Future Peeps this does NOT include the hemodynamics stuff

Cardio

Congenital Defects

• Present at birth

• Causes:

  • Idiopathic (most common)

  • genetic factors (chromosomal abnormalities)

  • environmental influences like an infection in the mother

    • TORCH

      • Toxoplasmosis

      • Other

      • Rubella

      • CMV

      • HSV

ASD - Atrial Septum Defect (LA and RA are connected)

• Fossa ovale stays foramen ovale

• Blood flows from LA to RA

  • oxygenated blood gets to the non-oxygenated side and makes the pulmonary circuit twice (NONCYANOTIC)

• Patients are often asymptomatic or can have murmurs, fatigue, SOB (especially on exertion)

• EKG is going to look wack but no specific changes

• Diagnosis is based on ECHO

• Long term effects are going to be pulmonary HTN and RV hypertrophy

VSD - Ventricular Septal Defect (LV and RV are connected)

• There’s a hole in the ventricular septum

• Starts out noncyanotic because the blood flows from the LV (oxygenated) to the RV (deoxygenated)

• HOWEVER, over time the RV has to work harder because it has more blood and we get RV hypertrophy. This leads to the RV being stronger than the LV. We go from a Left to right shunt, to a Right to left shunt and become cyanotic. (EISENMENGER SYNDROME)

  • If we get to eisenmenger’s syndrome we cannot fix this

• Long term effects are going to be pulmonary HTN and RV hypertrophy

• Symptoms: heart murmur, SOB, failure to thrive

• EKG is going to look wack but no specific changes

Tetralogy of Fallot (TOF) (Right to Left shunt)

• This is a combination of 4 heart defects (hence it being a TETRAlogy)

  • overriding Aorta

    • large aortic valve arises from both left and right

  • pulmonary stenosis

  • RV hypertrophy

  • Ventricular septal defect

• Heart is going to look like a boot on radiographs

• Murmur

  • diagnose with ECHO

• Patient Symptoms

  • Cyanosis (blue baby syndrome)

  • difficulty feeding

  • failure to thrive

  • Patients will often get into a squatting (Val Salva) position as it improves symptoms

• This can be fixed via the Blalock-Taussig-Thomas Shunt which connects the subclavian artery to the pulmonary

Ischemic Vascular Disease

Atherosclerosis Basics

• Atherosclerosis is a systemic disease affecting the arteries

• 3 things must occur:

  • Endothelial injury AKA inflammation

    • Step 1

  • lipid accumulation (LDL)

  • formation of atheromas (foam cells)

    • smooth muscle cells of the vasculature become the foam cells

    • When these burst Macrophages get activated and collagen is deposited leading to the hardening of the arteries

• The plaques are common sites for thrombosis and the weakened artery may bubble out into an aneurysm

• Location, Location, Location

  • Heart (coronary arteries)

    • leads to coronary artery disease or MI

  • Heart (aorta)

    • leads to aortic aneurysms

      • like a AAA

  • Cerebral

    • Leads to CVD (stoke)

  • Peripheral arteries

    • leads to peripheral artery disease (gangrene apparently)

• Risk factors:

  • Modifiable - to an extent

    • Diabetes - sugar in the blood is *VERY* inflammatory

    • High Cholesterol (hyperlipidemia)

    • HTN

    • smoking

    • obesity

    • sedentary lifestyles

  • Non-modifiable

    • age

    • gender

    • family history

• Major complications

  • MI

  • CVA

  • Aneurysm

  • Peripheral artery disease

• Protective factors

  • Exercise

  • lifestyle changes

  • weight control

  • Drugs for HTN, diabetes, hyperlipidemia

    • Statins/lupitor for hyperlipidemia
      

Coronary Artery Disease

• MI due to atherosclerosis (yikes)

• A lot of things affect how the patient is going to present like the

  • extent of occlusion

    • you cannot predict the patient symptoms based on the occlusion, someone’s dad is sitting at 96% occluded and is moving the damn yard

  • rapidity of ischemia

    • Slow, insidious, progressive

      • hypoperfusion, ischemia

      • angina pectoris

      • may progress to CHF

    • Sudden Occlusion (Popping plaques)

      • MI

  • extent of atherosclerosis elsewhere

  • Location of occlusion

    • Occlusions in the LAD (widow-maker) affect the anterior wall

      • Artery of sudden death

      • 50% of cases

    • Occlusions in the Left circumflex affect the lateral wall

      • 20% of cases

    • Occlusions in the Right coronary artery affect the RV and posterior wall

      • Involves posterior septum

      • 30% of cases

  • Presence of other diseases

    • big ones are HTN and hyperthyroidism

• Arteries are rigid and calcified

  • narrowed due to plaques which may rupture and cause clot formation

  • Older lesions may recanalize (blood flow returns, the river has been restored)

  • On the microscopic level:

    • Initially the nucleus is a little jacked up (pyknosis, karyorrhexis, karyolysis) so the cell is destroyed

    • At days 3-5 macrophages come in for clean up duty

    • At day 14 we get granulomas

    • Long term you’re gonna see fibrous scars

• Clinical Features

  • CHF - the heart is starving and don’t pump well

  • Angina pectoris is just chest pain secondary to the occulsion

  • MI

• Complications of MI - gotta be fast to the Cath lab bro

  • Infarct

  • Endocardial mural thrombus

    • can cause arrhythmias

    • can occur with reduced ejection fraction

  • Rupture

    • Softened necrotic myocardium may rupture with increased pressure

  • Aneurysm

    • Infarcts are replaced by scars which may bulge under pressure since’s there’s no contractile elements

  • Cardiac Tamponade

    • compression of the heart by blood/fluid in the pericardial cavity

• Diagnosis

  • EKG

    • if it’s a STEMI we are running to the cath lab period.

  • Troponin

  • CK-MB

  • For insidious occlusions imaging is an option

    • coronary angiography

    • ECHO

  • Stress testing

    • Not in an MI

    • Increase the need for demand (via exercise) and see if EKG changes

• Treatment

  • Lifestyle mods

  • medications

    • statins, ace inhibitors, nitro

  • surgery

    • PCI, bypass

Cerebral Atherosclerosis

• Plaque buildup in cerebral arteries leads to reduced flow to brain tissues

• Plaques may also rupture and form emboli

• Symptoms

  • TIA (mini stroke or a Transient Ischemic Attack)

    • basically a stroke where symptoms are temporary

    • MRI diagnosis

  • Stroke

    • ischemic

    • hemorrhagic

  • Cognitive decline

    • long term

Aortic Atherosclerosis

• Plaque buildup in the aorta leads to a weakening of the arterial wall and an increased risk of aneurysm formation

• Patients are often asymptomatic until it gets bad finding is often incidental

  • AAA (most common) presents with back pain and pulsating feeling in abdomen

• Complications

  • aortic aneurysm

  • Aortic dissection - the bubble pops and you die

• Types

  • Saccular

  • Fusiform

Peripheral Atherosclerosis

• Plaque buildup in arteries supplying limbs leads to reduced blood flow to extremities

• Patients present with intermittent claudication (leg pain) that aches, no muscular, numbness or weakness in legs, ulcers or sores that do not hearl

• Complications

  • critical limb ischemia

  • gangrene

HTN related disease

• Anything over 140/90 consistently

• Major risks for cardiovascular diseases

• Managed by lifestyle mods

  • Diet changes (reduce salt, increase fruits/veggies)

