinzmetals angina (vasopastic angina)
Intermittent coronary vasospasms (at rest)
Silent Myocardial ischemia
myocardial ischemia without pain
unknown eitology but found in diabetic patients
a group of disorders that affect the myocardium & are usually associated with disorders of myocardial performance which may be mechanical(heart failure) or electrical (arrhythmias)
They can be primary or secondary
disorders of the heart muscle that are confined to the myocardium.
conditions in which there is a cardiac muscle disease in the presence of a multisystem disorder
what are the 3 categories of primary cardiomyopathy?
Hypertrophic cardiomyopathy, most common, genetic, ppl dont' know they have it
- autosomal dominant disorder
- Hypertrophied ventricle becomes stiff and noncompliant and unable to relax causing a reduction in ventricular filling
- 1 out of 500 in general population
- common cause of sudden cardiac death in athletes
- signs & symptoms vary
Dilated Cardiomyopathy: extensively damaged myocardium reduces contractility causing a decline in systolic function and cardiac output (heart failure). There is left ventricular dysfuncion characterized by thinning of the ventricular wall. (still hypertrophied, but it's stretched out)
Restrictive Cardiomyopathy: Fibrosis and stiffening of the ventricle reducing the ability to relax and fill during diastole resulting in a decrease in cardiac output. Least common
Termed myocarditis or inflammatory cardiomyopathy. Its inflammation of the heart muscle and conducting systemw/o evidence of myocardial infarction
Focal or diffuse inflammation of the cardiac muscle which may be acute or chronic
- Inflammatory cardiomyopathy
- inflammation may lead to hypertrophy, fibrosis or inflammatory changes of the conduction system
- usually resolves spontaneously
- heart muscle weakens and contractility is reduced(during acute)
Causes of Myocarditis
Infection(bacterial, viral); radiation therapy, hypersensitivity immune reaction, toxins such as lead, chemicals, & cocaine, chronic alcoholism
most common cause is viral
Treatment- most cases are transient and resolve within several months
Complications of myocarditis
Arrhythmias & sudden death
infection of the endocardium, heart valves or cardiac prosthesis.
relatively uncommon, life-threatening
- causing deformities & destruction of valvular tissue & chordae tendineae causing rupture & valvular insufficiency
- collection of microorganisms, fibrin & platelets from vegetations that can cover the valve surface
- vegetations may break off and form septic emboli
- aka bacterial endocarditis
Causes of infective Endocarditis
Bacterial (most common) or fungal invasion
- Portal of Entry
- IV Drug abuse
- Damaged endocardial surface
- Presence of prosthetic heart valve
- Rheumatic heart disease
S/SX & Diagnosis of endocarditis
S/Sx: fever, chills due to bacterial infection
heart murmur due to turbulent blood flow (over valves that have been damaged by endocarditis)
positive blood cultures (most definitive & essential guide to treatment) blood cultures can identify causitive agent & sensitivity testing to make antibiotics
elevated WBC Count
Complications of endocarditis
acute renal failure
brain abscess (from septic emboli)
Rheumatic heart fever
an acute immune mediated, systemic, inflammatory disease of childhood that develops after infections with group A streptococcus.
- inflammation of heart, joints, CNS, skin, subcutaneous tissues
Rheumatic Heart Disease
The cardiac and valvular manifestations of rheumatic fever & is associated w acute inflammation of the myocardium, pericardium, and heart valves
- includes pericarditis, myocarditis, and endocarditis during early phase
- chronic valve disease in the later phase
Patients who develop acute rheumatic heart disease are not actively infected w Group A Streptococci but rather develop S/Sx weeks after infection has cleared
Pathophysiology of Rheumatic Heart Disease
GAS infection leads to autoimmune reaction in which antibodies produced to combat GAS affect connective tissues of the body
Antibodies may attack healthy body cells by mistake bc the bacterial antigens are similar to the bodys own cells
Pathophysiologic changes of RHD
polyarthritis caused by inflammation
firm movable subcutaneous nodules
Erythema marginatum skin rash found on trunk
Carditis with dyspnea and chest pain
sydenhams chorea is a CNS manisfestation
Complications of RHD
destruction of mitral and aortic valves
pancarditis (Inflammation of heart)
Treatment of RHD
prompt treatment of GAS with antibiotics
salicylates(aspirin) to relieve fever & pain
corticosteroids for carditis
Narrowing of heart valve opening
- blood accumulates in chamber preceding stenosed valve
- results in increased chamber pressure due to resistance to flow thru the valve
- may cause hypertrophy of cardiac wall on chamber preceding the stenosed heart valve
often results in decreased cardiac output and left ventricular hypertrophy. there is a heart murmur as blood is forced thru the narrow opening
occurs when heart valve leaflets don't completely close
- incompetent heart valves allow blood to flow both directions
- volume of pumped blood increases
- involved chambers dilate to accommodate increased volume
what is a murmur/?
