Resp and Endocrine Flashcards
(193 cards)
1
Q
Primary Billiary Chirrosis vs Primary sclerosing cholangitis
A
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)
2
Q
Hemochormatosis causes, iron studies, treatment
A
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.
3
Q
Wilsons disease
A
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
4
Q
HBV and HCV treatment
A
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
5
Q
TLC = what?
A
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
6
Q
FVC and FEV1
A
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).
7
Q
FEF 25-75
A
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)
8
Q
What tests are better for Obstructive vs restrictive disease
A
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
9
Q
DLco
A
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
10
Q
Asthma workup
A
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
11
Q
Distinguishing between COPD and Asthma
A
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.
12
Q
Alveolar - arterial Gradient
A
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.
13
Q
When you see pulmonary nodules what do you always do first?
A
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.
14
Q
New onset pleural effusion - what is next step?
A
Thoracocentesis!!
15
Q
Transudate vs exudate - effusion / serum ratios
A
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!!
16
Q
MCC Exudtavie
A
3 main causes.
- Cancer
- Pneumonia
- TB
PE can be either Exudative or Transudative.
17
Q
Transudative causes
A
Decreased oncotic - liver disease, nephrotic etc.
Increased hydrostatic - heart failure / liver disease
For transudative effusions - TREAT THE UNDERLYING CAUSE!!
18
Q
what are the types of pleural effusions?
A
- 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!!
19
Q
If any effusion is infected what do you do next?
A
stick in a chest tube!
20
Q
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?
A
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.
21
Q
what has a bad prognosis in asthma?
A
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
22
Q
Acute vs Chronic phase asthma workup
A
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
23
Q
Acute asthma exaccerbation treatment
A
- 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
24
Q
Chronic asthma treatment
A
- 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!
25
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)
26
How to differentiate between different COPDs?
two main types:
1. Emphysema:
decreased DLCO
more rapid breathing
2. 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.
27
How does COPD present?
very similar symptoms to asthma:
1. wheezing
2. dyspnea
3. 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)
```
28
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.
29
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
30
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.
31
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
32
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.
33
what are the only things at improve outcomes in COPD?
1. smoking cessation
2. Home O2 ( Pa02 < 55 or Pa02 < 59 and cor pulmonale)
3. Vaccines
Influenza yearly
Pneumococcal
H. Influenze once a lifetime
34
Home O2 is required in COPD when?
Home O2 ( Pa02 < 55 or Pa02 < 59 and cor pulmonale
35
Treatment in acute exaccerbation of COPD
just like asthma:
1. O2
2. Bronchodilators (ipatropium and albuterol)
3. systemic corticosteroids (IV)
4. Antibiotics!! (this is the big diff between COPD acute treatment and Asthma).
Give antibiotics even if CXR is normal --> Macrolides / cephalosporins, fluroquinolones
36
what is the differential for AST and ALT in the 1000s?
1. Acute infection of liver
2. Toxins / Drugs
3. Ichemic injury to the liver
37
When you have acities what do you do first?
Tap - parcentesis.
check fluid for 2 things:
1. Absolute neutrophil count.. if above 250 then it means you have SBP
2. Check the SAAG
38
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
```
39
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:
1. exertional dyspnea
2. fine crackles
3. clubbing
4. 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
40
Interstitial lung disease
Over 100 different diseases in ILD.
1. idiopathich pulmonary fibrosis
2. sarcoidosis
3. occupational lung disease
4. silicosis / asbestosis
5. wegners granulomatosis
6. churg strauss
etc etc
41
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.
42
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.
43
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:
1. Arthritis
2. Erythema nodosum
3. 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!!
44
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
45
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!!!
46
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
```
47
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.
48
Caplan syndrome
RA + pulmonary disease.
elevated IgA
positive RF
Positive ANA
Decreased C3
49
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.
50
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.
51
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
52
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.
53
Treating PE and DVT
Think of DVT and PE as the same disease!! treat the same.
1. always treat Proximal vein thrombosis
2. worry about distal DVTs propagating
3. dont worry about superficial thrombosis
4. Pregnant pts, IV catheters, --> look in uncommon places like pelvic veins, upper extremity veins etc.
54
can the superficial femoral vein cause thrombosis?
YES. Its a misnomer. its actually a deep vein.
55
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!.
56
how does nephrotic syndrome cause hypercoagulatility
losing AT3 in urine. will see lots of renal vein thrombosis.
57
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.
58
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.
59
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.
60
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.
61
Do heparin and warfarin lyse the clot?
no. They dont lyse clots. they prevent further propagation.
62
PE treatment
1. O2 and Heparin Immediatly
2. confirm diagnosis with CTA / VQ etc.
3. 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)
63
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)
64
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.
65
Sleep Apnea
Diagnosis - polysomnography
Treatment:
obstructive - weight loss, CPAP
central sleep apnea --> acetazolimide.
66
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.
