Internal Med 1

Front 1

Reduction in the amount of air exhaled forcefully in the first second of the forced exhalation (FEV1) may reflect what?

Back 1

- reduction in the maximum inflation of the lungs (TLC)
- obstruction of the airways (most common)
- respiratory muscle weakness

Front 2

Systolic Heart Failure: Defined as? 3

Back 2

impaired cardiac contractile function
- with reduced Left Ventricular Ejection Fraction (LVEF)
- chamber dilation
- defined as LVEF less than 50%

Front 3

Diastolic HF?

Back 3

abnormal cardiac relaxation, stiffness or filling
- normal Left Ventricular Ejection Fraction (LVEF) or > 50%
- diastolic dysfunction

Front 4

What is the average Left Ventricular Ejection Fraction for a healthy adult population?

Back 4

60 to 70% with the lower boundary being 55%

Front 5

Events during diastole?

Back 5

- Diastole begins with the relaxation of the contracted myocardium.

1. Isovolumic relaxation — the period between aortic valve closure and mitral valve opening during which LV pressure declines with no change in volume.

2. Auxotonic relaxation — During the period of auxotonic relaxation the LV fills at variable pressure beginning with mitral valve opening and ending by mid diastole in normal individuals and most patients.

Front 6

Chamber Remodeling found in diastolic HF? 4

Back 6

1. A normal or near-normal end-diastolic volume

2. Increased wall thickness and/or LV mass

3. An increased ratio of myocardial mass to cavity volume

4. An increased relative wall thickness (RWT).

Front 7

Potential triggers for decompensated DHF include 8

Back 7

Uncontrolled hypertension
Increased salt and water intake and/or retention
Tachyarrhythmias
Ischemia
Chronic kidney disease
Anemia
Chronic lung disease
Infection

Front 8

What are some things that may cause diastolic HF? 4

Back 8

1. Chronic hypertension with concentric remodeling.

2. Coronary artery disease and myocardial ischemia.

3. Valvular aortic stenosis.

4. Hypertrophic cardiomyopathy

5. Ischemia - demand ischemia, created by an increase in energy utilization that outstrips the available supply; (exercise)and supply ischemia, created by a primary decrease in myocardial blood flow (blockage)

6.

Front 9

Clinical manifestations of heart failure (HF) include 9

Back 9

1. dyspnea on exertion
2. paroxysmal nocturnal dyspnea
3. orthopnea
4. elevated jugular venous pressure
5. pulmonary rales
6. lower extremity edema
7. elevated brain natriuretic peptide (BNP)
8. N-terminal pro-BNP (NT-proBNP) levels
9. radiographic evidence of pulmonary edema

Front 10

What should be given to all patients suspected of an acute coronary syndrome without contraindication?

Back 10

1. Aspirin 160-325 mg on arrival and continue daily aspirin at 81 mg per day.
- Clopidogrel can be given to those with aspirin allergy.
2. ECG
3. Lab draw for Troponins, repeat 6 and 12 hrs =>elevated in both STEMI and NSTEM

Front 11

Typically presents with "tearing" pain radiating to back.
Smoking is a risk factor, but the two biggest risk factors are being over 60 and having hypertension.

Back 11

Aortic Dissection

Front 12

Typically worsened with inspiration and is constant.
Hallmark: alleviation of chest pain with position change from the supine to the sitting and leaning forward position. (Not typically exertional pain.)

Classic ECG findings are diffuse concave-upward ST segment elevations and a depressed PR segment. However, these findings are often transient and may not be present at all.

Back 12

Pericarditis

Front 13

Tobacco use
Exertional chest pain
Dyspnea
nausea, as well as other symptoms such as belching, indigestion, dizziness, and fatigue.
These are sx of what?

Back 13

Unstable Angina and Acute MI

Front 14

Should a normal ECG and troponins in the presence of chest pain change your opinion about unstable angina/ACS?

Back 14

A normal ECG in the presence of chest pain should not really change your opinion about unstable angina/ACS, and really only suggests that the patient has not had an MI in the past.

Normal troponins this early in an MI may also be expected, since a rise does not usually occur until four to six hours after the infarct.

Front 15

- substernal chest discomfort (Typically not exertional nor associated with dyspnea)
- Nausea
- mild epigastric tenderness on exam

What is this?