  • Exercise

  • weight management

  • stop smoking

• Meds - usually a combo, typically start with an ARB or ACE + a Diuretic

  • diuretics (decrease blood volume)

  • beta blockers

  • ACE inhibitors

  • Calcium channel blocker - drops that pressure lickety-split

  • ARBs (angiotensin II receptor blockers)

Primary

• No identifiable cause

• accounts for like 95% of cases

• Things like genetics, lifestyle, diet, and stress can contribute but if you fix these the HTN remains

Secondary

• Identifiable cause typically underlying conditions

  • renal disease

  • Pheochromocytoma

    • Warning: This is a zebra

    • Increased release of epi/norepi by the renal medulla leads to intermittent HTN

    • Diagnosed with urinary VMAs

Consequences of HTN

• Cardiomegaly

  • can lead to heart failure

  • enlargement of the heart (mostly the LV)

  • increased thickness of LV

• Vascular pathology

  • damage to aorta, major, minor, arteries and arterioles

  • accelerates atherosclerosis

    • damage to the vessels is step 1 so

• Hypertensive encephalopathy

  • HTN in the brain can cause ischemia

  • risk of hemorrhagic stroke

• Hypertensive retinopathy

  • The eyes are the only place where you can actually see the vessels (opthalmoscope)

  • They’ll look tortuous and wierd

  • But this changes vision → like in the ER where people lose their vision in hypertensive emergencies

Diseases as a Response to Infections

Rheumatic Heart Disease

• The reason we treat strep with antibiotics

  • Group A Beta-hemolytic streptococcus pyogenes produces a toxin that B cells will make antibodies to, just like normal

  • However (this is the widely accepted theory) these antibodies are cross-reactive with parts of the heart

  • So this involves antibodies and cell-mediated immune reactions

• Affects different parts of the heart but it’s mostly about valves

  • Endocarditis → inflammation of the inner heart surfaces

    • valvulitis (typically mitral or aortic), fibrin thrombi, valve deformities

    • Murmur, SOB, fatigue on exertion

  • Myocarditis → inflammation of the heart muscle

    • Aschoff bodies, myocardial fibrosis

  • Pericarditis → inflammation of the outer heart surface

    • Fibrinous exudate, chronic fibrosis, adhesions

• Diagnosed with a new onset on murmur, typically no labs, vegetation on valves on ECHO

  • On the Jones Criteria you need 1 major and 2 minor OR 2 major

  • 

Infectious Endocarditis

• Inflammation of the heart valves, commonly caused by bacterial infections

• In your average patient, mitral valve is the most common spot

• In your IV drug user patient, Right side valves are the most common spot

  • Bacteria comes through the veins duh

• Entry of bacteria into the blood stream leads to colonization of the heart valves

• This causes vegetations on valves

  • vegetations are just thrombi with bacteria in them

• Quirks:

  • Fever

  • heart murmur

  • embolic phenomena

  • Risk of heart failure and systemic emboli

Infectious Myocarditis

• inflammation of the heart muscle, often due to viral infections

  • VIRAL infection → immune response → myocardial cell damage

• Quirks:

  • Fever

  • Chest pain

  • Heart failure symptoms

  • Arrhythmias, sudden cardiac death

Infectious Pericarditis

• Inflammation of the pericardium - caused by bacterial, viral, autoimmune, trauma

• EKG kinda looks like an MI

• Can lead to cardiac tamponade

• Quirks

  • stabbing chest pain, patient will NOT sit still - typically want to be hunched over, refused to lie down

  • pericardial friction rub on auscultation (squeaky)

  • Pericardial effusion

Cardiomyopathy (The problem is in the muscle)

• Reminder: cardiomyopathy is a group of diseases that affect the heart muscle, leading to deterioration of structure and function. This allows the heart to become enlarged, thickened, rigid, or replaced with scar tissue (rare)

  • Heart failure: a group of symptoms as a result of the heart losing its ability to pump

• General symptoms: SOB, fatigue, edema, arrhythmias

• Diagnose with Echos, MRIs, genetic testing, EKG, biopsy

  • Biopsies are invasive but they give you good info

  • 1st line diagnostic studies are non-invasive like echos or ekgs

• Treat with beta-blockers, ACE inhibitors, lifestyle changes, heart transplant

Dilated

• Often idiopathic but can be due to alcohol, viruses, genetics

• Enlarged heart chambers with dilated walls

• Reduced systolic function - floppy ventricle

• Symptoms: fatigue, SOB, edema

Hypertrophic

• Caused by genetic mutations affecting the cardiac muscle proteins or it’s idiopathic

• Thickened walls especially the interventricular septum

  • Can block the aortic vavle

• Symptoms include chest pain, dyspnea, syncope, sudden cardiac death (fatal arrhythmias)

Restrictive

• Caused by infiltration of the myocardium with abnormal substances like amyloids or iron

• Stiff ventricular walls because of plaques in muscle fibers, impaired diastolic filling

• Symptoms include fatigue, SOB, peripheral edema (there’s problems with diastole so filling sucks, decreased venous return, increased venous pooling which leads to increase filtration)

Cardiac Tumors

• These are just growths of the valves that aren’t supposed to be there

• Tumors of the heart are rare because its a post mitotic tissue

• Primary tumors originate in the heart

• Secondary tumors metastasize to the heart

Atrial Myxoma

• Most common primary heart tumor

• typically benign and polypoid

• usually found in the LA → proclivity to the mitral valve

  • originates from multipotent mesenchymal cells

• Can obstruct blood flow causing symptoms similar to mitral valve disease

• Symptoms include: embolization, systemic like fever or weight loss

  • can be positional

• Diagnose via echo, MRI, histological exam

• Treatment is a surgical resection

Secondary tumors

• Tumors of the heart are almost secondary

• Tumors tend to reach the heart via the bloodstream, lymphatics, or by direct invasion

• Typically come from lungs, breast, lymph (lymphoma), melanomas

• Quirks:

  • depend on tumor size and location

  • Symptoms include pericardial effusion, arrhythmias, and heart failure

• Diagnose with echo, CT, MRI

  • Must confirm with biopsy (histological confirmation)

Vascular Diseases

• Veins, arteries, lymphatics

• Can lead to significant morbidity and mortality

Arterial

• Vasculitis

  • often caused by immune mechanisms

  • Large vessel vasculitis → giant cell arteritis

    • like the temporal artery in the face leads to temporarily blindness

  • Small vessel vasculitis → hypersensitivity vasculitis

  • Symptoms:

    • general: fever, fatigue, weight loss, myalgia, joint pain

    • organ specific symptoms depend on the vessel

• Raynaud Disease (hella blue fingers)

  • a condition causing episodic narrowing of the arteries due to a response to stress or cold

  • Involves vascular spasm of small arteries (fingers and toes are typically affected)

  • During attacks patients will complain of pain, tingling, numbness

  • Tricky to treat → basically just avoid cold weather

Venous

• Varicose Veins

  • enlarged, twisted veins commonly in the legs

  • caused be bad valves

  • Symptoms include: aching, heaviness, swelling, visible veins

• Thrombophlebitis

  • inflammation of a vein caused by a blood clot typically from an IV

  • Can occur in superficial or deep veins

    • deep = DVT

  • Symptoms: pain, redness, swelling, warmth in affected area

Lymphatic

• Lymphangitis

  • acute inflammation of the lymphatic vessels

  • Most often bacterial (streptococci)

  • Symptoms: red streaks like cellulitis, fever, chills, pain along the track of the lymph, swelling

  • Diagnose with clinical exam, blood test (cultures)

  • Treat with antibiotics and steroids

    • treat it fast!

