Resp and Endocrine Flashcards
Primary Billiary Chirrosis vs Primary sclerosing cholangitis
Primary biliarry cirrhosis: Autoimmune disease of middle aged women --> autoimmune destruction of BILE DUCTS in portal triad. Symptoms; chronic cholecystitis puritis - bile salts in skin Jaundice Hyperlipidemia
Diagnosis:
Normal total serum bilirubin levels
serum ALK PHOS ELEVATED
BIT is right upper quadrant US –> distinguish between intra and extra hepatic billiary obstruction.
ANTI-MITOCHONDIRAL ANTIBODY (90% sensitive) ABSENT in PSC.
Confirmatory diagnosis with BIOPSY (focal duct obliteration with granuloma formation)!!
Treatment: First line treatment = ursodeoxycholic acid (decreases symptoms). You can add Cholestyramine to bind salts in the intestines and thus decrease puririts.
Primary Sclerosing Cholangitis:
Strong association with IBD (especially UC) - will see a patient (mostly occurs in young MEN) with UC who is developing fatigue, jaundice, pruritis (all same symptoms as PBC).
Unknown etiology.. but chronic cholestasis in the bile ducts leads to their fiborsing –> narrowing and eventually obliteration –> ending up in cirrhosis.
Diagnosis:
serum alk phos elevated (same as PBC)
bilirubin is variable may or may not be elevated
BIT is direct choliangiography (Best by ERCP) - will show multiple short strictures and saccular dilatations, involving both intra and extra-hepatic bile ducts. –> beaded / strictured appearance .
Confirmation of diagnosis with Biopsy –> will show periductual fibrosis and inflammation and loss of bile ducts.
ABSENT mitochondrial antibody.
poor prognosis - strong association with developing cholangiocarcinoa and liver failure.
treatment:
Endoscopic Balloon dilatation of strictures
Endoscopic stenting of strictures to relieve symptoms
Possible liver transplant (must do before liver failure)
Hemochormatosis causes, iron studies, treatment
excess iron deposition in all tissues in body. May be primary or secondary. *Iron is not toxic to tissues, its the free radicals that generate because of the iron that damages teh tissues.
autosomal recessive
Primary: HFE gene mutation
Secondary: Too many transfusions, alcoholism (alcohol has high iron content),
Ferritin elevated
transferrin elevated
iron elevated
TIBC decreased
Treatment: Phelbotomys to decrease iron stores. Menses does this in women.. thats why in women it usually appears after menopause.
Deferoxamine - iron chelating agent.
Wilsons disease
A rare autosomal recessive disorder
Defect involves a copper transporting (cerruloplasmin) protein and is linked to chromosome 13
Characterized by impaired biliary excretion of copper
leads to excessive copper deposition in the LIVER and BRAIN
Usually presents in patients< 30 years old
Aggressive chronic hepatitis, which often progresses to cirrhosis liver symptoms include asterix jaundice mental status changes
Basal ganglia copper deposition leads to extrapyramidal tremors loss of coordination drooling dementia
Deposition in the joints causes a degenerative arthritis
spine and large joints are most commonly involved
Physical exam
pathognomonic Kayser-Fleischer rings in the cornea
hepatomegaly
Parkinsonian tremor
Diagnosis - serum cerruloplasmin is low. And Urine copper is high!!
Treatment: First step is dietary copper restriction. Penicillamine (a copper chelator) co-administered with pyridoxime oral zinc (increases fecal excretion) can be used for maintenance therapy
Liver transplant if drug fails
HBV and HCV treatment
HBV :
Tenofivir +/- Lamivudine (3TC)
monitor therapy with HBV DNA and alanine aminotransferase (ALT) levels
HCV:
sofosbuvir +/- ledipasvir +/- ribavirin
monitor therapy with HCV RNA and ALT levels
TLC = what?
TLC = VC + RV
TLC > 80% predicted = normal
TLC >80 % in obstructive disease –> due to air trapping
TLC < 80% in restricve disease –> due to decreased ability to expand and take in volume
FVC and FEV1
vital capacity over time
FVC = VC / Time
FEV1 = FVC in the first second
FEV1 / FVC = less than 80% in obstructive lung disease (obstruction in getting the air out)
in Restrictive - FEV1 / FVC is normal (80% and higher).