Back 15

GERD

Front 16

Sharp chest pain and dyspnea are frequent presenting complaints

Smoking

ECG is abnormal in 70% of patients

Two most common abnormalities - sinus tachycardia and nonspecific ST and T-wave changes

What is it?

Back 16

Pulmonary Embolism

Front 17

Stable angina ?

Back 17

Stable angina describes symptoms that have been occurring chronically and are predictable with exertion. It is thought to be caused by a stable atherosclerotic plaque.

Front 18

Unstable angina?

Back 18

Unstable angina is when the chest pain occurs at rest, is new, is increasing in frequency, or when its onset is triggered with a lower level of exertion. Unstable angina is caused by an unstable plaque that has ruptured and caused a non-occlusive thrombus.

Front 19

Acute MI results from?

Back 19

Acute MI results from rupture of an unstable plaque with subsequent occlusive coronary artery thrombosis and myocardial necrosis.

Front 20

Criteria for acute MI:

Back 20

Rise and fall of troponin or creatine kinase myocardial band (CK-MB) plus ONE of the following:

- Symptoms consistent with myocardial ischemia

- Electrocardiogram changes indicating myocardial ischemia (ST-segment elevation or depression)

- New pathologic Q waves

- Findings on percutaneous coronary intervention (PCI)

Front 21

Acute Management of Unstable Angina?

Back 21

1. Sublingual nitroglycerin
2. Beta Blocker - dec oxygen demand
3. Aspirin
4. Heparin
5. Angiography with PCl
6. Statin

Front 22

Inferior infarction is typically associated with?

Back 22

right coronary artery lesion

Front 23

Anterior or lateral infarctions are usually associated with?

Back 23

circumflex and LAD occlusions

Front 24

Complications of MIs?

Back 24

Complications of acute myocardial infarction include:

-arrhythmias (bradyarrhythmias and tachyarrhythmias)
-reduced ventricular function
-cardiogenic shock
-papillary muscle dysfunction with acute valvular dysfunction
-ventricular free wall rupture
-recurrent thrombosis

Front 25

When should ACE inhibitors be started after an MI?

Back 25

ACE inhibitors started within the first 24 hours of acute MI with ST-segment elevation in 2 anterior precordial leads or in those with clinical heart failure in the absence of hypotension (systolic BP < 100 mm Hg)

However, Mr. Monson does not have clinical heart failure or anterior MI so an ACE inhibitor is not indicated at this time.

Front 26

What drugs should be started in a pt suspected of having acute coronary syndrome?

Back 26

1. Aspirin - 160 to 325 mg, immediately upon presentation and continue daily aspirin at a dose of 75 to 325 mg/day.

2. Clopidogrel should be continued for a year after stent placement in addition to aspirin to prevent stent thrombosis.

3. β-adrenoceptor blockers should be started early in all patients with suspected ACS - Begin with oral β-blockers within a few days of the event, if not begun acutely, and continue them indefinitely. Goal heart rate is <70 and blood pressure <130/80.

4. HMG CoA reductase inhibitors (statins) (D) should be started while in the hospital in patients with ACS with a target LDL of <100.

5. Sublingual nitroglycerin should be sent home with patients post-admission.

Front 27

Leads V1-V4 ?

Back 27

reflect the anterior wall

Front 28

Leads II, III and AVF ?

Back 28

reflect the inferior portion of the heart

Front 29

Leads I, AVL, V5 and V6 ?

Back 29

correspond to the lateral myocardial wall

Front 30

Hyperbilirubinemia post hepatic causes?

Back 30

- obstruction of the bile drainage (extrahepatic cholestasis)

1. gallstones
2. tumors
3. primary sclerosing cholangitis
4. neoplasms
5. pancreatitis.

Front 31

Hyperbilirubinemia intrahepatic causes?

Back 31

1. Gilbert's disease
2. inflammation that disrupts bilirubin transport or due to hepatocyte dysfunction. This can be acute, as in the case of toxin injury, ischemic injury, drug injury, or acute viral hepatitis. It can be chronic, as is the case in chronic viral hepatitis, alcoholic hepatitis, Wilson's disease, hemochromatosis, non-alcoholic steatohepatitis, alpha-1-antitrypsin deficiency, and autoimmune hepatitis. There are two rare hereditary conditions that cause decreased excretion of bilirubin from hepatocytes: Dubin-Johnson syndrome and Rotor's syndrome.
3. Stasis of bile within the small bile ducts (intrahepatic cholestasis) can be caused by primary biliary cirrhosis, primary sclerosing cholangitis, drugs or toxins, granulomatous diseases, sepsis, pregnancy, viral or alcoholic hepatitis, malignancy, graft vs. host disease, or liver transplant.