67
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
68
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
69
Bronchogenic Cancer types
1. Squamous - PTH like peptide
2. Small cell - SIADH, Cushing, Lambert Eaton
3. Large Cell
4. Adenocarcinoma (bronchoalveolar) - non smokers
Small cell is uncurable!
70
bronchogenc cancer presentation
1. cough (most common symptom)
2. weight loss, dyspnea
3. hemoptysis
4. recurrent pneumonia
5. hoarseness
6. SVC syndrome
7. pancoast sydrome
8. Horner syndrome
9. Effusion
71
When is a lung cancer treatable?
What are the 5 scenarios that a lung cancer is not treatable?
1. Outside the lung
2. In the Pleura
3. Metastasis to the other lung as well
4. If its in the main stem bronchus
5. Low PFTs --> cant take out part of lung when they wont have enough pulmonary function to live.
72
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.
73
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.
74
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!
75
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!.
76
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
77
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!!!
78
Cervical Cancer screening
start screening at 21 yo.. stop at 65 if 3 negative tests in a row.
HPV + Pap Smear --> and they are both negative.. then you can do screening every 5 years
If just pap smear.. and its negative --> screening every 3 years.
79
Prostate cancer screening
We dont use PSA to screen.. however if another provider measured PSA and it was elevated.. then the next step is Digital Rectal Exam and BIOPSY!!!
If cancer is diagnosed then you stage it.. most prostate cancers you dont really do anything
80
Do you screen prostate cancer?
no.
And especially not with PSA.
If someone else does it and its elevated.. then you have to follow it up.. but DONT SCREEN FOR IT!!!
81
someone goes to a malaria endemic area how do you prophylax?
give MEFLOQUINE :
1 week before they go
the whole time they are there
2 weeks after they get back.
Round trip coverage.
Mefloquine causes bad side effects --> psych.. bad dreams.
If they cant take mefloquine then use doxycycline.. issue is now they have to take doxy daily.
In prego patients use CHLOROQUINE not doxy or meflo
82
how do you treat travelers diarrhea?
Loperamide + hydration
if there is systemic symptoms or bloody diarrhea then add antibiotics (CIPRO)
83
Immunizations
1. influenza
everyone should get it
pregnant patients should get it in 2nd and 3rd trimester
patients with TRUE egg allergy should NOT get the flue shot.
Side effects from Influenza:
swelling and redness at site of injection
causes flu like symptoms.. but NOT THE FLU
2. Pneumococcal vaccine
everyone 65 and older should get it
asplenic patients, lung disease, cirrhosis, heart disease, HIV all should get the vavccine..
asplenics give booster shots.
3. zosster vaccine --> everyone over 65 should get this
84
Smoking cessation
ask about smoking cessation every visit
If theyr ready to quit set a contract
Nicotine patches
Bupropion ( DO NOT use in patients with seizures.. this exaccerbates it)
Varenicline (patient must continue this med for 6-9 months AFTER quitting).
85
Osteoperosis screening
all women above 65 should get a DEXA scan.
If they have risk factors (low vita D, family history) then they should get the DEXA at 60yo!
treatment of osteoperosis is:
calcium + vita D + bisphosphanates
86
Cholesterol
check fasting LDL in all men above 35 with no risk factors.
if there are risk factors for CAD or hypercholesterolemia then start cholesterol screening at age 20.
If treating.. treat the LDL levels with Statins!
Normal LDL is 130 and less. Optimal is 100 and lower.
87
HTN screening
every visit do BP check
to diagnose someone with HTN they have to have elevatged BP for 2 or more visits.
88
DM screening
Fasting glucose above 126 on 2 seperate visits.
*Screen for DM in patients who have HTN
89
Alcohol abuse what is the single best test do diagnose?
CAGE questionnaire!!!!!
2 or more + answers in CAGE is positive finding. --> refer them to AA!
Dont do:
ETOH levels .. transaminases.. none of that.
90
Screening questions
Always ask about domestic violence. --> cant call authorties on patient if they dont want it.
DO call authorities in elderly or child abuse.
Always ask about guns at home
Always ask about seat belt use in car.
91
Anterior pituitary vs Posterior Pituitary
anterior pituitary--> adenohypophysis horomones
FSH / LH/ TSH / ACTH
Posterior pituitary --> neurohypophysis:
Oxytocin and ADH release
92
What are the majority of the tumors in the pituitary
they are non functioning
pressure on the optic chiasm --> bitemporal hemianopia.
93
Patient comes in with galactorrhea what do you do?
check the following:
1. pregnancy test
2. prolactin level
3. TSH
94
Hyperprolactenemia
excess prolactin --> presents with amenorrhea and galactorrhea
in men it will present with hypogonadism
Prolactinoma is the most common functioning adenoma in the pituitary.
Etiology:
1. nursing / stress / stimulation
2. drugs --> haloperidol / reseripine / H2 blockers
3. hypothyroidism
Dopaine blocks prolactin in the tuberoinfundibular pathway.