FEF 25-75
FEF 25-75 is the exact same thing as FEV1/ FVC
If FEF 25-75 is less than 80% its obstructive
if FEF 25-75 is 80% or higher its normal (seen in restrictive diseases)
What tests are better for Obstructive vs restrictive disease
best test for obtructive is measuirng FEF25-75 or FEV1/ FVC
because these are abnormal in obstructive but normal in restrictive
Best test in restrictive is PFTs –> TLC / FVC / RV
because these are abnormal in restrictive
DLco
what is a nomral value for DLco? 80% or higher (just like for TLC just like for FEF25-75 just like for FEV1/FVC)
helps you distinguish between types of disease within obstructive or restrictive for example:
Obstructive pattern on FEV1/FVC how do you know if its emphysema vs asthma?
Asthma / COPD / = normal DLco
Interstitial lung disease / Emphysema = decreased DLco.
diseases with normal DLCO vs Abnormal DLCO
Normal DLCO: Asthma COPD Obesity KYPHOSCOLIOSIS!!!
Abnormal DLCO:
Pulmonary Fibrosis
Emphysema
Interstitial lung diseases - pneumoconisosi, sarcoid, scleroderma
Asthma workup
Asthma can have normal PFTs (since its reversible). so they may come in with asthma symptoms but when you do the PFTs the PFTs are normal. so in these patients you do the METHACHOLINE challenge test.
This will constrict bronchioles (bronchoprovocation). Positive test is 20% decrease in FEV1/FVC
Distinguishing between COPD and Asthma
patient comes in with PFTs showing a obstructive pattern (FEV1/FVC < 80%) Elevated TLC. Hyperinflation of lungs on CXR.
How do you distinguish between COPD and Asthma.
DO the Bronchodilator reversibility test. Asthma Is reversible. COPD IS NOT!!!
After giving bronchodilator if FEV1/FVC improves by 20% on bronchodilator test then its asthma.
Alveolar - arterial Gradient
A-a gradient = (150-1.25 x PaCO2) - PaO2
PAO2 is the ALVEOLAR oxygen that we are trying to solve for using the below values and the above equation.
PaO2 is arterial oxygen and is found from the ABG.
PaCO2 is the arterial CO2 and is found from the ABG also.
Using these 2 values we can use the above equation to derive the PAO2
Normal PaCO2 = 40
Normal PaO2 is around 95
thus A-a gradient in a normal patient is
150 - 1.25(40) - 95 = 5
So why do we calculate it?
Because if its above 15 then we know there is a problem with gas exchange from the alveoli to the blood.. AKA ventilation perfusion problem..like an obstruction in the alveoli, PE, Intestital disease etc.
When you see pulmonary nodules what do you always do first?
ask for OLD XRAY!!
if present on old xray and no change then not worried.
New Nodule:
Low Risk: pts who have no tobacco history and the nodule is less than 3 CMs
Follow up with CXR Q3 months for 2 years
*If durring the every 3 month CXR or low Dose CT imagings you see changes or growth then send this patient in for a biopsy
High risk: pts with tobacco history, and over 45 yo.
MUST BIOPSY you can do it a few ways.. if its in the lungs in an area that close to the trachea you can do a bronchoscopy.
If its in the peripheray you can do a CT guided biopsy.. If this is not an option then you will have to do an open lung biopsy.
New onset pleural effusion - what is next step?
Thoracocentesis!!
Transudate vs exudate - effusion / serum ratios
Transudate: LDH effusion = <200 LDH effusion / Serum = 200 LDH effusion / Serum = >.6 Protein effusion / serum = >.5
If any one of these 3 values fits the exudative profile then its EXUDATIVE!!
MCC Exudtavie
3 main causes.
- Cancer
- Pneumonia
- TB
PE can be either Exudative or Transudative.
Transudative causes
Decreased oncotic - liver disease, nephrotic etc.
Increased hydrostatic - heart failure / liver disease
For transudative effusions - TREAT THE UNDERLYING CAUSE!!
what are the types of pleural effusions?
- parapneumonic - next to the pneumonia
- hemmhorragic effusion
- lymphocytic exudative effusion –> Tb / infections
- Malignant pleural effusion
1st step with any effusion is thoracocentesis.
If any effusion is infected you stick a CHEST TUBE in!!
If any effusion is infected what do you do next?
stick in a chest tube!