Respiratory

Infectious

• Upper respiratory tract → nose diseases, URIs

  • Most of the infections involve upper respiratory

• Middle respiratory tract → trachea/bronchi

• Lower respiratory tract → pneumonia

  • 5000 people die every year of pneumonia

• Accounts for 75% of all human infections

URIs (aka the Common Cold)

• Acute inflammation typically involving the nose, paranasal sinuses, throat and or larynx

  • In children, it can spread through the eustachian tubes to the middle ear causing otitis media

• Can extend to the trachea/bronchi and be complicated by pneumonia

  • can also be complicated by a bacterial superinfection

    • this is when you’ll see purulent nasal discharge, sinus/ear pain, or deep throat expectoration

• Most are viral, short-lived, and resolve on their own

  • 50% are from a strain of rhinovirus

  • No scientific evidence that it’s caused by bad weather

• Physical exhaustion, old age, and general poor health can predispose individuals

• Symptoms include: nasal congestion/inflammation, rhinorrhea, throat pain/discomfort, general malaise, myalgia, headache, fever

• Typically last 2-3 days

Middle respiratory Infections*

• Includes the larynx, trachea, and major extrapulmonary bronchi

• Prevalent among children

• Croup

  • acute possibly life-threatening infection of the larynx

    • Severe cases will put the child in the ICU, maybe intubated

  • Peds less than 3 y/o

  • Vocal cords spasm leading to stridor on inspiration, barking/brass cough

  • Typically caused by parainfluenza virus

  • No specific treatment but steroids, nebulized epi, and a cool mist may help

  • Steeple sign on CXR shows inflammation of airway

• Epiglottitis*

  • Most often caused by Haemophilus influenzae

    • incidence has been reduced by vaccination

  • Peak incidence in school aged kids and teens

  • Sudden loss of voice, accompanied by hoarseness and throat pain on swallowing

  • Epiglottis is inflamed (red and swollen), this and the pharyngeal mucus leads to the narrowing of the air passage

    • Severe cases may require intubation to maintain the airway

      • due to swelling this may basically be a blind procedure or a cricothyrotomy may be done

  • Treated with antibiotics with supportive humidified oxygen mask

  • Can be prevented with vaccination

• Bronchiolitis*

  • An acute childhood disease that involves the bronchi and bronchioles

    • Affects infants and small children, epidemics are usually fall-spring

  • Viral infection most common (80%)

    • Typically RSV (respiratory syncytial virus) but can also be parainfluenza, rhinovirus

  • Invades the epithelial cells of the bronchi/bronchioles → cell death and desquamation

    • this causes obstruction of the bronchi/bronchioles

  • Characterized by wheezing respirations, low-grade fever, SOB

  • Spontaneous recovery ensures usually in 7-10 days

Lower Respiratory Infections*

• Pneumonia is the just inflammation of the lung

  • Alveolar pneumonia is within the alveoli itself

  • Interstitial pneumonia involves the alveolar septa

• Infection occurs via the inhalation of pathogens, aspiration of infected URI secretions or infected particles of gastric contents, from the blood, or contaminated foreign material

• Alveolar pneumonia is usually bacterial

  • Can be focal or diffuse, may involve only alveoli or both alveoli and bronchi

  • Bronchopneumonia: pneumonia that is limited to the segmental bronchi and surrounding lung parenchyma

  • Lobular pneumonia: limited to single lobules

  • Lobar Pneumonia: widespread or diffuse alveolar pneumonia (large portions of pulmonary parenchyma)

    • Spreads from lobule to lobule until the entire lung is involved

  • As exudate accumulates it replaces air, and the lung parenchyma becomes consolidated (denser than normal, shows up on x-ray as “infiltrates or consolidation of parenchyma)

• Interstitial pneumonia is usually diffuse and bilateral*

  • usually viral or mycoplasma pneumoniae

  • inflammation affects the alveolar septa and does not result in exudations of PMNs (neutrophils) into the alveolar lumen

  • Reticular pattern (lots of lines) no major consolidations

  • Most just cause minor alveolar damage and resolve without sequelae

    • however, some progress to chronic stage characterized by interstitial fibrosis and destruction of functioning lung parenchyma

• Atypical AKA Walking Pneumonia

  • Doesn’t present with classic symptoms

  • Typically viral or mycoplasma pneumoniae

  • Symptoms are milder: low grade fever, mild cough, maybe dyspnea, minimal changes on CXR, no leukocytosis, no signs of sepsis

  • Diagnosis is based on finding IgM to mycoplasma or viral pathogens

• Pulmonary Tuberculosis (TB)*

  • Chronic bacterial infection caused by Mycobacterium Tuberculosis

    • Rod shaped bacteria with a waxy capsule

    • Acid fast bacillus - stains pink/red on a gram stain

    • Causes the formation of granulomas with a caseous (cottage cheese) necrotic center

  • Affects ~13,000 Americans every year (used to be a lot more but has decreased since the 50s)

  • Primary Pulmonary TB is clinically unrecognized in most incidents (>95%), so true incidence may be higher

    • Primary infection is localized lung infection, symptoms are short lived and may go unnoticed

      • Associated with mild pulmonary disease and low grade fever

    • Develops lesions (Ghon complex/granulomas) in lung parechyma and regional lymph nodes

      • in 95% of cases the Ghon complex will heal spontaneously and calcify

      • These calcifications can be reactivated → secondary TB

  • Secondary TB develops after a reactivation of the dormant primary infection (most of the cases) or a reinfection

    • Bacteria tend to consolidate in the APEX of the lungs causing a granulomatous lobular pneumonia

    • Confluent granulomas produce cavities known as Cavernous TB

      • Cavities are the source of the hemoptysis, which may be fatal

    • Symptoms of Secondary: dry cough, low grade fever, loss of appetite, malaise, night sweats, weight loss

  • Dissemination of the bacilli occur through lymph, pulmonary vessels, or air spaces

    • Miliary TB - widespread seeding in lungs and organs, small granulomas

    • TB pneumonia - severe spread through airspaces leads to massive lobular/lobar pneumonia and may involve the same or opposite lung

    • Complications of dissemination include: pleuritis, extrapulmonary TB (infect larynx, GI tract)

  • Clinical Quirks

    • Variety of symptoms, but most are nonspecific

    • Hemoptysis is a BIG one, and SOB

    • For diagnosis you need CXR, acid-fast bacilli sputum stain

    • Tuberculin skin test can pop a false negative in patients with a weakened immune response

    • A positive bacteriologic culture of M. Tuberculosis is the gold standard for diagnosis

    • Treatable with 6 months of antibiotics unless its a drug resistant stain

      • AIDS patients may not respond to treatment

• Complications of Pneumonia

  • pleuritis chronic lung disease

    • pleuritis: extension of inflammation to the pleural surface commonly leads to pleural effusion

      • Pus gets trapped in fibrous tissues which as it heals usually results in pleural fibrosis of the entire lung

      • The lungs cannot expand during inspiration, restrictive lung disease

  • Abscess formation

    • Usually associated with highly virulent bacteria (S. Aureus)

  • Chronic lung disease

    • unresponsive to treatment

    • Pus inside of bronchi leads to their destruction of their walls and bronchial dilation (bronchiectasis)

    • Destruction of the lung parenchyma and fibrosis transform the lung into a structure known as honey-comb lungs