blood going thru a valve
syndrome that occurs when the heart cannot pump enough blood to meet the bodys needs (pump failure)
- results in intravascular and interstitial volume overload and poor tissue perfusion
- classified as Left sided or Right sided
Left sided heart failure
Pumping ability of left ventricle fails
cardiac output falls
blood backs up into left atrium
right-sided heart failure
Pumping ability of right ventricle fails
blood backs up into right atrium and peripheral circuation
peripheral edema develops
what are 2 most common causes of heart failure?
Acute Pulmonary edema
most dramatic symptom of left heart failure.
A life-threatening condition in which capillary fluid moves into the interstitial and causes lung stffness, makes lung expansion more difficult & decreases gas exchange in lungs
an acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate blood supply resulting in cellular hypoxia
Diminished cardiac output that severely impairs tissue perfusion (pump failure)
- the left ventricle initiates a series of compensatory mechanisms that attempt to increase cardiac output
- the actions initially stabilize and later deteriorates as oxygen demands increase on an already compromised heart
Causes of Cardiogenic shock
acute myocardial infarction (most common)
end stage cardiomyopathy
Circulatory dysfunction and inadequate tissue perfusion caused by reduced intravascular blood volume.
venous return is reduced and cardiac output fails
- acute loss of 15%-20% of blood volume
Causes of hypovelemic Shock
blood loss; burns; GI fluid loss
tachycardia restlessness; reduced urine output; hypotension; cyanosis
oxygen, fluids, blood replacement
Mechanical obstruction of blood flow
- great veins
aortic aneurysm; pneumothorax; pulmonary embolism (most common)
inqadequate tissue perfusion and circulatory collapse in response to infection
caused by loss of blood vessel tone and enlargement of vascular compartment
capacity of vascular compartment expands such that normal blood volume will not fill the circulatory system
Causes of Distributive Shock
decreased sympathetic activity: neurogenic
- brain or spine injury, anesthetics,, insulin shock, emotion
vasodilator substances in blood
- type 1 hypersensitivity (anaphylactic shock)
- inflammatory response to infection (sepsis)
- gram negative sepsis (70%)
Pathopysiologi changes of distributive shock
chills & fever due to infection
reduced urine output
complications and treatment of distributive shock
death, heart failure, renal failure
test with blood cultures
treatment: antibiotics therapy, medications to increase cardiac output oxygen
What are the primary functions of the Respiratory System?
Oxygenation of blood
Removal of CO2 Carbon Dioxide
What are the secondary functions of the Respiratory System?
Protection (ciliary blanket, macrophage0
What 2 zones is respirator broken down into?
Conducting Airways - consists of nasal passage, mouth, & pharynx, larynx, trachea, bronchi, bronchioles
Respiratory tissue - area distal to the terminal bronchi and consists of respiratory bronchioles, alveolar ducts and alveoli
What are the components of the conducting airways?