In asthma exacerbation
what is the best drug to relieve symptoms asap?
what is going to decrease hospital stay?
what is contraindicated in asthma exacerbation?
best drug to relieve symptoms right away - albuterol
what is going to decrease hospital stay? steroids
what is contraindicated in asthma exacerbation?
long acting beta agonists - salmeterol!!!
even in outpatient setting (not acute exacerbation).. if patient will need LABA like salmeterol you NEVER give it without also giving them corticosteroids.
what has a bad prognosis in asthma?
getting it at an old age..
very difficult to control in old people when onset happens in old age.
Poor prognosis: old age elevated CO2 use of intercostal muscles acidosis
Most common precipitants of asthma attacks?
- viral infections
- Aspirin and Beta blockers and NSAIDS
- exercise
Acute vs Chronic phase asthma workup
Acute exacerbation:
- ABG
- CXR
- Pulse Ox
Chronic phase eval (non-acute)
- PFTs to confirm diagnosis
- if PFTs are normal (Methacholine challenge test)
If PFTs show obstructive pattern - do the albuterol challenge test to confirm its asthma vs copd.
- CBC to check peripheral eosinophilia
Acute asthma exaccerbation treatment
- O2
- Albuterol (MDI or Nebulizer)
- Start IV steroids (methylprenisolone is IV) then after a few days can switch to oral steroids (prednisone) for 7-14 days
Chronic asthma treatment
- daily inhailed corticosteroids (stunts growth / causes thrush, long term will cause cataracts etc).
- albuterol as needed
If these dont work then you can add the following:
- LABA - salmeterol .. only give when this patient has nocturnal symptoms (this will allow them to sleep at night and not wake up for albuterol).. remember do not give LABA in acute exaccerbation or ALONE.. must be taking steroids also if this is being perscribed.
- Leukotrine modifiers - montelukast
- last resort is systemic steroids
WE DO NOT USE:
epinephrine, aminophylline, theophylline for asthma treatment!
What is first line treatment for COPD?
Inhaled Ipratropium and Anticholinergics
(because beta agonists cause tachycardia.. anticholinergis dont.. most patients with COPD are old and you dont want to induce tachy in them)
How to differentiate between different COPDs?
two main types:
- Emphysema:
decreased DLCO
more rapid breathing - Chronic bronchitis
productive cough for multiple months for multiple years
normal DLCO!!!
Both have:
non-reversible obstruction
non-inflammatory in chronic state.. but significant inflammation durring acute exacerbations.
How does COPD present?
very similar symptoms to asthma:
- wheezing
- dyspnea
- productive cough (more so in chornic bronchitis)
PE: distant heart sounds ronchi, wheezing CLUBBING Cor PULMONALE facial plethora (caused by excess RBC production due to the hypoxia)
Cor Pulmonale
right sided heart failure due to pulmonary hypertension due to the lung disease.
this will cause JVD and facial plethora
as soon as the patient develops cor pulmonale the morbidity and mortality increases by 5x.
patients will either die of either lung disease or heart disease.
Testing in COPD
CXR:
hyperinflated lungs
flattened diaphragms
PFTs:
obstructive pattern and not reversed with albuterol
ABG:
Hypercapnia, hypoxemia
“60-60” group (CO2 is high and O2 is low)
Labs:
polycythemia
how should you treat the patients hypoxia in COPD?
give them O2 but make sure you dont take it above 95%!! very high yield.. IF you go above that you will destroy their respiratory drive.
COPD management in chornic setting
Anticholinergics:
inhaled ipatropium - most effective bronchodilator in COPD
Beta Agonists: inhaled albuterol (less effective and more side effects)
Theophylline - only added if above not sufficent
Theophylline toxicity
do NOT give theophylline with Macrolides (ACE) or with Fluroquinolones!!
both of these antiboitcs effect p450 –> theophyline levels rise and lead to arrhythmias.
what are the only things at improve outcomes in COPD?
- smoking cessation
- Home O2 ( Pa02 < 55 or Pa02 < 59 and cor pulmonale)
- Vaccines
Influenza yearly
Pneumococcal
H. Influenze once a lifetime
Home O2 is required in COPD when?
Home O2 ( Pa02 < 55 or Pa02 < 59 and cor pulmonale
Treatment in acute exaccerbation of COPD
just like asthma:
- O2
- Bronchodilators (ipatropium and albuterol)
- systemic corticosteroids (IV)
- Antibiotics!! (this is the big diff between COPD acute treatment and Asthma).
Give antibiotics even if CXR is normal –> Macrolides / cephalosporins, fluroquinolones
what is the differential for AST and ALT in the 1000s?