If you have hypothyroidism.. you will have low TSH.. and this will result in high TRH --> TRH activates prolactin release
Treatment:
1. In microadenoma first line treatment is Dopamine agonists --> cabergoline (less side effects), bromocriptine they have equal efficacy
If there is severe mass effect on the pituitary / optic chaiasm.. then do surgery
2. surgery
3. XRT
95
Acromegaly
Excessive GH
Gigantism in children
in adults --> acromegaly
Macroadenomas --> large tumors --> these will very often cause bitemporal hemianopia.. make sure you do physical exam to identify this.
Enlargment of hands, feet tounge, mandible,
heart --> CHF
Carpal tunnel --> median nerve compressed
Diabetes. GH should nomrally block the effect of insulin. the excess GH counter-regulates insulin --> high blood sugar
Diagnosis:
1. IGF / Somatomedins --> Somatomedins is what is used to monitor disease activity.!!!
2. Glucose Load test --> When you give someone glucose.. in a normal person, growth hormone should be decrease. But in a patient with acromegally GH is still high after giving glucose.
3. MRI --> view the pituitary
Treatment;
1. octreotide --> Somatostatin analogue
2. dopamine agonists --> cabergoline and bromocriptine can be used to lower the release of GH.. however this IS NOT THE TREATMENT.. may be a pharma question tho.
3. surgery (commonly used here) since these are macroadenomas you often have to go to surgery here.
96
Does growth hormone cause tissue growth?
no. GH stimulates the liver to release IGF --> IGF is what causes growth
97
Hypopituitarism
lesions in the pituitary - hypothalamic region:
crainiopharyngiomas in kids
TB, sarcoidosis
GH, Gonadotropins --> lost early
ACTH --> lost last
how do you diagnose?
give the patient insulin --> insulin causes drop in glucose --> GH should be high. If GH does rise.. then you know this patient is fine. In hypopituitarism GH goes first.. so if it rises like in a normal person then that iwll rule it out.
DIagnosis --> decreased GH levels after hypoglycemia or arginine
98
sheehan syndrome
a type of hypopituitarism
peripartum necrosis
inability to lactate
99
Pituitary apoplexy
A type of hypopituitarism
prior adeoma --> causes necrosis and bleeding in the pituitary --> wipes out pituitiary function
headache
altered mental status
confusion
mengismus
looks like meningitis.. make sure you differentiate.
this patient will have bleeding in the pitutiatry on CT scan!
This is an emergency.. take patient to surgery!
100
Empty sella syndrome
when the meningies herniate into the sella turcia.. pushing the pituitary off to the side.
THese patients have NO ENDOCRINE PROBLEMS!!
SO then why would this patient get an MRI and find this if there are no symptoms?
Patient got an MRI for another reason and found this on accident.
101
Posterior pituitary --> diabetes insipidus (no ADH)
1. ADH deficiency or unresponsiveness
2. Central vs Nephrogenic
3. Polyuria / polydipsia
4. low urine osmolality
5. hypernatremia and increased serum osmolality
To diagnose --> water deprivation test. In a normal person the Urine will become more concentrated when deprived of water.
In Diabetes insipidus the urine will stay dilute.
102
How do you distinguish between Central and nephrogenic?
Give desmopressin.
If urine osmolality increases then its central.
If urine osmolality does not change then its nephrogneic.
103
Central (primary) DI
Causes:
1. neoplastic
2. sarcoid
3. surgery
4. radio therapy
5. head injuries
teratment = Desmopressin Intranasally
*this is what is given in vWF disease and Hemophilia a also.
104
Nephrogenic (damaged V2 receptors) DI
1. hypercalcemia
2. sickle cell disease
3. Drugs --> lithium, demeclocycline, colchicine
treatment --> HCTZ, Amiloride, chlorthalidone --> these diuretics work by removing salt from the body. Giving these will allow the patient to lose more salt then water.. adjusting the hyperosmolality of the serum!
105
SIADH
euvolemic hyponatremia ( NO EDEMA!!!)
Free water retention
extra cellular volume expansion
symptoms come when hyponatremia is severe --> irritability, confusion, seizures (EXACT SAME manifestations as hypernatremia btw)
1. hyponatremia
2. decreased plasma osmolality
3. small amounts and concentrated urine
4. high urine sodium
5. inappropriate naturiesis
6. Low BUN, Low URic aicd
normal thyroid and adrenal function
SSRIs, vincristine, vinblastine can cause SIADH
106
Treatment of SIADH
1. treat underlying cause
2. Fluid restriction
3. Demeclocycline or lithium
If patients develop severe confusion / convulsions because of the hyponatremia.
give hypertonic saline (5% saline) --> this is the only disease you would even think of doing this.. Make sure not to correct to quickly or it cna result in cerbeallar pontine myelinolysis
107
What is the best initial test for all thyroid disease?
What is the main hormone secreted by thyroid?