Outer layer- supporting connective tissue layer- provides support and protection
Middle Layer - Smooth muscle layer that circle the airway
Inner Layer - Mucosal Lining, pseudostratified columnar epithelium with hair like projections called cilia intermingled are goblet cells that secrete mucus. mucus forms ciliary blanket
Type 1 Alveolar cell
95% of surface, primary function is gas exchange
Type 2 Alveolar cell
1. lowers surface tension within the alveoli therby keeping the alveoli open
2. Increases lung compliance or the ease of inflation
3. Provides stability and more even inflation of the alveoli
4. assists in preventing pulmonary edema by keeping alveoli dry
encases the lungs; the pleura is thin, transparent, double layered serous membrane,
Functions to reduce friction during breathing
What is involved with the transportation & exchange of gasses
Ventilation, perfusion, diffusion
The movement of air bw the atmosphere and the alveoli of the lungs
Process of blood flowing thru lungs
The actual movement of gas b/w alveoli & blood
How is Oxygen & CO2 transported?
Oxygen: can be carried as a dissolved gas in plasma
or in combination with hemoglobin (98%)
CO2 - carried in blood but is converted to bicarbonate and transported in that form
What is partial pressure?
when oxygen and CO2 are dissolved in plasma.
Normal partial pressure for Oxygen is 80-100 mmhg
Normal partial pressure for CO2 is 35-45 mmhg
has become preferred method to measure PO2 in arterial blood gas.
It measures total percent of O2 that is saturated with oxygen (SpO2)and the PO2 is determined using the Oxygen-Hemoglobin Dissociation Curve. This is an INDIRECT measure of PO2 and PO2 must be calculated.
How is CO2 transported in blood?
As dissolved CO2 (10%)
Attached to Hemoglobin (30%)
As Bicarbonate, HCO3 (60%)
PO2 <60 mmHg
Impaired function of vital centers
- agitated or combative behaviour, euphoria, convulsions, delirium
- retinal hemorrhage
- hypotension & bradycardia
Activation of Compensatory mechanisms
- sympathetic system activation
PCO2 > 50 mmHg
- increased respiration
- decreased nerve firing
- CO2 narcosis
- Decreased muscle contraction
- headache, conjunctival hyperemia, warm flushed skin
Where is the respiratory Center
Medulla (the rate) & Pons (how deep your breath is)
Regulation of breathing : Chemoreceptors
monitor oxygen & cabon dioxide & pH
Central Chemoreceptors - hypercapnic drive- located in brain stem
- monitors PCO2 levels
- the primary stimulus for respiration
Peripheral Chemoreceptors - hypoxemic drive
- located in carotid arteries and aorta
- monitors PO2 levels (oxygen)
- a back up system for respiration
Regulation of breathing: lung & chest wall receptors
monitors breathing patterns and lung function
Stretch Receptors: located in smooth muscle of conducting airways & responds to changes in airway pressure
Irritant receptors: Located bw the airway epithelial cells, stimulated by irritants, like smoking
Juxtacapillary: J Receptors: located in alveolar wall & sense lung congestion
caused by a virus & has 3 distinct types: A B or C
36,000 deaths annually in US
A&B can cause epedemics bc they can mutate C cannot
Antigenic Drift- minor mutation (epedemic)
Antigenic Shift - Major Mutation (pandemic)
an acute inflammation of the parenchyma of the lungs (alveoli & bronchioles). Leading cause of morbidity & mortality world wide.
The interstitial tissues & alveolar spaces become infiltrated & filled with exudative fluid, leukocytes, and local macrophages
Development of pneumonia
1. Virulence of organism
2. size of innoculum
3. effectiveness of host defense
Classification of pneumonia
Type of Agent
- Typical Vs Atypical
Anatomic Pattern (distribution)
- Lobar vs bronchopneumonia
- community acquired vs hospital
Pneumonia Type of Agent- TYPICAL
Bacteria in the alveoli
- mulitply extracellulary
- cause inflammation
- fluid in alveoli (decreases diffusion & affects respiration)
Viral, mycoplasma and chlamydia
infections of alveolar septum or interstitium
Affects entire Lung
Affections patchy distributions over more than one lobe
What is the mos common cause of bacterial pneumonia?
