Internal Medicine Tips Tricks and Techniques Part I Flashcards
What is the mechanism of Digoxin
Inhibits Sodium potassium ATPase
What are some common anti-arrythmic drugs
…
maxalt
rizatriptan
What is the treatment of bells palsy
steroids for anti-inflammatory.
Studies have not shown a decrease in symptoms when steroids are combined with acyclovir (up to date)
What is the SPIKES protocol
- SET up the Interview
- Assess the patients PERCEPTION
- Obtain the patients INVITATION
- Giving KNOWLEDGE and information to the patient
- Address the patients EMOTIONS
What is the antibiotic treatment for Cat Bites
- Monotherapy with a beta-lactam/beta-lactamase inhibitor, such as one of the following:
a) Ampicillin-sulbactam
b) Piperacillin-tazobactam
c) Ticarcillin-clavulanate - A third generation cephalosporin
- Metronidazole 500 mg IV every eight hours
What is the treatment for increased ammonia levels
- Lactulose (45-90grams QD) You want to create 2-3 soft stools per day with a pH less than 6. 2. Oral antibiotic such as Neomycin or rifaxmin
What does QHS mean
At bed time
What does QAC mean
with meals
What does QD
daily
What does QOD mean
every other day
efudex
fluorouracil topical
Lexapro
Escitalopram
Victoza
Liraglutide
What is liraglutide
activates glucagon-like-peptide-1 (GLP-1) receptor, increasing insulin secretion, decreasing glucagon secretion, and delaying gastric emptying (incretin mimetic)
Also helps with weight loss
Glucosamine Sulfate
A dietary supplement not a drug. Used to help prevent joint degeneration
Name the rapid acting insulin
Lispro,
Aspart,
Glulisine,
Onset in 15 - 30 minutes
Regular (30 minutes - 1 hour)
Name the intermediate acting insulin
NPH;
Onset in 1-2 hours
Name the long acting insulin
Glargine (onset in 4-6 hours)
Detemir (onset in 3-4 hours)
Used for basal insulin control
When should a sliding scale insulin be used
In patients with only intermittent minor BG elevations
How often should insulin be measured in patients taking insulin
at least 4 times per day;
Preprandially and at bed time
What is tested for when looking for ketones associated with DKA
b-hydroxybutyrate in the serum;
urine ketones are also often present
What are the big 3 that is used in the treatment of DKA
Fluids
Insulin
Potassium
If a patient has DKA and is hypotensive, how is their fluid load
greater 10% loss of fluids
What are major classes of T2DM
Metformin, insulin secretagogues, DPP IV Inhibitors, GLP mimetics, TZD's,
All are effective with in days to weeks except TZD’s which may take weeks to months
First line treatment for T2DM
BG 200 combination therapy and possibly insulin
What are the insulin secretagogues
SFU's, Non SFU's, Biguanides, a-glucosidase inhibitors, TZD's, DPP-4 Inhibitors, Bile Acid sequesterants, Dopamine receptor agonist, GLP agonist
What is the mechanism of SFU’s
Increase insulin secretion by binding to specific receptors in B cells. Must be taken 30 - 60 minutes before meals to prevent hypoglycemia
What is contraindication for glyburide
Impaired renal function and used with caution in the elderly
Name the non SFU’s
Repaglinide,
Nateglinide
Name the biguanides
metformin
Name the a-glucosidase inhibitors
acarbose
miglitol
Name the thiazolidinediones
Rosiglitazone
Pioglitazone
Name the DPP 4 inhibitors
Sitagliptin
Saxagliptin
Vildagliptin
Name the bile acid sequestrants used in the treatment of T2DM
colesevelam hydrochloride
Name the dopamine agonist used in the treatment of T2DM
Bromocryptine Mesylate
Name the GLP Agonist
Exenatide
Name the amylin analogues
Pramlinitide acetate
What are the common side effects of SFU’s
hypoglycemia and weight gain
What are the common side effects of Non SFU’s
Hypoglycemia and weight gain
less severe than the SFU’s
What are the main adverse side effects of Biguanides
Diarrhea
nausea
abdominal pain or cramping
Lactic acidosis
What are the main adverse side effects of TZD’s
Weight gain, edema
CHF
anemia,
increased fractures in women
What are the main adverse side effects of sitagliptin
Angioedema,
Steven-Johnson syndrome,
URI
What are the main adverse side effects of saxagliptin
urticaria
facial edema
URI
What are the main adverse side effects of bile acid sequestrants
constipation
reduced absorption of some medications
What are the main adverse side effects of dopamine agonist
Nausea asthenia dizziness headache constipation diarrhea
What are the main adverse side effects of GLP agonist
Nausea
vomiting
GI distress
pancreatitis
What are the main adverse side effects of Amylin analogues
Nausea vomiting diarrhea headache hypoglycemia
What is the mechanism of metformin
inhibits hepatic glucose output and stimulates glucose uptake in peripheral tissues
What is the mechanism of a-glucosidase inhibitors
Block polysaccharide and disaccharide breakdown and decrease postprandial hyperglycemia when administered with food.