Main secretory hormone is T4
T3 is more potent
Only free T3 and T4 are active. 99.9 % is bound to albumin.
High T3 and T4 negatively feedback TSH
BIT for all thyroid diagnosis = TSH!!!
If TSH is normal then the patient is euthyroid.
108
what is thyroglobulin
it is co-secreted with T3 and T4.
It is a measure of endogenous production of T3 and T4.
If you are suspecting exogenous use..check thryroglobulin levels to rule it out.. if its low but T3 / T4 is high then its exogenous.
When is the times you check thyroglobulin?
1. To rule out exogenous
2. To follow cancer activity.
109
why is it important to look at free T4 and T3 instead of total T4/T3?
Because total is not always accurate. TBG binds T3 and T4.
increase in TBG levels:
1. pregnancy
2. OCPs
Bound T3/T4 will not show up.. this will falsely decrease T3/T4 levels
decreased TBG levels in:
1. nephrotic syndrome
2. liver disease
110
what is the normal RAI of the thyroid?
10-40%
if the thyroid has above this on RAI uptake scan then its a sign of hyperthyroidism.
If the whole thyroid has excess update --> graves disease
If there are specific spots that have high uptake --> toxic multi-nodular goiter.
111
when do you do RAI scan?
when the patient has hyperthyroidism and you are unsure of the cause.
if pts is hyper thyroid and the scan shows the following:
1. whole thyroid has excess uptake --> graves
2. SPecific spots have high uptake --> toxic multinodular goiter.
3. Decreased uptake (less than 10%) --> de-quirvans thyroidoitis
112
Graves disease
MCC of hyperthyroidism
Hyperthyroidism + Diffuse Goiter + Exopthamlos
if patient has exopthamlos this can ONLY BE GRAVES!!
+ TSI --> these are essentially TSH copy cats --> hyperthyroid.
linked to autoimmune disorders:
1. pernicious anemia
2. myasthenia gravis
3. diabetes
Presentation:
1. nervous symptoms
2. high output heart failure.. dyspnea, palpitatoins, CHF
3. inablity to sleep, tremors
4. diarrhea, sweating
5. pretibial myxedema
113
What is the only symptom of hyperthyroid that can become worse with treatment initially?
Exopthalmos
If patient has exophtalmous its automatically GRAVES!!
114
How do you diagnose Graves?
If the patient has exopthamous --> no further testing needed.
BIT is TSH.
TSH will be low.. and free T3 / T4 will be elevated
next do a RAI scan (usually not needed) --> diffuse increased uptake.
3. TSI will be positive (usually not needed)
115
Graves disease treatment
Immediate treatment:
1. propanolol (to control adrenergic symptoms)
2. Antithyroid drugs (PTU or Methimazole)
In pregnant give PTU (only one safe in prego)
Long term Tx:
1. RAI ablative therapy --> this will make them hypothryoid.. but that is much safer than hyper.
2. Thyroidectomy (rarely)
116
when do you do surgery in graves?
1. pregnancy
2. pressure on the thryorid
3. children
117
Toxic Multinodular goiter
Older patients
Lumpy - bumpy thryoid
Presentation:
1. arrhythmias --> A-FIB (always work up an elderly patietn with a-fib for hyperthyroid)
2. CHF
NO OPTHALMOPATHY
118
Thyroid storm
extreme thyrotoxicosis caused by very high thyroid hormones.
1. High fever
2. Hypotension/ CHF (hypotension caused by heart failure)
3. Delirium / coma
Percipated by stress / surgery / trauma.
Treatment: This is an emergency
1. Antithyroid drugs --> PTU
2. Iodine or iodide (large bolus to down regulate T3/T4 production)
3. BBs
4. Dexamethasone
5. IVF, cooling blankets
119
What is the most common cause of hypothyroidism?
Hashimoto thyroiditis is the MCC!!!
```
Hashimotos
or
Iatrogenic (RAI ablative therapy)
or
Drugs (lithium)
```
These are the only 3 causes in the U.S.
120
Hypothyroidism presentation
```
Slowed deep tendon reflexes on the relaxation phase (not on the way up)
elevated cholesterol
hoarse voice
carpal tunnel syndrome --> caused by edema from hypothyroid..
dry hair and skin
pseudodementia
cold intolerance
constipation
```
121
How do you treat the hypercholesterolemia in Hypothyroidism???
TREAT the Hypothyroidism!!
Levothyroxine.
not statins.
122
what are the places you see bilateral carpal tunnel?
1. Hypothyroidism
2. amyloid deposition
3. pregnancy
4. acromegaly
123
hypothyroidism management
1. Levothyroxine (T4).. we use T4 in the U.S not T3.
T4 is given for LIFE!!
TSH levels take 6 weeks to equilibrate
suspicion of secondary hypothyroidism--> give hydrocortisone first.
124
Myxedema Coma
the opposite of thyroid storm.
Untreated long standing hypothyroidism.