• Clinical Picture of Pneumonia*

  • Patients are typically younger than 5 or older than 70

  • Categorized into 2 groups

    • Community-acquired pneumonia (primary) affects previously healthy people (strep pneumonia)

    • Nosocomial (secondary) affects people with pre-existing illness (like homies in the hospital), older people, those debilitated/sick are at a higher risk

      • Other risk factors are smoking, alcoholism, immunosuppressed

  • Systemic signs of infection: high fever, chills, weakness

  • Local signs of irritation: plugging of airways/mucus, bronchial irritation, coughing, expectoration

  • Airway obstruction: impaired gas exchange (get a VBG/ABG) due damaged alveoli leading to SOB, tachypnea

  • Inflammation and destruction of tissues caused by inflammatory exudate leads to mucopurulent, blood-tinged, rusty sputum or even hemoptysis

• Findings of Pneumonia (what are ordering)

  • CXR

  • Bacteriologic studies of sputum

  • CBC should show leukocytosis if bacterial or elevated lymphocytes if viral

  • VGB/ABG should show Hypoxemia, high CO2 (hypercapnia), respiratory acidosis

  • Treatment: support vital functions and antiobiotics

Fungal Diseases

• Acquired by inhaling dry fungi and their spores

• clinically resemble TB

  • induce the formation of granulomas, which heal by calcification

• Patients may be asymptomatic, solitary pulmonary lesion, numerous small nodules

• Histoplasmosis is widespread in the midwest US

• Coccidioidomycosis in the southwestern deserts

• Nosocomial fungal infections may presents in terminally ill, cancer, AIDS patients

  • Most common pathogens tend to be P. jirovecii, C. albicans, A. fumigatus

Lung Abscess

• localized, destructive, and suppurative (pus forming) lesion

• Typically bacterial in nature

  • S. Aureus, K.pneumoniae, P. Aeruginosa

• Develop in these conditions:

  • complication of necrotizing staphylococcal pneumonia

  • Aspiration of infected material

  • Distal to bronchial obstruction by tumors

  • Septic lung emboli

• Tend to connect with airways, erode the bronchial wall, and extrude their pus content into the airways

Chronic Obstructive Pulmonary Disease (COPD)*

• lung diseases characterized by chronic airway obstruction

• Chronic bronchitis and emphysema can coexist

• Early form of smoking-related lung disease

• Later stages are characterized by scarring with obstructs airways

• Treat the symptoms and supportive measures

  • advanced lesions are irreversible → no smoking kids

Chronic Bronchitis (“Blue Bloaters”)

• Excessive production of tracheobronchial mucus causing cough and expectoration for at least 3 months during 2 consecutive years

• Smoking is the cause for 9/10 cases (stop smoking, symptoms get better)

  • Air pollution, occupational exposure, various respiratory infections can contribute

• Walls of the bronchi/bronchioli are thickened, lumen contains thick mucus

• Mucosa is infiltrated by lymphocytes, macrophages, and plasma cells

• Characterized by mucous gland hyperplasia, chronic inflammation and fibrosis

• A common complication of chronic bronchitis is bronchiectasis (permanent bronchi dilation)

  • associated with bronchiolectasis (dilation of the bronchioles)

  • The dilation is due to the persistent inflammation, as enzymes are released by bacteria and leukocytes. This leads to mechanical pressure increase and traction of the fibrous scars.

  • Big bronchi tend to show saccular (cystic) dilation while smaller ones show cylindrical

  • Mucoprulent material typically can’t be cleared with a cough

  • Infection can spread to adjacent alveoli → recurrent pneumonia

• Characterized by prolong bouts of coughing, expectoration of purulent mucus, SOB

  • Hypoxia causes cyanosis

• Affects the pulmonary vasculature and can lead to pulmonary hypertension and chronic cor pulmonae (right sided heart failure)

Emphysema (“Pink Puffers”)*

• The destruction of alveolar walls with enlargement of the air spaces

• Seen in chronic smokers as its related to the chemicals in cigarette smoke

  • rare in nonsmokers but there is a genetic component (a1-AT)

• Proteolytic enzymes from the leukocytes cause the damage

• Centrilobular Emphysema: widening of air space in the center of a lobule and involves respiratory bronchioles

  • Most common form

  • found in smokers

• Panacinar Emphysema: involves all the air spaces distal to the terminal bronchioles

  • typically a1-AT

  • Most prominent in lower parts of lungs/anterior margins

• Characterized by there being NO bronchial obstructions/irritation, the chest is over-expanded (barrel chest), patients tend to hyperventilate to compensate (preventing hypoxia)

Immune*

• Also includes allergic rhinitis (hay fever)

Asthma*

• Can be acute or chronic and is a reversible inflammatory airway obstruction

• “Asthma Attacks” are characterized by wheezing on expiration, cough, SOB

  • often precipitated by exposure to allergens

• Affects ~10% of kids and 5% of adults in the US

  • twice as common in males

  • more than half of cases begin in childhood

• Two major forms

  • Atopic (type 1 or extrinsic) - an exposure to exogenous allergens and represents a type I hypersensitivity reactions

    • typically affects children and is associated with other allergies (atopic dermatitis and hay fever)

    • Many have spontaneous improvement, but 50% persist

    • wheezing on expiration, cough, SOB

    • You can use a skin test, inhalation test or serum test but all you need to diagnose is allergen → attack.

  • Nonatopic (intrinsic) - precipitated by NO immune mechanism but can be due to physical factors such as hot or cold, exercise, psychological stress, chemical irritants, infection, aspirin

    • typically appears in adulthood

    • attacks may occur at random

    • May progress to COPD in patients with chronic, relentless asthma

• Bronchi show that mucosal infiltrates full of chronic inflammatory cells and eosinophils. Also the walls show hyperplasia of the bronchial gland which would explain the overproduction of mucus

• Smooth muscle cells are large and increase in number, explaining the bronchial spasms

• Treat the symptoms and prevent bronchospasm and bronchial inflammation*

  • drugs that prevent degranulation (no histamine) of mast cells

  • Inhalation therapy with corticosteroids → reduces the inflammation and immune aspects

  • Bronchodilations with sympathomimetics is an efficient way of stopping the attack

• Prognosis is good, deaths secondary to severe protracted attacks (status asthmaticus) are rare

Sarcoidosis*

• Multisystemic granulomatous disease of unknown etiology

• Presumably a Type IV hypersensitivity

• Affects 5/10,000

  • more common in African Americans

    • 2x more common in females

• Typically affects the lungs and the mediastinal lymph nodes

  • Lungs are infiltrated by T cells (mostly CD4s)

    • CD4s outnumber CD8s 10:1

• Granulomas of sarcoidosis may involve any organ

  • most commonly though are the lungs, lymph nodes of the neck and thorax, and the liver

  • In 1/3 of patients the lacrimal and salivary glands are affected

• 50% of patients are asymptomatic

• CXR shows enlarged hilar pulmonary lymph nodes, nonspecific lung abnormalities, pulmonary modules

• Most common symptoms include SOB, cough, wheezing

  • lymphadenopathy, hepatomegaly, splenomegaly, skin nodules

• Diagnosis based on a biopsy of the lymph nodes, bronchi, liver, skin, or enlarge salivary glands

  • You should see typically granulomas (epithelioid macrophages and giant cells with a narrow rim of lymohocytes)