What are the main adverse effects of the a-glucosidase inhibitors
gas
bloating
diarrhea
abdominal pain
What is the mechanism of the TZD’s
increase insulin sensitivity in muscle, adipose tissue and liver.
When is TZD’s contraindicated
compromised cardiac function NYHA Class 3 and 4
What is the mechanism of DPP 4 inhibitors
Blocks the enzyme that breaks down endogenous GLP, which is an incretin secreted from the intestinal L cells. Increased levels of GLP reduce BG concentration by inhibiting glucagon secretion from the pancreatic alpha cells and by stimulating insulin secretions
What is the mechanism for GLP agonist
peptides are structurally similar to GLP-1 but resist breakdown by DPP enzyme. Have a longer half life than native FLP 1 and reach higher blood and tissue levels
What is the treat of NKHS
- correct the fluid imbalance
- electrolyte replenishment (potassium)
- Gradual correction of hyperglycemia with fluid and insulin
What are some complications of NKHS
Thromboembolic events
cerebral edema
adult respiratory distress syndrome rhabdomyolysis
What is the problem with correcting hyperglycemic episodes too rapidly
osmotic encephalopathy
What is the main purpose of controlling BG in DM
prevention of chronic microvascular insufficiency
- Diabetic Retinopathy
- Diabetic Neuropathy
- Diabetic Nephropathy
Prevention of chronic macro vascular insufficiency
- CHD
- PVD.
Miscellaneous Complications
- Erectile Dysfunction
- Diabetic Foot Ulcers
What is heart failure
A clinical syndrome in which either structural or functional abnormalities in the heart impair its ability to meed the metabolic demands of the body
What are the two classes of heart failure
Systolic dysfunction
Diastolic dysfunction
What are the stages of heart failure
- Asymptomatic
- Mild symptoms (mild SOB/Palpitations with physical activity)
- Marked limitations in activity (walking 20-100 meters)
- Severe limitations (at rest)
What are the classes of heart failure
A. No structural disease/ symptoms. Has risk factors
B. Abnormal LV systolic function
C. Structural heart dz and HF symptoms
D. Refractory heart failure symptoms to max medical management
What are the initial labs for suspected HF
CBC CMP Fasting lipid profile Urinalysis Thyroid function BNP (>400 to rule in <100 to rule out)
What is a concern when using vasodilators with HF patients
patients with a fixed cardiac output (aortic stenosis or HCM or with a predominately diastolic dysfunction)
What is the medical mainstays for HF treatment
Beta blockers
Vasodilators
Diuretics (for volume overload)
Why do ARB’s not cause cough and angioedema.
ACE’s will increase bradykinin while ARB’s will not.