1. Stupor
2. hypothermia
precipitated by infection / cold exposure.
TX:
1. High dose T4/T3
2. Corticosteroids
3. warming blankets
4. IVF
125
Thyroiditis Subacute
Giant cell, De quervains
causes HYPERthyroid
Viral origin
thyroid pain
lower jaw pain
Labs:
1. elevated ESR!! (100% of the time)
2. Inital elevation of T4 and T3
3. Decreased ratioactive iodine uptake
Painful thyroid on palpation
Tx: for symptomatic --> ASA, Prenisone
DO NOT GIVE THEM PTU / MEHTIMAZOLE !!!
the disease will go away by itself.
126
Hashimotos Thyroiditis
HYPOthyroidism
Chronic inflammation --> leads to hypothyroid
lymphocytic infiltratoin
Findings:
1. Antithyroglobulin antibodies
2. Rubbery Goiter
3. Hypothyroidism
4. Goiter may or may not be symmetrical.
Diagnosis --> antimicrosomal antibodies
Management --> Thyroxine (T4)
Type II hypersensitivity reaction: anti-TSH receptor antibodies are formed that inhibit thyroid hormone release (opposite of Grave's disease)
1. anti-microsomal and anti-thyroglobulin antibodies are formed that lead to destruction of thyroid stroma
*Do not confuse with anti-mitochondrial in primary biliary sclerosis
127
Sick Euthyroid syndrome
When people are very sick.. possibly sepitc and T3 / T4 are low
TSH will be normal in these patients
128
If a patient has normal TSH what is the diagnosis?
EUTHYROID.. this patient does not have any of the diseases that cause hypo or hyper thyroidsims.
129
Thyroid Nodules and THyroid Cancer workup
All non-functioning nodules are presumed to be due to cancer until proven otherwise!!!
Step 1: examine the thyroid and get TSH
Step 2: Fine needle aspiration (under ultra sound guidance)
FNA will tell us if its either benign or cancer.
130
What is the most common thyroid cancer?
papillary. --> associated with radiation
spreads via lymph nodes
does not spread via blood
131
Thryoid cancers
1. Papillary
2. Follicular --> very curable.. But also often metastasizes to bone / liver
3. Medullary associated with MEN2a and 2b.
4. Anaplastic
Medullary --> high familial link.. if there is a family history of thyroid cancer its probably medullary thyroid cancer.
Treatment for all thyroid cancers:
1. Thyroidectomy--> full removal of thyroid.
2. Suppress TSH. Give very high dose of thyroid hormones (T3/T4) for 10 years to completely suppress TSH.. so that the TSH does not stimulate the cancer cells
132
How do you follow thyroid cancer?
thyroglobulin
133
for every 1 unit Albumin is dropped how much does calicum drop by?
.8
134
Hypercalcemia symptoms
lethargy, confusion
abdominal pain, constipation
NDI (polyuria, polydipsia) stones
135
Hypercalcemia causes?
Hyperparathyroidism
Malignancy (PTH like peptide, bone mets)
Sarcoid --> hyper vita D3
Prolonged immobilization
Familial hypocalciuric hyper calcemia --> Kidney cannot excrete calcium--> hypercalcemia.
Test by checking urine calcium. in these patients it will be low. in a normal patient when you have high calcium you should be urinating it out (high urine calcium) but in these patients thats not happening.
Drugs --> HCTZ
* loops get rid of calcium.. HCTZ dont!
136
Hypercalcemia Management
what causes the most severe hypercalcemia?
cancer
what is the MCC of hypercalcemia?
hyperparathyroidism
Treatment:
1. IVF (normal saline) FLUIDS, FLUIDS, FLUIDS!!!!
2. Furosemide.. give fluids then furosemide to get rid of the calcium
3. Calcitonin - works quickly but also has short half life
4. Bisphosphonates (pamidronate) - takes long to effect but has very long half life
give calcitonin and bisphosphanates at same time.
137
Hyperparathyroidism
75% of the time its a single adenoma in 1 of the 4 parathyroid glands.
25% of the time its all 4 glands.
Diagnosis --> elevated PTH
Management:
Surgery is the definitive treatment! this is the treatment for the majority of patients.
Medical management:
fluids
bisphosphanates
MEN1:
hyperparathyroid
pituitary
pancreatic (zollinger ellison etc)
MEN2:
Hyperparathyroid
medullary cancer
pheochromocytoma
138
How do you follow hyperparathyroidsim post parathyroidectomy?
you get hypocalcemia because of the lack of parathyroid hormone --> hungry bone syndrome (misnomer).
tenatus like symptoms --> chvostek and truseau sign
post surgery --> monitor calcium
Give these patients CALCIUM!!
139
Hypocalcemia etiologies
what is the first thing you do when you have low calcium?
check albumin!! if its low then calcium is falsely low.
Hypomagnesemia can cause hypocalcemia.