- Acute infection of liver
- Toxins / Drugs
- Ichemic injury to the liver
When you have acities what do you do first?
Tap - parcentesis.
check fluid for 2 things:
- Absolute neutrophil count.. if above 250 then it means you have SBP
- Check the SAAG
Bronchiectasis
Permanent dilatation of bronchi both medium and small sized bornchi.
can be both local or diffuse.
Localized - had an infection whe nyou were young.. it destroyed part of the lung and permanently dilated the bronchi
Diffuse - cystic fibrosis, Kartagners syndrome
Pneumonia + chronic daily productive cough (lots of sputum)
Patients will get recurrent pneumonias,
may get hemoptysis.. if the bronchiectasis is advanced
diagnosis:
CXR - tram tracking appearance
BIT = High resolution CT - permanent dilated bronchi
PE:
Thin
Resp distress
Diminished breath sounds in a part of the lung
For acute treatment: Treat this patient with an ABX that covers PSEUDOMONAS!! Aminoglycosides - GNATS Ceftazidime, cefipime pipericilin / tazboactm imipenem / meropenem
Chronic treatment: Bronchodilators chest physiotherapy antibiotics vaccinations surgery for localized disease
Interstitial lung diseases
Chronic inflammation –> leading to fibrosis of the interstitium –> leads to disrupted gas exchange (decreased DLco) –> hypoxemia.
all the diseases will have similar symptoms:
- exertional dyspnea
- fine crackles
- clubbing
- cor pulmonale
All will have similar findings on imaging:
CXR - Reticular pattern / ground glass apperance.
Similar PFTs
intrapulmonary restrictive lung disease
decreased DLco
BIT in all interstitial is CXR
follow up with high res CT –> this will help localize where we need to do a biopsy from.
MAT = Biopsy.. must do to confirm diagnosis
Interstitial lung disease
Over 100 different diseases in ILD.
- idiopathich pulmonary fibrosis
- sarcoidosis
- occupational lung disease
- silicosis / asbestosis
- wegners granulomatosis
- churg strauss
etc etc
Idiopathic pulmonary fibrosis
PE:
positive JVD
Lung exam: fine crackles on inspiration
3. postive clubbing
CXR shows diffuse reticulonodular pattern
When you do Biopsy - shows non-specific fibrosis.
SO all same symptoms as all other Interstitial lung diseases.. but we have no idea why it happens. and all findings on biopsy and bronchoscopy are non-specific but rule out other disease.
ALso ONLY affects the LUNG!! no other area affected.
Treatment is steroids for now.. we may be moving to anti-fibrotic agents once approved… treatment is questionable.
Idiopathic pulmonary fibrosis treatment and followup
since treatment is up in teh air.. the question the USMLE may ask is what is teh best test for follow up..
best test for follow up will be PFTs before and after treatment.
Sarcoidosis
Chronic granulomatous disease of unknown origin - non caseating granulomas!
Painful erythematous papulses, joint swelling, symmetrical polyarticular arthropathy, well demarcated 3cm papules over anterior leg.
looks a lot like RA.. however on CXR you will see bilateral hilar lymphadeonopathy!!!
So Sarcoidosis comes with 3 things:
- Arthritis
- Erythema nodosum
- Bilateral hilar lymphadenopathy
can also get eye symptoms –> Uveitis!
when you get eye symptoms treat quickly with high dose steroids.
Hypercalcemia – hyper vitaminosis D3. More so in summer because of activation via sunlight in the skin.
Hypercalcemia in sarcoid –> MUST BE TREATED WITH STEROIDS!!
MAT –> biopsy. MUST DO BIOPSY to make diagnosis.
Treatment = STEROIDS!!
Patient with bilateral hilar lymphadenopathy comes in with no symptoms.. what do you do for him?
Asymptomatic patients - just follow up in a few months to see if symptoms develop.
80% of sarcoid self resolves.
MUST TREAT symptoms like uveitis, hypercalcemia
Pneumoconisios - occupational lung diseases
Asbestosis
Silicosis
CWP
Inhaled fibers –> alveolar macrophages –> inflammatory process –> fibrosis.
Most important –> must have history of exposure to one of the above causes!!
typically manifests 20-30 years after exposure.
Classic interstitial lung disease presentation:
ground glass / reticular bodies
1. exertional dyspnea
2. fine crackles
3. clubbing
4. cor pulmonale
decreased DLCO / restrictive pattern (decreased TLC and FVC normal FEV1/FVC).