How are ACE inhibitors excreted
through the kidneys… need to titrate the dose for renal insufficiency
How do nitrates reduce cardiac ischemia
decreasing ventricular filling pressures and by directly dilating coronary arteries
How does nitroprusside work
Primarily an arterial vasodilator with less potent vasodilatory properties
What diuretic is useful for patients with a low GFR
Metolazine
Its actions are are at the proximal as well as the distal tubule. It may be used in combination with a loop
What are some common side effects of loops
hyperuricemia hypocalcemia ototoxicity rash vasculitis
Remeron
Mirtazipine
What is primary bilary cirrhosis
autoimmune disease of the liver marked by the slow progressive destruction of the small bile ducts (bile canaliculi) within the liver. When these ducts are damaged, bile builds up in the liver (cholestasis) and over time damages the tissue
Keflex
Cephalexin (1st generation cephalosporin)
Xenical
Orlistat
Inhibits gastric and pancreatic lipases, reducing fat absorption
Actos
Pioglitazone
Flexeril
Cyclobenzaprine
glucotrol
glipizide
Tikosyn
Dofetilide (anti arrhythmic: prolongs action potential during phase III)
What is a cox maze procedure
is a type of heart surgery for atrial fibrillation. May use a less invasive minimaze procedure too.
Livalo
Pitavastatin (reduced myalgia than other statins)
Tofranil
Imipramine (Tricyclic antidepressant)
Penlac
ciclopirox topical
Fioricet
butalbital + acetamenaphen + caffeine
What are the major classes of valvular heart Disease
Mitral Stenosis (MS) Aortic Stenosis (AS) Mitral Regurgitation (MR) Aortic Regurgitation (AR)
What is the predominant cause of MS
Rhuematic
What is the pathophysiology of MS
increase in the transvalvular flow (CO) or decrease in diastolic filling time (tachycardia)
What is the clinical presentation of MS
physical exam may have an:
- opening snap (OS)
- Mid diastolic rumble
With regards to MS what does the OS-A2 time duration signify
the duration is inversely proportional to the severity.
The shorter the duration, the more severe the stenosis
With regards to MS what does the duration of the murmur signify
The duration of the murmur is directly related to the severity of the stenosis.
The longer the murmur the more severe the stenosis
What are some diagnostic testing for MS
EKG CXR TTE (candidacy for PMBV) Exercise testing with echo TEE Cath
What will an EKG show for MS
ECG will have P-wave duration greater than 0.12 secs
What are the findings for severe MS
Mean gradient > 10 mmHg
PASP > 50 mmHg
Valve area less than 1 square cm
What is the treatment for MS
Medically - decrease Pulmonary HTN
AFIB - high risk of AFIB (30-40% of patients)
PMBV
Surgery
What is the survival with severe pulmonary HTN
mean survival is 3 yrs
How common is AS
2% over age 65
4% over age 85
What causes AS
Calcific/degenerative disease (most common in US)
Bicuspid
Rheumatic (most common world wide)
What is the history in a patient with AS
Classic triad of:
- Angina
- Syncope
- HF
What are the physical exam findings of AS
- Harsh crescendo/decrescendo murmur heart best at the apex
- Diminished or absent A2
- Opening snap suggest Bicuspid valve
- S4 reflects poor compliant ventricle
- Pulsus parvus et tardus (late peaking and diminished carotid upstroke in Severe AS)
What diagnostic testing is used for AS
- EKG
- CXR
- TTE
What findings signify severe AS
peak jet velocity > 4 m/s
Mean gradient > 40 mmHg
Valve area less than 1 square cm
Patients maybe asymptomatic until the valve area is less than 1 cm. Once symptomatic, average survival is 2-3 years with high risk of sudden death
What is the treatment for AS
Only surgery… no medical treatment
Severe AS is a deadly disease
What are the two types of MR
Organic - caused primarily by lesions to the valves and or chord tendonae;
Functional - caused primarily by ventricular dysfunction ussually with accompanying annular dilation
What causes MR
DCM
Degenerative Dz
Ischemic (post infarct)
Rheumatic
What is the presentation of a patient with MR
SOB
Palpitations
fatigue
What are the physical exam findings of a patient with MR
Tachycardia
Systolic murmur usually at the apex
S2 maybe widely split due to an early A2
What is the treatment for MR
Medically:
While awaiting treatment,
aggressive afterload reduction;
Percutaneous;
Surgery (repair is more common than replacement; no surgery for DCM)
What are common causes of AR
Rheumatic
Calcification
Bicuspid
What are the physical exam findings of AR
Tachycardia
Wide pulse pressure
Brief diastolic murmur heard best at Erb’s point
Austin Flint murmur (low pitch rumbling presystolic)
What is the treatment for AR
Medical tx is limited (reducing HTN or antibiotics for infective endocarditis);
Surgery (the aortic root may need to be prepared at the same time as the valve)
What are the common prosthetic valves
Bileaflet is the most common mechanical.