Causes:
1. Low PTH
2. Hypomagnesemia --> low calcium levels
3. Low vitamin D (no sun exposure... malabsorption syndromes)
Low vita D will result in High PTH and low calcium.
140
what happens to calcium with vitamin D deficency
calcium will be low
PTH will be high
IF PTH is high then phosphate will be decreased.
Low vita D
Low ca
HIGH PTH
LOW phosphate!
141
what happens in end stage renal disease to calcium?
In renal disease you cant activate vita D
so calcium will be low
PTh will be high
Vita D will be low obviously
when PTH is high normally phosphate should be very low.. however phosphate is excreted by the kidney.. in ESRD you cant get rid of phosphate so in these cases the phosphate is high!!
142
Treatment of hypocalcemia
acute stage --> IV calcium gluconate!
maintantenace therapy --> Oral calcium, vita D
ESRD --> hyperphosphatemia give phostphate binders.. CaCO3 / aluminum hydroxide.
143
Diabetes melitus
type 1 = no insulin = DKA
type 2 = insulin resistance = Hyperosmolar hyperglycemia
Definition of diabetes = fasting glucose > 126 on 2 separate occasion
or
if fasting is above 200
144
how often should you check HbA1c?
HbA1c will NOT be differnt from the last reading for 3-4 months.. so it doesnt make sense to check it earlier than that.
145
How do you lower the risk of MI in DM?
Statins! control the cholesterol
tight glycemic control will control the microvascular complications not MACRo like cardiac.
146
Microvacular complications in DM?
1. Retinopathy --> get yearly eye exam (type 2 diabetics go right away)
2. Neuropathy --> autonomic.. so gastroparesis.. ED.. orthostasis
3. Nephropathy--> microalbuminuria --> Start ACEI right away
147
how do you calculate anion gap?
Na - (bicarb + chloride)
148
If someone comes in with DKA what is the workup?
rule out percipiating causes first:
1. CXR
2. Blood cultures / UA
149
why do patients have hyperkalemia in DKA?
low insulin!
2nd is the acidosis causing hydrogen to go into cells and potassium to come out.
HOw do you treat the hyperkalemia?
Insulin!
150
Pseudohyponatremia?
when glucose is high.. it makes sodium look low.
151
Treatment of DKA
1. admit to ICU!
2. Insulin IV then SQ
3. Aggressive IVF --> .9% saline
4. confirm ketones in blood or urine
5. blood and urine cultures
6. in patients with 'normal' serum k on admission with DKA give KCl
152
Treatment of hyperosmolar hyperglycemia
1. admit to ICU!
2. aggressive IVF (.9 normal saline)
3. Insulin IV then SQ
4. EKG (silent heart attack)
5. Blood and urine cultures / CXR --> looking for percipitating factors
153
Hyperosmolar hyperglycemia vs DKA
DKA --> High Ketones and elevated anion gap
Glucose in the 400-500
HHS --> No Ketones, Normal Anion gap and GLucose in the 1000s!
154
Follow up exams required in diabetes pateints
Yearly eye exams:
Type 1: 1st exam needs to be 5 years after the diagnosis of DM and then every year after that
Type 2 need to go right away and do one every year after that.
Foot exams yearly!
155
Type 2 diabetes treatment
1. Life style mods + Metformin! (metformin inhibits gluconeogensis)
2. if metformin alone is not controling sugar then ADD a sulfonylurea --> glipizaide, glyburide,
3. pioglitazone --> sensitizes insulin
these are the ONLY 3 we use.
Sulfonylurea side effects --> they work on the beta cells to increase insulin secretion --> weight gain is a big side effect. cant use in kidney failure.
Metformin DOES NOT cause hypoglycemia or Weight gain.
Most common side effect with metformin is GI side effects
Most dangerous side effect is lactic acidosis (rare).
So you CANNOT use Metformin in CKD or ESRD
156
Metformin uses and contraindications
Metformin DOES NOT cause hypoglycemia or Weight gain.
Most common side effect with metformin is GI side effects
Most dangerous side effect is lactic acidosis (rare).
So you CANNOT use Metformin in CKD or ESRD
157
sulfonylurea contraindicaitons
Sulfonylurea side effects --> they work on the beta cells to increase insulin secretion --> weight gain is a big side effect. cant use in kidney failure.
158
What do you use in diabetics who have chornic kidney disease?
INSULIN!!!
cant use metformin or sulfonylureas or pioglitazone!
159
Insulin management
Ultra short acting insulin: lispro / aspart --> give these right before meals
short acting:
intermediate acting: NPH
long acting: Glargine (lantis) --> used to set a baseline
160
when do you add insulin in type 2?
you only add it after they are already on metformin, sulfonylureas and pioglitazone and its still not controlled!
161
what is required for the diangosis of HYPOglycemia?
1. low glucose
2. symptoms from low glucose
3. reversal with glucose.