    • No central necrosis

  • Labs are not specific or really that helpful

• No specific therapy most patients spontaneously recover with in a year or 2

  • only like 10% have a lethal outcome

Hypersensitivity Pneumonitis*

• An extensive allergic alveolitis immune disorder caused by repeated inhalation of foreign antigens

• Most are derived from mold and fungi growing on organic material (hay, tree bark) or in contaminated fluid/air-conditioning equipement

  • bird droppings, animal dandruff, and wood dust are common

• Acute pneumonitis is mediated by antibodies that react with inhaled antigens in the alveoli

  • occurs several hours after the exposure

  • Remove the antigen, patient gets better

• Chronic pneumonitis mediated by T lymphocytes and is characterized by a type IV hypersensitivity

  • granulomas in the alveolar septa lead to focal destruction, leading to fibrosis

  • Loss of parenchyma, scarring and cystic dilation → honey comb lungs

  • Biopsy shows signs of hypersensitivity but its difficult to determine the antigen

  • Destructive lung disease can cause chronic SOB, hyperventilation, and respiratory failure

  • Only treated with lung transplant

Pneumoconiosis - Environmentally Induced*

• Lung diseases caused by inhalation of mineral dust, fumes and various organic/inorganic particulate matter

• Most classified as occupational and due to long term exposure

• lung injury depends on duration, concentration of particles, size/shape/solubility of particles, and the biochemical composition of the inhaled dust

Coal Workers Lung Disease (CWLD)

• Coal miners working in reasonably well conditions have minor health problems like anthracosis with is just black discoloration of the lung due to carbon particle accumulation

• Coal minors in poor conditions without PPE may develop CWLD

  • Autopsy will show lungs that are black, fibrotic, and structurally abnormal

    • black due to accumulation of carbon particles

  • Other minerals like silica are present and contribute to lung destruction

• If coal particles are overwhelming or if the dust has other compounds macrophages cannot clear the bronchi, so they accumulate, incite fibrosis and contribute to the destruction of parenchyma

• Symptoms vary

• No effective treatment

• Improved conditions and use of PPE (shout out to the unions) have reduced CWLD

Silicosis

• Lung disease caused by inhalation of silica crystals during stone cutting, mining, and sand blasting

• Disease develops after 10-20 years of exposure

• Most common lung disease caused by mineral particles

• Characterized by fibronodular lesions in the parenchyma

  • Destroy the parenchyma and cause massive pulmonary fibrosis

  • after lesions develop it’s irreversible

• Silica gets taken up by macrophages, which get damaged in the process, they die release the silica crystals and cytokines that stimulate fibroblast.

• TB is a complication because the silica loaded macrophages can’t combat the disease

• Generally mild unless TB or bilateral fibrosis occurs

• Does not predispose individuals to cancer

Asbestosis*

• Seen in pulmonary fibrosis and malignant mesothelioma

• Pathogenesis is unknown, but short, straight fibers enter the aveoli and are taken up by macrophages which activates them to release various fibrogenic cytokines and growth factors

  • extensive pulmonary fibrosis

• Coarse bilateral pulmonary fibrosis and pleural plaques

  • fibrous tissue contains beaded bodies with knobbed ends (asbestos bodies)

  • Bodies are coated with hemosiderin pigment

    • but these are a minority its like a 1:10 ratio so most can’t be seen with light microscopy

• Presents with restrictive lung disease and SOB

  • SOB persist for years and rarely progresses to respiratory failure

• Plaques that are small or solitary typically have no symptoms

• Malignant mesothelioma is the most important neoplastic complication of asbestos fibers

  • Increase chance of lung cancer 4-5X

    • if you also smoke that jumps to 50X

Misc.*

Idiopathic Pulmonary Fibrosis

• unknown cause but possibly viral pneumonitis or allergic/immune disease

• Fibrosis is the most significant finding → widespread/bilateral, associated with destruction of alveolar structures

• Presents with Honey comb lung, restrictive lung disease, progressive respiratory impairment

• Usual Interstitial pneumonia (UIP) is a common disease in thing group

• Treat with corticosteroids but eventually will need a lung transplant

Acute Respiratory Distress Syndrome (ARDS)*

• ARDs AKA noncardiac pulmonary edema

• Changes in the lungs, resulting fro acute lung injury (ALI), which cause acute respiratory failure

• ARDS develops either as an injury to endothelial cells in pulmonary capillaries or as an injury to the cells in the alveolar lining

• Terminal airway (alveolar walls) and function is severely affected

• Impaired pulmonary blood circulation strains the heart leading to cardiopulmonary failure

• Lungs are going to show diffuse alveolar damage (DAD)

  • in an autopsy lungs are heavy and filled with fluid, airless

• On a biopsy you show see alveolar space dilated, filled with proteinaceous edema which extravasates into the alveoli, clots and forms fibrin-rich hyaline membranes

• Symptoms occur with in 24 hours

• Symptoms: severe SOB, gasping for air

  • 1/3 die within days, 1/3 die of pneumonia or heart failure, 1/3 recover

    • 40% of recovered patients

• Labs confirm hypexemia (low O2), hypercapnia (high CO2)

• CXR: diffuse consolidation of the lung

• Most patients are placed on a ventilator

• Patients are prone to develop pneumonia and tend to have chronic problems

Atelactasis (lung collapse)

• incomplete expansion or collapse of lung

• minor focal atelectasis is common and may accompany other pulmonary diseases

• Atelectasis of the are entire lungs less common and is associated with more significant symptoms

• Important causes of atelectasis

  • deficiency of surfactant (type II)

  • compression of the lungs from outside

  • resorption of air distal to bronchial obstruction

• Usually reversible (based on diagnosis/time)

Neoplasms (not on Patho 3 test)

GI

Mouth

• Infections can be as a result of systemic disease or an isolated condition

  • Typically viral, fungal, or bacterial in nature

Herpesvirus Infection (cold sores)

• In the US HSV1 is the most common oral form of herpes

  • In other countries its HSV2

• Presents with vesicles on the lips

• 

Candida albicans (Thrush)

• Yeast infection of the mouth common in AIDS and late stage cancer patients

  • can be dangerous in this population

• The infected mucosa has a white surface layer

• Can also occur in babies, patients with dentures, inhaled corticosteroids, or DM

• Can spread to heart, brain, etc.

Aphthous Stomatitis (Canker sores)

• superficial ulcers of unknown etiology that form in the mouth

• painful, recurrent

• not contagious

• Heal spontaneously in about a week or two

Cancers

• Can occur any where in the mouth

• Most tumors are classified as squamous cell carcinomas

  • often related to tobacco smoking (pipe, cigar, snuff, cigarettes)

    • frequency raises the risk

    • Snuff is bad because the tobacco is up against the tissue

  • Alcohol is a risk factor

  • Diet may play a role → get those orange fruits and veggies

• Frequently develop from pre-cancerous lesions

  • leukoplakia or erythroplakia

    • Leukoplakia: white elevated plaque

      • most don’t progress to oral cancer

    • Erythroplakia: red elevated plaque

      • more likely to become cancer

  • Early detection is critical because if these turn malignant then tend to spread quick-like

    • Dentist got to check for these lesions

    • Without the early detection → 25% 5 yr survival rate

• Morphologically these can present as

  • plaques

  • Ulcers

  • Craters

  • Nodules

Salivary glands

Sialadenitis

• Inflammation of salivary glands

  • infectious or autoimmune

    • infections typically originate from mouth

      • Most common bacteria: S. aureus, S. Viridans

      • Mumps is most common viral

    • Autoimmune - Sjorgren’s Syndrome

• Clinically presents as swelling of the glands with either dry mouth (xerostomia) or excessive spit (sialorrhea)