Anticoagulation is required for a mechanical replacement.
Bioprosthetic (bovine or porcine)
Homograft is rarely used
What is CAD
Greater 50% luminal stenosis of any epicardial coronary artery
What is the leading cause of morbidity and mortality in the western society
CAD
What causes CAD
results from luminal obstruction by atheromatous plaque
What percentage of stenosis is generally required to generate Angina
Greater 70% stenosis
What are some risk factors for CAD
HTN; DM (2-4 times greater incidence); Obesity; Dyslipidemia; Family history; Smoking
When do we begin screening for CAD
Begins at age 20 and 5 year intervals (Framingham study)
How do we prevent CAD
Screening;
High risk CV patients receive aspirin;
Statin for patients with elevated CRP;
Exercise (minimum of 30 minutes 5 days a week);
NOT INDICATED hormone replacement in postmenopausal women
What are the two types of Angina
Typical and atypical
What is typical angina
Includes all 3:
Substernal chest discomfort or heaviness;
precipitated by stress;
relieved by nitroglycerin
What is atypical angina
Includes 2 of the 3.
Substernal chest discomfort or heaviness; precipitated by stress;
relieved by nitroglycerin;
Non cardiac chest pain will only have 1 of the 3
How do we quantify angina chest pain
Canadian cardiovascular Society classification system;
CCS 1 - angina with strenuous activity;
CCS 2 - Angina with moderate activity (>2 blocks);
CCS 3 - Angina with mild activity (<2 blocks);
CCS 4 - Angina with any activity or at rest
What symptoms will be presented with CAD
Angina; dyspnea; Diaphoresis; nausea; vomiting; dizziness
Female patients or CKD or DM will present with what symptoms of CAD
Minimal or atypical symptoms;
dyspnea;
epigastric pain;
nausea
What is the diagnostic testing used for CAD
Stress testing; Excercise stress testing; Myocardial perfusion imaging Echocardiography imaging with stress; MRI
What is the bruce protocol
3 minute stages of increasing treadmill speed and incline.
BP, HR and ECG are monitored through the study and recovery period
What is the duke treadmill score
Exercise stress test:
Minutes exercised - (5 X maximum ST segment deviation) - (4 X angina Score);
0= no angina; 1 = angina that is not stress limiting; 2 = test limiting angina;
total score >5 use medical therapy;
total score -10 to 4 further testing; total score <-10 coronary angiography
What is the gold standard for CAD diagnosis
Coronary angiography
What is the major goal for treatment of patients with stable angina
prevent MI, cardiac death and to reduce symptoms
What are the medical treatment goals for CAD
improve myocardial oxygen supply, reducing myocardial oxygen demand, controlling exacerbating factors, and limiting the development of further atherosclerotic disease
What are the medical treatment options for CAD
Aspirin; B blockers; Calcium channel blockers (avoid short acting DHP's); Nitrates; Ace Inhibitors; Ranolazine; Cholesterol lowering agents (Statins)
What is ranolazine
a novel antianginal agent that does not depend upon reductions in HR or BP. Its exact mechanism of action is unknown:
however, it appears to have effect on cardiomyocyte metabolism and sodium ion channel function.
When should coronary revascularization be attempted
after 2 and preferably 3 antianginal agents have failed
When is PCI or CABG indicated
Angina refractory to medical therapy; Angina and reduced LV function; Severe activity limiting angina (CCS 3 and CCS 4);
Angina in the presence of left main or severe three vessel CAD
What type of revascularization is preferred in diabetic patients
CABG
What are the alternative procedures for CAD for patients that are unable to have PCI or CABG surgery
Transmyocardial laser revascularization;
Therapeutic angiogenesis
What is COPD
expiratory airflow limitation that is not fully reversible
What are two conditions largely associated with COPD
Emphysema;
Chronic Bronchitis
What is the pathology of emphysema
enlargement of the distal airways, destruction of the acinus and absence of associated fibrosis
What is the pathology of chronic bronchitis
productive cough on most days for at least 3 consecutive months per year for at least 2 consecutive years in the absence of other lung disease that could account for the symptoms.