162
Insulin and glucose examples studies:
A normal response to low glucose is LOW INSULIN!!
example 1:
low glucose, low insulin, low c-peptide
STARVATION / FASTING
example 2:
low glucose, elevated insulin, elevated c-peptide
Sulfonylurea use.. or insulinoma
example 3:
glucose low, insulin high, c-peptide low
Exogenous insulin use
163
what is the most reproducible test in diabetes?
fasting glucose
follow up is done with hba1c
164
what do you do for a diabetic showing up with hypoglycemia?
1. admit them and give glucose
2. get a good history
if its sulfonylurea usage --> observe them
if its a new excersie regimen.. bring glucose back up and dc
165
how do you diagnose cushings syndrome?
Overnight dexamethasone suppresion test --> give very high dose dexamethasone. this should suppress cortisol levels in the blood in normal patients.
In cushings.. even after high dose dexamethasone.. the cortisol will be high.
24 hour urine free cortisol is the gold standard (this one is hard to do so people do the overnight test first.. but this is the best one to do)
if 24 hour urine coritsol is high then you have cushings.. if its not.. then you dont.
If they give you both options overnight dexa or 24 hour free urine.
the answer is 24 hour free urine cortisol!!!
166
once you confirm cushings how do you localize it?
Give very high dose dexamethasone --> if this decreases cortisol levels.. then you know that this is caused by ACTH release from the pitutiary!
if this doenst suppress it then you have to see if its lung vs adrenal?
so here you will have high cortisol obviously.. how do you differentiate lung vs adrenal?
look at ACTH. If ACTH is high then its lung. If its low then its adrenal.
167
what affect does ACTH have on aldosterone?
NONE!!!
168
Hyperaldosteroneism (Conns)
High sodium --> increased intravasc volume --> HTN
low potassium
alkalosis
Low renin
MUSCLE WEAKNESS (secondary to hypokalemia)!!
Aldosterone : Renin ratio is very high
this is renin independent hyperaldosteroneism
169
what happens to aldosterone in hypovolemia?
decreased intravascular volume -->increased renin --> increased aldosterone --> increased NA and decreased K+ and H+ --> alkalosis
Since aldosterone and renin are both high here you have a LOW aldosterone: renin ratio.. they are BOTH HIGH..
IN conns syndrome you have a HIGH aldosterone: Renin ratio because the hyperaldosteronism is independent of the renin in this disease.
170
adrenal insufficiency
idiopathich or autoimmune causes
World wide Tb is the main cause
Addisons disease (primary):
Hypotension (no aldosterone)
hyperpigmentation (high ACTH and thus MSH)
Hyperkalemia
hypoglycemia
eosinophilia (unknown reason. but REMEMBER THIS)
Secondary (Low ACTH)
no hyper pigmentation here
also in this ONLY CORTISOL is low here.. ACTH has no control over aldosterone.
Diagnosis:
ACTH stimulation test!
Give ACTH and measure coritsol levels. If ACTH raises cortisol levels then its secondary.
If ACTH does not raise cortisol levels then its Addisons disease!
Treatment for adrenal insufficiency:
Hydrocortisone and Fludrocortisone
171
In what scenario will secondary adrenal insufficiency not respond to the cosyntropin test?
in chronic secondary adrenal insufficiency.. because the adrenal glands will have been atrophied!!!
if atrophied giving ACTH will not increase cortisol production.
172
Pheochromocytoma
diagnose by measure free catecholamines (metanephrines in urine)
next step do MRI to localize the lesion.
DO NOT do imaging until the patient has either urine or blood metanephrines found. MUST HAVE THIS FIRST!!
Treatment = alpha blockers first then surgery!!
173
Klinefelters (primary hypogonadism)
gynecomastia, smal testes
47xxy
hypogonadism --> low testosterone --> causing high fsh and lh and Gnrh
treatment = testosterone
high risk of BREAST CANCER
174
Kallmans syndomre (scondary hypogonadism)
Decreased GnRH --> low LH and FSH --> resulting in low testoterone
Different mech then klienfelters
this is caused by and x-linked single gene defect
pts also have anosmia, gynecomastia, small testes
Treatment = testoterone or Synthetic GnRH (this is the better answer)
175
patient on anitthyroid drugs (PTU or MEthimazole) develops sore throat what do you do?
discontinue.
If the cell count drops below 1000 then permanently discontinue.
176
Patient with diabetes takes insulin glargine at bed time. when she wakes up her blood glucose is within normal range.. however her random glucose check and her hba1c are elevated. What is happening and how can you fix it?
This patient is likely haveing postprandial hyperglycemia.
Glargine is a long acting.. good for setting a baseline. However certain patients may need a rapid acting mealtime insuline (insuline aspart) to prevent POSTPRANDIAL HYPERGLYCEMIA..
177
What is the dawn phenomenon
When patients wake up with hyperglycemia due to the diurnal spikes in GH and Cortisol in the morning.
Dawn phenonmenon is seen in fasting glucose (when they wake up) rather than post meal time.