Cancers

• Neoplasms may affect minor or major salivary glands

• Most (more than 60%) are benign

• Most common tumor: pleomorphic adenoma

• Rare only like 3% of tumors in the head

• lots of pain

• treat with surgery - tumors can be difficult to remove

  • >85% 5 yr survival rate

Esophagus

• Present with dysphagia, esophageal pain (retrosternal/colic), aspiration/regurgitation

Developmental Abnormalities

• Atresia with or without esophageal-tracheal fistula

  • Most common developmental defect in esophagus

  • Ends in blind pouch instead of attaching to stomach

  • Fistula allows GI contents to enter respiratory tract

    • aspiration pneumonia infection

  • Found pretty quickly after birth → babies vomit up all their feedings or you’ll see aspiration pneumonia infection

  • Death by starvation occurs without surgery

Hernia

• hiatal hernia is the most common type of gastro-esophageal disease

• If small particularly the sliding → no problems

• If big particularly the paraesophageal → can cause significant symptoms and may require some intervention (surgical repair due to bursting or twisting risk)

• Stomach acid backs up into esophagus → heartburn, stomach pain, belching, nausea

• Sliding:

  • displacement of the esophagus in which the stomach moves through the esophageal hiatus of the diaphragm

  • most common

  • Treat with self care measures and meds to relieve symptoms

• Paraesophageal:

  • A portion of the stomach pushes through the esophageal hiatus and forms a bulge at the base of the esophagus

  • Less common

  • more likely to have serious complications due to bulge

Achalasia

• The LES fails to relax properly when swallowing

  • spasms cause constrictions triggering stenosis of the areas surrounding the esophagus sphincter

  • The esophagus above the spasm becomes dilated

  • These leads to dysphagia

• Idiopathic

Varices

• Circulatory disturbance of vessels in the esophagus

• Can cause hematemesis

  • Most important cause of upper GI bleeds

• Bulbous gross veins as a result of portal hypertension

  • if they dilate enough they become weak and burst

• High mortality especially when the bleeding starts

Esophagitis

• inflammation of esophagus

• NG tubes can cause mechanical irritation

• Peptic Esophagitis - reflux of gastric juice

  • #1 cause

  • Malfunction of LES usually due to hiatal hernia

  • nonspecific inflammation and change of the epithelium

  • damaged squamous epithelium areas get replaced by glandular columnar epithelial cells (metaplasia) AKA Barrett’s esophagus

    • more likely to have ulceration and to become malignant

    • treated with tissue freezing to kill the glandular so the squamous comes back

• Infection (Immunosuppressed peeps)

  • Virus

    • shallow ulcers

  • fungi

    • shallow ulcer

  • bacterial superinfection

    • secondary to viral/fungal ulcer

• Chemical irritants

  • Exogenous chemicals

    • Kids swallow some stuff

  • Drugs

    • NSAIDS

Cancer

• Accounts for 4% of all cancers (8000 cases per year in US)

• Higher incidence in Asia and Africa

  • soil or food carcinogens maybe

  • maybe genetic

• Correlates with alcohol and tobacco use

• More common in men

• More common in black people

• Poor prognosis with a ~2 year survival rate

• Sqaumous

  • most common

  • highly correlated to smoking and drinking, with a bad diet

• Adenocarcinoma

  • on the rise due to Barrett’s esophagus

Stomach and Duodenum

• Characterized by pain (midline/upper abdomen), vomiting, bleeding (melena (chronic), hematemesis (acute)), dyspepsia (indigestion)

  • May have systemic consequences: iron deficiency anemia (chronic blood loss), vitamin B12 malabsorption (pernicious anemia)

Congenital Stenosis

• The most important and most common developmental abnormality of stomach and duodenum

• pretty rare

• stenosis of pyloric sphincter so you can’t go through the intestines and projectile vomit (exorcist style)

• Symptoms appear early in neonatal period

• Can be surgically corrected, relieve the contracture

• more common in males

Gastritis

• inflammation of stomach

• Acute (erosive) caused by circulatory disturbances, food, exogenous chemicals, and drugs

  • short lived

  • heals spontaneously usually

  • defect in mucosal lining

    • erosion = superficial

    • ulcer = deeper

  • Circulatory disturbances like shock leads to ischemia in the mucosa so damage is more common

  • Stress affecting the brain (trauma, burns, surgery) can trigger ulcers that extend through the entire mucosa → Cushing ulcers which are associated with bleeding

    • GI and brain connection maybe due to overstimulation of vagal nuclei, which increase ACh, which increase hydrochloric acid secretion

• Chronic atrophic gastritis

  • Often the cause is unknown but these things are related to it

    • H.pylori related

    • TB

    • Chrons

    • Sarcoidosis

    • Autoimmune with pernicious anemia

    • Atrophic gastritis

    • Atherosclerotic thrombi

    • bile reflux

  • Symptoms depend on causal agents

    • Asymptomatic or pain/burning in upper abdomen, belching, boating, feeling of fullness

    • Severe symptoms: palor, tachycardia, severe SOB, chest pain, hematemesis/melena

Peptic Ulcer

• Chronic, Multifactorial

• Mucosal ulcerations that extend all the way to the muscle layers

• any part of GI tract in content with gastric juice

  • duodenum = #1 site

  • Stomach = #2 site

• 4 million Americans at any given time are affected

  • 10% of money spent to GI diseases go here

• Contributing factors include:

  • excessive gastric juices

    • HCl, pepsin

    • Treat with H2 blockers and proton pump inhibitors

  • Mucosal Barrier defects due to stress, shock, NSAIDs, alcohol abuse

    • Smoking reduces resistance

  • H. Pylori is found in most patients

    • cure infection, cure ulcer

• Can be complicated by

  • hemorrhage (most common), melena is more common, iron deficiency anemia, in bad ulcers we get hematemesis

  • Acute pancreatitis (penetrates pancreas)

    • those in the duodenum

  • Peritonitis (perforation)

    • those in the duodenum

  • Stenosis (cicatrization)

    • scaring can contribute to stenosis of the small intestine

Gastric Tumors

• Benign epithelial tumors AKA polyps 5%

  • Hyperplastic, tubular, villous

  • Asymptomatic discovered during endoscopy

  • can progress to carcinoma or be associated with carcinoma in adjacent mucosa

  • Take’em out of there

• Benign stromal tumors 5%

  • leiomyoma - smooth muscle cell tumors

  • lymphoma - In the MALT

    • may be secondary from lymph gland or bone marrow

    • Primary MALT tumors are easy to remove

• Malignant Tumors

  • adenocarcinoma (most common) 90%

    • affects 25,000 people a year

      • more common in Japan/Chile (8X)

        • related to pickle and preserved foods maybe

      • has decreased in the US over the last 70 years

        • 14,000 deaths

    • Etiology is unknown, H. Pylori or nitrosamines (nitrates/nitrites) in food are thought to have a role

      • cigarettes and alcohol together may be a factor

Intestine

Developmental abnormalities

• Hirchsprung’s Disease

  • abnormality in innervation of the rectum and sigmoid colon resulting in permanent spasms

• Meckel’s

  • congenital diverticulosis

Diverticulosis, Obstructions, Hernias

• Can be congenital (Meckel’s) or acquired

• Characterized by the formation of diverticula (bulging of intestinal wall)