When should you suspect an a-1-antitrypsin deficiency
minimal smoking;
early onset COPD;
family history of lung disease;
lower lobe predominant emphysema
What are the main pathophysiologic processes associated with COPD
- Inflammation;
- Imbalances of proteinases;
- oxidative stress;
- apoptosis
Where are the pathophysiologic changes found in COPD
central airways;
peripheral airways;
lung parenchyma;
pulmonary vasculature
What are the common symptoms of a patient with COPD
dyspnea; cough; sputum production; wheezing; Weight loss often occurs in end stage COPD
What are the physical exam findings of a patient with COPD
prolonged breath sounds (>6 secs on a maximalforced expiration); Decreased breath sounds; use of accessory muscles; Chest hyperresonance to percussion; Expiratory Wheezing
Is clubbing a feature of COPD
NO;
presence should prompt an evaluation for other conditions, especially lung cancer
What are treatment options for smoking cessation
- Nicotine replacement;
2. Nonnicotine pharmacotherapy
What are the nicotine replacement options
- transdermal patch
- Oral (chewing gum, lozenges, inhaler)
- Nasal Spray
What are the non-nicotine pharmacotherapy options
- Bupropion ER (Zyban)
2. Varenicline (Chantix)
What diagnostic testing is used in the diagnosis of COPD
Pulmonary function testing
How is the severity of COPD scaled
GOLD classification (Global strategy for diagnosis, management and prevention of COPD)
What is required for the diagnosis of COPD
expiratory airflow limitation on spirometry, defined as a forced expiratory volume in the first second/forced vital capacity (FEV1/FVC) to be less than 0.70
What are the stages in the GOLD classifications
All stages have FEV1/FVC ratio less than 0.70; Stage I - Mild: FEV1 > 80% predicted; Stage 2 - Moderate: 50 - 79% predicted; Stage 3 - Severe: 30-49% predicted; Stage 4 - Very Severe: <30% predicted
What labs should be ordered to monitor COPD
ABG;
bicarbonate;
CBC
What is significant with a CBC for COPD
polycythemia may reflect a physiologic response to chromic hypoxemia and inadequate supplemental oxygen use.
What is the only proven chronic medical therapies proven to increase survival in COPD
smoking cessation and the correction of hypoxemia with supplemental oxygen
What is the stepwise approach to COPD therapy
Mild:
smoking cessation,
vaccination, and
short acting B agonist prn;
moderate:
all mild + long acting bronchodilators and
pulmonary rehabilitation;
severe:
all moderate + inhaled corticosteroids if repeated exacerbations.
Oxygen if needed;
Very severe:
all severe + considerations for surgical treatment
Name the short acting beta agonist used for COPD
Albuterol;
Levalbuterol (Xopenex);
Pirbuterol (Maxair)
Name the long acting beta agonist used for COPD
Salmeterol (Serevent);
Formoterol (Foradil);
Arformoterol (Brovana)
Name the anticholinergics used for COPD
Ipratropium (Atrovent);
Tiotropium (Spiriva)
What should be accompanied with an inhaled bronchodilator
proper use of an MDI (metered dose inhaler)
Are steroids indicated for COPD
Yes.;
Inhaled corticosteroids;
Systemic corticosteroids are used in patients with severe disease that are not responding to other therapies
How is the use of supplemental oxygen determined
A room air resting ABG is the gold standard for determining supplemental O2;
PaO2 < 55 mmHg; SaO2 < 80%; SaO2 < 92% and (pulmonary HTN, Polycythemia, or HF)
How will the CBC indicate polycythemia
hematocrit > 55%
How is a lung transplant indicated in COPD
BODE score
What is an acute exacerbation of COPD
increased dyspnea, often accompanied by increase cough, sputum production, sputum purulence, wheezing, chest tightness or other symptoms and signs in the absence of other pathology
When is hospitalization indicated for COPD
significant increase in symptom severity;
significant comorbidities;
failure to respond to initial medical management;
insufficient home support
When is the ICU indicated for COPD
invasive mechanical ventilation; hemodynamic instability; severe dyspnea; mental status changes; persistent worsening hypoxemia, hypercapnia or respiratory acidosis