BIOPSY IS MANDATORY!!!
Asbestosis
Brake linings
insulation
ship yards!!
absbests fibers - dumbeslls in macrophages –> feroginous bodies.
On CXR if you see PLEURAL PLAQUES –> that is pathagnomonic for Asbestosis!!!
another big clue,
Asbestosis affects the lower lobes of the lungs!!
as opposed to…
silicosis effects upper lobes
Asbestosis increases the risk for.. #1 is Bronchogenic cancer #2 is Mesothelioma
Silicosis
silica dust
sand blasting
mining
glass and pottery (quartz)
UPPER LUNG infiltrates
Nodular pattern, “egg shell calcification” (calcified lymph nodes)
diagnosis.. same as all others..
BIT = CXR
then follow up with high res CT
Confirm with Biopsy!
Increased risk for Tb in SILICOSIS@!
what do you have to do with this patient every year?
yearly ppd test.
Caplan syndrome
RA + pulmonary disease.
elevated IgA
positive RF
Positive ANA
Decreased C3
Pulmonary Embolism
normal CXR
elevated RR and HR
Lung and Heart exam are unremarkable on Physical exam.
resp alkalosis.. decreased Co2
What is the next step in a patient with symptoms of PE?
CTA! (its a CT with contrast) –> this is the gold standard for diagnosis.
What is the next step in a patient with symptoms of PE?
CTA! (its a CT with contrast) –> this is the gold standard for diagnosis.
Where do you have to have a clot to get PE?
MUST be above the knee to cause a PE.
What is the risk of getting a clot from a distal DVT (below the knee)?
0 chance
PEs can also be caused by DVTs in the following:
upper extremities –> subclavian and internal jugular (in patients with IV catheters).
In pregnancy –> Pelvic veins
What is the risk of getting a clot from a distal DVT (below the knee)?
0
however this clot can advance to above the knee.. forming a proximal DVT and this can then become a PE.
Treating PE and DVT
Think of DVT and PE as the same disease!! treat the same.
- always treat Proximal vein thrombosis
- worry about distal DVTs propagating
- dont worry about superficial thrombosis
- Pregnant pts, IV catheters, –> look in uncommon places like pelvic veins, upper extremity veins etc.
can the superficial femoral vein cause thrombosis?
YES. Its a misnomer. its actually a deep vein.
What is the most common cause of an inherited hypercoagulable state?
Factor 5 leiden deficency.
Protein C and Protein S are natural anticoagulants (thats why when warfrin blocks them.. there is initially a hypercoag state).
In a factor 5 mutation.. protein C cannot bind and INACTIVATE factor 5.. leaving factor 5 always activated!.
how does nephrotic syndrome cause hypercoagulatility
losing AT3 in urine. will see lots of renal vein thrombosis.
PE Diagnosis
ABG - Hypoxemia with elevated A-a
CXR - normal CXR most of time… may see a hamptons hump sign which is a peripheral wedge shaped mark.
EKG - will see tachy
CTA - gold standard
D- dimer - normal D-dimer rules out PE 100% sensitivity.. if D dimer is not elevated it no PE or DVT.
PE General concepts
1st step = CXR
2nd step = CTA
Normal CTA = No PE
Normal D-DImer (RULE OUT TEST) - no PE or DVT
Normal V/Q scan = NO PE
Always give Heparin!! anti-coagulate patients suspected / high risk patients while waiting for diagnostic tests to be complete.
If you have contraindication to CTA with contrast what do you do to diagnose PE?
contraindications:
ESRD / Kidney disease (cant take contrast)
Do VQ scan in these patients.
pregnancy do CTA still.
When bridging heparin - warfarin what if the INR becomes therapeutic before 5-7 days?
Doesn’t matter.
Must continue both together for 5-7 days even if INR is therapeutic.
Do heparin and warfarin lyse the clot?
no. They dont lyse clots. they prevent further propagation.
PE treatment
- O2 and Heparin Immediatly
- confirm diagnosis with CTA / VQ etc.
- after diagnosis is confirmed anticoagulate with LMWH Heparin and Warfarin!
LMWH given for 5-7 days
warfarin for 6 months
In pregnancy warfarin is contraindicated so use LMWH
For patients who recently had recent headtrauam / brain or eye surgery.. cant use anticoag – > place IVC filter.
Thrombolytics not used routinley in PE.. however used in the following situations:
1. hemodynamically unstable patients (hypotension, right heart failure).