Streptococcus or Pneumococcal
virulence factors- capsule prevents or delays digestions by phagocytes
Spleen is helpful in clearing bacteria from blood
Immunization for preventioin
Bacteria, Acquired from the environment
gram negative rod
warm stagnant waters
incubation period is 2-10 days, abrupt onset of malaise, weakness, diarrhea, high fever & cough
Treatment- quick antibiotics
Worlds foremost cause of deat from a single infectious agent.
Caused by myobacterium which are acid fast with a waxy cell wall.
Lesions that contain macrophage, T Cells and INACTIVE TB.
Diagnosis of TB
Bacterial culture (can take up to 12 weeks)
M. TUberculsosis DNA amplification technique
Sputum identification (nonspecific)
skin test (PPD) - cannot distinguish bw active & latent
Treatment for Active TB
isoniazid, rifamycin, pyrazinamide, ethambutol
4 types of lung cancer
Squamous cell carcinonma
Small Cell Carcinoma
Large cell carcinoma
Lung cancer therapeutically classified as:
Small cell carcinoma & non-small cell carcinoma
Small cell Carcinoma
death within 3 months w/o treatment
cant do surgery usually, only chemo
Non-small cell carcinoma
Adenocarcinoma- most common (in women & non smokers)
Squamous cell- most common in men, smokers
in children under 5,
a "cold gone bad"
upper airway infection, primarily with vocal chords
barking cough, worsens at night
Upper airway infection;
etiologic agent: historically- haemophilus influenza
now: streptococcus or staphylococcus
Very sudden onset that can be life threatening bc airways become occluded
Cherry-red epiglottis, drooling, chin thrust forward, sick looking
Lower airway infection, occurs in children less than 2 yrs old
etological agent: Respiratory Syncytial Virus (RSV)
Preceede by stuffy nose, cold symptoms
may progress to respiratory failure but usually slower onset
Inflammation of the pleura
Parietal Pleura - abrupt onset, unilateral
Causes: neoplasm, Inflammation (pneumonia)
Must differentiate: Musculoskeletal Pain and Heart pain (angina)
fluid accumulation in pleural space
Serous, water like fluid
Pus cells & infectious fluids
Air in pleural space
partial or complete collapse of the affected lung
Types: spontaneous, traumatic (open or tension)
Traumatic Pneumothorax (Open)
Penetrating chest injury or surgery, air flows into pleural space
Traumatic Pneumothorax (Tension)
Intrapleural pressure exceeds atmospheric pressure.
air enters pleural space but cannot exit
Bleb ruptures (or a blister0
Obstructive Asthma Disorders
Bronchial Asthma (acute)
Chronic Obstructive airway disease
- Chronic Bronchitis
Episodic acute airway narrowing
- cough, bronchospasm
- Dyspnea (shortness of breath)
- Tachypnea (rapid breathing)
- Tachycardia (rapid heart rate)
Basically- inflammatory airway disease, causes spasm, excessive mucous production & edema causes obstruction
Extrinsic (Atopic) Asthma
type 1 hyersensitivities (childhood, allergies)
Mast cells inflammatory mediators cause acute response within 10-20 minutes
Airway inflammation causes late phase response in 4-8 hrs.
Caused by External factors- pollen,
Intrinsic (non-atopic) asthma
Respiratory infections (epitheleal damage, IgE production)
Caused by internal factors- exercise, cold air
Chronic obstructive pulmonary disorders Mechanisms
inflammation and fibrosis of bronchial wall
hypertrophied mucus glands, excess mucus (obstructs airway flow)
loss of alveolar tissue (decreased surface area for gas exchange)
Loss of elastic lung fibers (airway collapse, obstructed exhalation)
4th leading cuase of death in US
Enlargement of air spaces and destruction of lung tissue
abnormal permanent enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of the walls of the alveoli w/o fibrosis
Chronic Obstructive Bronchitis
Increased mucus production and obstruction of small airways
condition in which chronic productive cough is present for 3 months per year for at least 2 consectutive years and the absence of other causes of chronic cough
uncommon, secondary condidtion
infection and inflammation destroy smooth muscle airways, causing permanent dilation of airways