  • can be solitary or multiple

  • at any part of GI tract (the most important ones clinically involve the sigmoid colon)

    • Diverticulosis of the sigmoid colon is common in constipated old people

      • pressure increases chance of bulging and the sigmoid colon is not very elastic, so it won’t return to the OG shape

      • These diverticula can become obstructed with fecal material and lead to bleeding or trigger inflammation (diverticulitis)

  • Diverticula complications include perforation, abscess formation, rupture, and development of fistula

  • In severe cases you may have to resect the intestine

  • If there’s no inflammation it’s diverticulosis

• Obstructions (ileus) can be caused by

  • Paralytic Ileus (Adynamic) - results from neuromuscular paralysis

    • There’s an interruption/inflammation of the nervous system coming to the intestine

    • Complication of spinal cord injury and acute peritonitis

  • Mechanical obstructive ileus (atresia/stenosis, stricture (narrowing), intussusception (invagination bad), volvulus, hernia, adhesions, neoplasms)

Vascular Disorders

• Hemorrhoids (piles)

  • varicosities of the anal and perianal region

  • Internal = above the anal-rectal line

  • external = below the anal-rectal line

  • 5% of US adults are affect

  • Genetic component, more common in those with varicose veins and inguinal hernia, secondary to portal hypertension (liver cirrhosis)

  • Presents as dilated veins filled with blood and thrombi

  • burst easily and bleeding is common

  • Protruding lesions may become strangulated and infarct

• Angiodysplasia

  • localized vascular lesion of the colon that may cause unexplained bleeding in old people

  • formed by dilated thin walled blood vessels that serve as an anastomoses between the arterial and venous circulation

  • etiology is unclear, evidence suggest these anastomoses open up to protect against HTN

• Ischemic Bowel Disease (a number of disorders that impair blood flow to segments of the intestinal arteries)

  • Chronic ischemia - incomplete blockage blood flow but not all the way (typically Non-occlusive)

    • nonspecific symptoms usually goes undiagnosed

      • constipation, diarrhea, etc

    • Typically caused by atherosclerosis

      • could trigger a acute

      • multiple scattered infarcts of the mucosa

  • Acute - complete blockage of blood flow (occlusive)

    • less common

    • sudden occlusion leads to high mortality rate

      • large transmural infarction

    • Typically caused by thrombi or emboli

Inflammatory Bowel Disease

• Crohn’s Disease

  • Incidence is 20-40/100,000 per year in the US

• Ulcerative colitis

  • Incidence is 70-150/100,000 per year in the US

• In 20% of cases it is impossible to tell them apart due to symptoms overlap

  • unclear if they’re even different diseases

• Cause unknown but may be familial

• Patients will require at least one surgery to manage their bowel disease

• Jewish ancestry seems to be involved

• extra-intestinal complications → skin, liver, eyes

• transmural → affects entire wall of intestine

• Crohn’s is treated surgically with resection if serious

  • it’ll come back though

• UC is treated by taking out the colon

Infections

• Originate from overgrowth of GI flora (C.Diff after antibiotics) or exogenous pathogen

• Fairly common

• Can be mild upset stomach or even lethal diarrhea

• Can be bacterial, viral, or protozoal

• Bacterial Diarrhea

  • usually due to bacterial toxins (food poisoning, travelers diarrhea)

  • Invasive bacteria (salmonella)

  • Psuedomembranous Colitis

    • marked by pseudomembranes form in the colon

    • Mostly caused by overgrowth of C. Diff

    • Infection tend to occur post-antibiotics

    • Acute diarrhea

    • YOU’RE GETTING VANC BABY

    • Can recur (25% of cases)

• Viral Gastroenteritis

  • common but unreported since symptoms are mild

  • rotavirus in unvaccinated infants and young children

  • Norovirus in adults and children

    • winter vomiting bug

• Protozoal enteritis

  • Not common in US

  • Contaminated water

    • G.lamblia

    • Entamoeba Histolictica → tropic vacations, traveler’s diarrhea

• Small intestinal infection

  • E.coli, V. Cholerae, G.Lamblia, rotavirus

• Large Intestine infection

  • E.coli, Shigella, Norwalk virus, Entamoeba

• Acute appendicitis

  • The one and only intestinal infection that requires quick-like surgery (appendectomy)

  • trigger by a blockage of the lumen of the appendix leading to bacterial overgrowth and bacterial toxins lead to ulceration

  • Purulent inflammation

  • Can become necrotic or rupture causing peritonitis

  • Marked by Sudden fever, epigastric/RLQ pain, leukocytosis (neutrophils)

  • Treatment by antibiotics may be able to delay surgery

• Acute Infectious Peritonitis (most common and caused by infection of enteric origin)

  • Inflammation of the peritoneal lining

    • Due to

      • Rupture of stomach

      • Spread of infection from fallopian tubes

      • Abscess rupture

      • Infection of pre-existing ascites (alcoholic cirrhosis)

    • Exudate is purulent

• Noninfectious peritonitis (steril, irritation of peritoneal lining)

  • Acute pancreatitis → enzymes irritate lining

  • Rupture of the gallbladder → bile irritates lining

  • Post-surgical peritonitis by talc or chemicals used in surgery (iatrogenic)

  • triggers congestion and edema of the intestines and visceral peritoneum leading to transudation in abdominal cavity

• healing may become fibrous and form adhesions

Malabsorption syndrome

• Malabsorption results from abnormalities involving:

  • Intraluminal digestion of food

  • Uptake and processing of nutrients within intestinal cells

  • Transport of nutrients from intestine to the liver

• Defective Intraluminal digestion

  • Deficiencies of Gastric Juices

    • Postgastrectomy conditions

    • Atrophic Gastritis

  • Deficiency of bile or brush border enzymes

    • biliary obstruction

    • liver disease

    • Crohns

    • Short bowel syndrome

  • Deficiency of pancreatic juices

    • Chronic pancreatitis

    • Cystic fibrosis

  • Overgrowth of microorganisms

    • G. Lamblia

• Defective uptake of nutrients

  • Damage to absorptive surface

    • Celiac Sprue - gluten sensitive enteropathy

    • Tropical Sprue - bacterial infection for tropic visitors

    • Infectious enteritis (e.coli, rotovirus)

    • Crohn’s

    • Whipple’s disease - bacterial infection caused by T. Whipili

  • Loss of absorptive Surface

    • Short bowel syndrome - post surgical resection

• Defective Transport of nutrients

  • Lymphatic obstruction

    • GI lymphoma

  • Intestinal Ischemia

    • CHF

    • Atherosclerosis

  • Inadequate lipoprotein synthesis

    • congenital abetalipoproteinemia - no protein component of lipoproteins

Neoplasms

• Colon is most often affected

• sporadic or familial (sporadic 8x more common)

• benign or malignant (benign 3x more common)

• solitary or multiple

• Primary or secondary

  • primary are more common

• Epithelial tumors (Adenomas and carcinomas) account for 90% of all tumors

• Classification

  • Non-neoplastic (pseudo) polyps (hyperplastic, inflammatory, juvenile, Peutxz-Jeghers, lymphoid,)

  • Benign neoplasms (true polyps) (All the adenomas (tubular, villous, tubulovillous) and benign stromal tumors (leiomyoma))

  • Malignant neoplasms: adenocarcinoma, carcinoid, lymphoma, sarcoma

• Large Intestinal Carcinoma AKA colorectal cancer AKA colon cancer

  • 3rd most common cancer of internal organs

  • Affects 190,000 people a year in the US

  • Early stages are easily treated and discovered by colonoscopy (no family history, get at 50)