What symptoms will Asthma patients have
paroxysms of cough;
dyspnea;
chest tightness;
wheezing
What are the mechanisms that asthma classified
based on the level of impairment;
Risk;
responsiveness to treatment
How is asthma classified on initial assesment
Intermittent (Day 2 week, night 3-4 month); Moderate Persistant (daily, >1 week); Severe persistent (continous during day, and night)
how is asthma control staged
Well controlled (similar to intermittent);
not well controlled (similar to mild persistent);
very poorly controlled (similar to severe persistent)
What is the leading chronic illness among children
Asthma (20-30%)
What are some factors that contribute to the development and persistence of asthma
Severe viral infection early in life, particularly RSV and rhyinovirus
What is the pathophysiology of asthma
Characterized by airway obstruction, hyperinflation, and airflow limitations resulting from:
chronic airway inflamation by activated eosinophils;
Bronchial smooth muscle contraction;
epithelial damage;
airway remodeling
What are the physical findings of asthma
wheezing;
prolonged expiratory phase;
During respiratory distress peak airflow <25%
How is asthma diagnosed
Severe distress or FEV1 < 40% predicted;
PaO2 < 60 mmHg;
PFT with improvement of >12% after bronchodilator;
heightened airway responsiveness to a methacholine;
challenge (drop in FEV1 of 20%)
How is the severity of asthma exacerbation classified
Mild: PEF or FEV1>70%;
moderate: PEF or FEV1 40-69;
Severe: PEF or FEV1 <25%
How do treat asthma
Initiate treatment at the highest level that occurred over the last 2-4 weeks.
Recheck every 3 months to step down treatment as necessary
What are the primary step wise treatment options for asthma control
PRN: Short acting bronchodilators; Step 1: None; Step 2: Low dose ICS; Step 3: Low dose ICS +LABA; Step 4: Medium dose ICS + LABA; Step 5: High dose ICS + LABA; Step 6: Add OCS to step 5
What are some alternative treatment options for asthma control
Leukotriene modifiers; Cromolyn sodium; Anti IgE therapy (omalizumab); Methylxanthines; IV Mag sulfate; Inhaled heliox
What are the leukotriene modifiers
Leukotriene receptor antagonist (LTRA's): Montelukast; zafirlukast; 5-lipoxygenase inhibitor; zileuton
When should a LTM be considered for initial therapy
patients with aspirin sensitive asthma or for individuals who cannot master the use of an inhaler
What are side effects of SABA
tremor; anxiety; tachycardia; decrease in serum potassium and magnessium;
mild lactic acidosis;
prolonged QT
What are side effects of ICS
oral thrush and systemic effects;
patients should be instructed to rinse their mouth after use.
What are the side effects of LTM
churg-straus vasculitis;
Ziuleten can cause a reversible hepatitis
How do patients monitor their asthma at home
max PEF;
Green is 80-100;
Yellow is 50-79;
Red is <50
What is the sign called of a clinched fist over the heart
Levines sign. A symbol of ischemic chest pain
What is tissue connecting the septum to the wall of the right ventricle
…
What are the two major classes of IBD
Ulcerative colitis;
Crohns disease
Where is the inflammation in ulcerative colitis
Limited to the colon and the rectum. Inflammation is limited to the mucosal lining.
Where is the inflammation in crohns disease
transmural inflammation in any part of the entire GI tract
What is the presentation of IBD
diarrhea;
weight loss;
abdominal pain
Crohns disease can also present with
fistula formation; strictures; abscesses; bowel obstruction
How is IBD diagnosed
Endoscopy is the preferred method.
CT and MRI scans;
Serologic markers
What will differentiate crohns disease from UC histopathologically
UC: Chronic mucosal inflammation with crypt abscess and cryptitis;
Crohns: multinucleated giant cells and noncaseating granulomas in CD
What are the serologic markers used to distinguish UC from Crohns
CD: Anti-Saccharomyces cerevisiae antibodies;
UC: pANCA (perinuclear antineutrophil cytoplasmic antibodies)
How is treatment determined for IBD
Based on the severity of the symptoms
How is the severity of disease classified for IBD
Mild;
Moderate;
Severe