Front 32

What is Gilbert's disease? When does it cause problems?

Back 32

decrease in the enzyme glucuronosyltransferase that leads to decreased hepatocyte uptake of heme.

Bilirubin in Gilbert's disease tends to increase during stress, illness and fasting.

Front 33

When does acetaminophen occur?

Back 33

toxicity can occur with acetaminophen doses of > 4 grams/day, although most cases occur in patients taking > 10 grams.

Front 34

"Which of these medications commonly cause elevated aminotransferases?" 4

Back 34

1. Statins
2. Phenytoin
3. Isoniazid
4. Carbamazepine

Front 35

What are the risk factors for NASH? Non-Alcoholic Steatohepatitis

Back 35

1. Obesity
2. DM
3. Hyperlipidemia

Front 36

Which of the following are genetic liver diseases that should be in the differential diagnosis of elevated aminotransferases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT])? 3

Back 36

1. Hemochromatosis

2. Wilson's disease

3. Alpha-1 antitrypsin deficiency

Front 37

1

Back 37

Hemochromatosis is a genetic multi-organ iron deposition disorder. It is associated with bronzing of the skin, diabetes, liver disease, heart failure, hypogonadism, and arthritis. All of these symptoms are due to an autosomal recessive genetic defect of the HFE gene. It occurs with a frequency of 5:1,000 in patients of European descent.

Associated findings: Hemochromatosis is associated with an extremely elevated ferritin level (>1000 ng/mL), but ferritin is an acute-phase reactant (meaning it will increase with any acute stress on the body).

Screening: The initial screen should measure transferrin saturation, calculated by dividing the serum iron by the total iron-binding capacity. A percentage greater than 45% is very suggestive.

Diagnosis: The currently recommended, noninvasive way to confirm the diagnosis is with genetic testing. In the past, liver biopsy was required, but this has been largely replaced with genetic testing.

Front 38

11

Back 38

Wilson's disease is a genetic disorder of biliary copper excretion leading to copper deposition in the liver and other organs.

Associated findings: It usually presents in the young adult with asymptomatic elevation of liver enzymes and can progress to neuropsychiatric changes as the patient ages. Kayser-Fleischer rings are usually seen on eye examination.

Screening: The initial screening test is ceruloplasmin which should be decreased.

Diagnosis: The next test to evaluate would be a 24-hour urinary copper with the final confirmatory test being a liver biopsy. Too many genetic defects make genetic testing currently not feasible.

Front 39

1

Back 39

Alpha-1 antitrypsin deficiency is a cause of emphysema in the young. It is also a rare cause of elevated liver enzymes.

Associated findings: It is associated with a low level of the alpha-1 antitrypsin enzyme.

Diagnosis: Genetic tests confirm the condition.

Front 40

Calculate CL?

Back 40

CL = (0.693 X Vd) / T1/2

Front 41

First line medication for trigeminal neuralgia? Mechanism?

Back 41

Carbamazepine - depresses nuc ventralis of the thalamus and limits influx of sodium ions

Front 42

Valgus stress on the knee means?

Back 42

The distal foot going lateral. - testing medial collateral ligament.

Front 43

Varsus stress on the knee means?

Back 43

The distal foot going medial and testing the lateral collateral ligament.

Front 44

What is Behcet syndrome?
Associated with?
Treated with?
Pathophysio?

Back 44

oral and genital ulcers + uveitis + joint arothopathy + panniculitis (erythema nodosa) = inflammation of subcutaneous fat layers

- HLA - B51

- TNF inhbitors and corticosteroids are used to treat

- Pathophysio = activation of complement by circulating antibody complexes

Front 45

A man with schizophrenia presents with milk from his nipples...what drug could cause this as a side effect?

Back 45

Haloperidol = dopamine antagonist that inhibits the pituitary gland that could cause hyperprolactemia.

Front 46

If a baby is lacking in T cells what will happen?

Back 46

Example: DiGeorge Syndrome.
- viral and fungal infections (more intracellular infections)

Front 47

If a child has dec plasma cells or B cells...what happens?

Back 47

More extracellular bacterial infections with polysaccharide capsules => Strep. pneumoniae, H. influnzea, and Neisseria meningitis)