  • Etiology is unknown most of the time

    • May be genetic

      • Familial Polyposis coli - lots of polyps in colon, autosomal recessive

      • Gardner’s syndrome - lots of polyps in colon, extracolonic tumors, autosomal dominant

      • Hereditary nonpolyposis Colorectal cancer - autosomal dominant, increase tumors in ALL epithelial tissue

    • Diet is involved → low fiber, high carb, bbq not a good look

    • Interaction of carcinogen and oncogenes and tumor suppression genes

• Gastrointestinal Carcinoids

  • 90% occur in the intestines

    • appendix is the most common site

  • small tumors remain localized

    • larger ones can metastasize

  • May be multiple, especially in terminal ileum and stomach

  • Composed of neuroendocrine cells that contain granules visible via electron microscope

  • Low grade malignancy (not as bad as carcinomas)

  • Tumors secrete polypeptide hormones (gastrin and secretin) that are locally active

    • leads to diarrhea and hypermotility of the intestines

  • Tumors that do metastasize to liver causes which is a systemic disease carcinoid syndrome

    • blushing, bronchial wheezing, heart valve damage

Pancreas

Pancreatitis

• Inflammation of the pancreas

• Typically sterile in nature, secondary to tissue destruction caused by enzyme release from exocrine cells

  • self digestion

Acute

• Acute response to tissue necrosis caused by the release of enzyme

  • These can trigger release of those enzymes: obstructive biliary disease, gallstones, reflux of bile into pancreas, disruption of pancreatic cells (surgery/MVC), injury to pancreatic cells from cytotoxic drugs, overstimulation of pancreatic cells (fatty foods and alcohol)

• Common causes alcohol abuse, gallstones, and unknown

  • alcohol and gallstones make up 80%

  • Idiopathic make up 15%

• Rare causes surgery, drugs, metabolic disease, infection (Mumps) → 5%

• Complications:

  • Massive edema, hemorrhage

  • Fat necrosis, calcifications, hypocalcemia

  • Ascites (sterile peritonitis)

  • Shock (hemodynamic instability)

  • Massive necrosis (psuedocyst - large fluid filled sacs)

    • forming abscess formation

  • Chronic Pancreatitis

    • 20% of cases

    • usually when this acute is recurrent

  • DM

    • hyperglycemia during attacks but rarely transcends to permanent DM

Chronic

• 4/100,000 adults in US

  • 3X more common in males

• Progressive and irreversible

  • eventually you’ll get exocrine and endocrine insufficiency

    • usually exocrine 1st

• Pathology

  • Fibrosis of the pancreas

    • replacement of parenchymal tissue

  • Atrophy and loss of acini (functional cells)

  • calcifications - seen on X-ray

  • Islets of Langerhans are preserved but in late stages they reduce in number

    • endocrine tissues is typically the last to be destroyed

• Causes

  • Chronic alcoholism (70%)

  • Trauma

  • Systemic metabolic/endocrine disease

  • Idiopathic (20%)

• Clinical Quirks

  • Insidious Onset

    • slowly overtime and fairly silent until its too late

    • Most cases are independent of the acute form

  • Pain in upper abdomen (epigastric) that radiates into the back

  • Malabsorption caused by pancreatic insufficiency

    • presents as steatorrhea and weight loss (malabsorption of fat)

  • X-ray evidence of calcifications

  • Secondary DM

    • polyuria, polydypsia, polyphagia

Neoplasms

• In 95% of all cases tumors are derived from ducts (exocrine), solid, malignant, and functionally silent (no hormones)

  • affect your ability to secrete enzymes

Adenocarcinoma of the pancreas (exocrine)

• 4th major cause of death in men, 5th in women

• 25,000 new cases a year in the US

• Smoking increases risk 3x

• Chronic pancreatitis increases risk 2x

  • minor cause overall

• Rare before the age of 40, but then incidence increases with age

• Poor prognosis - most dead in 2 year

• Clinical Quirks

  • weight loss, loss of appetite, nausea, jaundice if the cancer is in the head of the pancreas (obstruction of the common bile duct), gallbladder distention (Courvoiser’s sign), radiating pain if tumor is in body/tail

  • Commonly metastasizes to the lymph nodes (40%), liver, lungs, bones

    • only 20% of people have NO metastasize at time of diagnoses

  • Use endoscopic retrograde cholangiopancreatography (ERCP) with aspiration cytology important for diagnosis (differentiates adenocarcinoma and chronic pancreatitis)

  • CT scan is the most reliable tool for finding pancreatic cancer

• Most important neoplasm of the pancreas

• 60% of tumors are in the head of the pancreas, 15% in the tail, 25% are diffusely involved

Islet Cell Tumors (Tumors of the Endocrine Part of the Pancreas)

• Rare 10X less common than adenocarcinoma

• typically benign so prognosis is better

• Hormones can determine type of tumor

• Insulinomas are characterized by hyperinsulinemia → hypoglycemia → syncope, profuse sweating

  • Reverse with glucose infusions

  • Most common

  • small and solitary

• Glucagonoma

• Somatostatinoma

• VIPoma

• Gastrinoma (Zollinger-Ellison Syndrome) - hypersecretion of gastric juice and multiple peptic ulcers that are unresponsive

  • May be a part of MEN1 (multiple endocrine neoplastic 1)

  • Pancreas is the most common site for gastrin secreting tumor

  • 25% of pancreatic endocrine tumor

  • While the pancreas has no gastrin secreting cells, the gastrin secreting cells share a common precursor cell to the islet cells

    • gastrinomas originate from the precursor cells in the pancreas

  • Can be Multiple and malignant

DM

• Inadequate production of or lack of response to insulin

• Primary (complex interaction between genetics and environment)

  • Type 1 - no production (less than 10% of cases)

    • may be proceeded by a viral infection

    • You have to destroy at least 80% of the beta cells before symptoms

    • Insulin dependent

    • More likely to progress to coma and DKA (too much glucose)

  • Type 2 - no response to insulin (insulin resistance)

    • You have to use more and more insulin to get a response

• Secondary (other disease states)

  • Pancreatic disease

  • Endocrine disease

  • Drug related

  • Genetic syndromes (hemochromatosis, hyperlipidemia)

• Pathogenesis

  • Diabetes is a result of islet cell insufficiency, increased demand for insulin, peripheral tissue resistance

  • Polyuria, polydypsia, polyphagia

• Complications (long term, gotta manage that blood glucose)

  • Eyes

    • Cataracts

      • sugar gets converted to alcohol

    • Retinopathy - Retinal micro aneurysms, hemorrhage, exudates

    • Glaucoma

  • Kidney

    • Glomerulosclerosis

      • since kidney is suffering it thinks everything is so it increases pressure

    • Pyelonephritis

  • Nervous System

    • CVD (stroke or dementia)

    • Peripheral neuropathy (loss of sensation, pain/tingling)

      • If you can’t feel pain, you won’t know something is infected

  • Cardiovascular (endothelial cells are damaged that’s step 1, plus hemoglobin is more sticky)

    • Most common cause of death in DM patients

    • Most common cause for non-traumatic amputations

    • Arteriolosclerosis (peripheral changes)

    • Atherosclerosis DVD Gangrene of extremities

      • You know it when you smell it

• Complications of DM are what lead to death (most of the time)