178
Patient with Thyroid Cancer --> what are next steps?
Must do ALL 3.
1. Removal of thyroid
2. Radioiodine
3. High dose thyroid hormones to suppress TSH
179
Calcitonin is a marker for which thyroid cancer?
Medullary Thryroid Cancer --> arises from the PARAfollicular C cells of the thyroid gland.
Papillary and Follicular cancers arise from Thyroid Epithelial cells.
180
what will cortisol and ACTH be in a patient who was on chronic glucocorticoid therapy for years and abruptly discontinued it?
Cortisol and ACTH will be low due to suppression of the hypothalamic-pituitary-adrenal axis.
Patients with a CUSHINGOID appearance are likely to have a suppressed HPA axis (big indicator).
Following discontinuation of glucocorticoids.. normal HPA axis function may not fully return for up to 6-12 months!
181
How do OCPs or pregnancy effect thyroid hormones?
Oral estrogens decrease clearance of Thyroxine-Binding Globulin (TBG) --> thus leading to elevated TBG levels.
Patients with normal thyroid can compensate and produce more thyroid hormone to fill the excess TBG binding sites and also make more so that there is free thyroid hormone available as well.
In HYPOthyroid patients.. they cant make enough thyroid hormone (they rely on exogenous thyroid hormone) and thus we need to INCREASE THE DOSE of L-THYROXINE (Levothyroxine). Same scenario in pregnant patients.. in crease the dose if they are hypothryoid.
182
Does estrogen inhibit the conversion of T4 to T3?
no.
GLucocorticoids, BBs, and PTU do.
BUt estrogen does NOT.
183
How can diabetes cause dizziness?
causes AXONOPATHY of large and small nerve fibers through microvascular injury, demyelination, oxidative stress, and deposition of glysocylation end products.
Small fiber injury - Pain , parasthesias, allodynia (exaggerated pain with slight touch)
Large Fiber injury - Numbness, LOSS OF PROPRIOCEPTION AND VIBRATION SENSE, diminished ankle refelx.
184
21 hydroxylase deficency. What will mineralcorticoids, glucocorticoid and androgen levels be?
Decreased glucocorticoids and mineralcorticoids.
ELEVATED androgens. (zona reticularis)
185
Thyroid nodule management. What is the first step when you palpate a nodule?
obtain TSH and ULTRASOUND!
then do FNA.
186
In DKA or HHS what kind of fluids are used for volume resuc?
Normal saline (.9%). Use this no matter what the sodium level.
Afterwards.. once intravasc volume is restored and serum sodium is either normal or slightly elevated.. then switch to .45% saline.
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in type 2 diabetics what causes the altered sensorium.. delerium?
Hyperosmolarity.
In type 2 diabetics there is severe hyperglycemia --> this causes GLYCOSURIA and OSMOTIC DIURESIS --> results in HYPOVOLEMIA and DEHYDRATION.
As hypovolemia worsens.. GFR decreases leading to reduced renal glucose excretion and worsenting hyperglycemia.
The neuro symptoms ranging from confusion to coma are due to the HIGH SERUM OSMOLARITy.
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what is the difference in the MOA of graves / toxic multinodular goiter vs painless thyroiditis / subacute thyroditis
Graves and Toxic multinodular goiter --> OVERPRODUCTION of thyroid hormone.
Painless thyroditis and Subacute thyroiditis --> RELEASE of PREFORMED hormone.
189
Thyroid Peroxidase autoantibodies are found in Hashimoto thyroiditis. What is the only other disease they are found in?
PAINLESS Thyrdoitis.
Hyper thyroid (High T4, and low TSH) + Painless thyroid on exam and LOW uptake of Radio active iodine.
There is no specific therapy for PAINLESS thyroiditis. You can give a BB to help control symptoms (palpations and tremulousness)
190
what effect does albumin have on calcium?
Calcium is bound to albumin about 40% of circulating calcium.
Hypoalbunemia will decrease the TOTAL calcium
Hyperabluminemia will increase the TOTAL calcium
Neither will affect the ionized fraction.. and thus albumin changes can NEVER CAUSE calcium related symptoms.
191
acromegaly will have what effect on the heart?
CONCENTRIC MYOCARDIAL HYPERTROPHY.
This will lead to HTN, Heart failure or valvular disease.
192
Starting what drug will cause symptoms in a apatient with mild primary hyperaldosteronism who was previosly symptomless
Diuretics. they will cause an exacerbation of the primary hyperaldosteronism and it will present with one or more of the folowing:
1. Hypokalemia
2. Hypernatremia
3. metaboli alkalosis
Best screening test - Measuring early morning plasma aldosterone concentration to plasma renin activity ratio.
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in sick euthyroid syndrome.. what do you see as far as thyroid hormone levesl?
Sick euthyroid syndrome AKA low T3 syndrome.
Total and free T3 levels are LOW. while T4 and TSH are normal.
treatment - fix underlying illness.