(streptokinase / tpa)
when to use thrombolytics in PE?
Thrombolytics not used routinley in PE.. however used in the following situations:
1. hemodynamically unstable patients (hypotension, right heart failure).
(streptokinase / tpa)
ARDS
increased alveolar - capillary permeability
non-cardiogenic pulmonary edema
hypoxemia
Etiology: sepsis - mCC is gram - sepsis Trauma DIC drowning..
occurs within first 5 days.. but usually within first 24 hrs
Findings:
Dyspnea
Crackles and ronchi
Hypoxemia +/- hypercapena
X-ray - fluffy white-out apperance –> thats pulmonary edema.
Elevated pulmonary artrey pressure
Treatment –> treat primary disorder and give mechanical ventilation if needed.
Sleep Apnea
Diagnosis - polysomnography
Treatment:
obstructive - weight loss, CPAP
central sleep apnea –> acetazolimide.
Pancoast tumor
tumor in the right upper lobe of the lung.. can press on the brachial plexus and sympathtic nervous system –> horners. vena cava –> superior vena cava sydnrome
oncological emergency–> must do XRT right away.
What is the leading cause of death in men and women?
Lung cancer.
Non smoker = adenocarcinoma.
ALL LUNG CELL CANCERS assoicated with SMOKING.. if you smoke you have a higher risk of getting ALL lung cancers.. even adenocarcinomas!
at what point will a previous smokers risk for cancer be equal to someone who never smoked?
NEVER.
Smokers have a 10x higher risk than non smokers.
No good screening test exists for lung cancer risk
Smoking screening.
Pts who have smoked within the last 15 years
and
65-75 y/o
screen with low dose CT every 1 to 2 years
Bronchogenic Cancer types
- Squamous - PTH like peptide
- Small cell - SIADH, Cushing, Lambert Eaton
- Large Cell
- Adenocarcinoma (bronchoalveolar) - non smokers
Small cell is uncurable!
bronchogenc cancer presentation
- cough (most common symptom)
- weight loss, dyspnea
- hemoptysis
- recurrent pneumonia
- hoarseness
- SVC syndrome
- pancoast sydrome
- Horner syndrome
- Effusion
When is a lung cancer treatable?
What are the 5 scenarios that a lung cancer is not treatable?
- Outside the lung
- In the Pleura
- Metastasis to the other lung as well
- If its in the main stem bronchus
- Low PFTs –> cant take out part of lung when they wont have enough pulmonary function to live.
Dyspnea 24 hrs after a surgery.. what is the cause?
its not a pneuonia.. that would take atleast 48 hrs to develop..
this is atelectasis –> collapse of part of / entire lung immediately post op.
atelectasis
in baby - think obstruction from aspiration of something
in smoker - think obstruction from cancer causing collapse
diagnosis via CXR –> will see tracheal deviation
Treatment –> incentive spiromotery.
Colonoscopy screening
start at age 50 and do colonoscopy every 10 yrs
If there is positive family history –> start screening at 40 y/o or 10 years before the diagnosis in the family member.
Gold standard is colonoscopy –> because when you see a poly you take it out and thats diagnostic and therapeutic.
If you find polyps –> colonoscopy every 5 years after finding the polyp.
If patient doesnt want to do colonoscopy then you can do a FOBT instead. But this has to be done every year.
If FOBT is positive.. then they have to get a colonoscopy!
52 yo man is found to have 3cm dysplastic polyp on colonoscopy when do you screen next?
56 yo man is found to have a 3.5 cm adenomatous polyp.. when do you screen next?
pts comes in with normal colonoscopy and incomoplete prep
52 yo man
in 10 years.. If its not adenomatous then you dont have to worry.. its benign
56 yo man
In 3-5 years.. adenomatous polys require more frequent screening / surveilance.
incomplete prep –> must re-do the colonoscopy!.
Breast cancer screening
Most common cancer in women
what age group has shown that survival is improved by yearly mamogram?
50-75
screen women from 50-75 years old.
Family HIstory start 10 years before the diagnosis in the relative and do it every year from then.
Once you start the screening then you MUST do it every year form then on
GOLD STANDARD = MAMMOGRAM
IF a patient or provider finds a breast mass what is the next step?
Next step is to do a biopsy.. but before you biopsy you will be doing a mamogram to localize the lesion and then see if there are any other masses that will need to be biospied…. then MUST DO BIOPSY!!!
