Internal Medicine

Question 1

The first step in evaluating a patient presenting with chest pain is a ——— to look for ———

Answer 1

12-lead ECG

ST segment elevation

Question 2

Chest pain observed with MI/angina

Answer 2

Substernal or left-sided chest heaviness, pressure, or pain, typically radiating to the left arm, shoulder, or jaw. Often described as “an elephant sitting on my chest.” Commonly accompanied by diaphoresis or dyspnea.

(A key question to ask is does the chest pain worsen with exertion and get better with rest.)

Question 3

Chest pain observed with pericarditis

Answer 3

Chest pain radiating to the shoulder, neck, or back; worse with deep breathing or cough (pleuritic); relieved by sitting up and leaning forward.

Question 4

Chest pain observed with aortic dissection

Answer 4

Severe chest pain radiating to the back, can be associated with unequal pulses or unequal blood pressure in right and left arms. Often described as a “tearing” pain.

Question 5

Chest pain observed with Thoracic abscess or mass

Answer 5

Often sharp, localized pain; can be pleuritic.

Question 6

Chest pain associated with Pulmonary embolism

Answer 6

Often pleuritic. Frequently associated with tachypnea and tachycardia.

Question 7

Chest pain associated with Pneumonia

Answer 7

Pleuritic, frequently associated with cough, sputum, and hypoxia if severe.

Question 8

Chest pain observed with GERD/esophageal spasm/tear:

Answer 8

Burning pain, midline, substernal; may be associated with dysphagia. Pain made worse with lying flat, certain foods, accompanied by a bitter taste in the mouth known as “water brash.” May be similar to pain of MI.

Question 9

Chest pain observed with Costochondritis/musculoskeletal:

Answer 9

Sharp, localized pain with reproducible tenderness (touch chest wall and feel the pain); often exacerbated by exercise (second or third costochondral junction inflammation, aka Tietze syndrome).

Question 10

Chest pain isn’t the only presentation of MI—women often only complain of (2) as their “anginal equivalent.”

Answer 10

nausea or dizziness

Question 11

MI can be silent, particularly in people with ———, due to ——— or ———, due to ———.

Answer 11

diabetes, due to neuropathy

transplanted hearts, due to denervation

Question 12

Stable angina:

Answer 12

A chronic, episodic, predictable pain syndrome due to temporary myocardial ischemia. The pattern of pain is similar to that of acute MI, but resolves with rest or medication. Doesn’t change (i.e., it’s stable).

Question 13

Stable angina: Treatment

Answer 13

Beta blocker (reduces myocardial oxygen demand), aspirin, nitroglycerin.

Question 14

Patients with angina can benefit from ——— such as ——— to help control symptoms.

Answer 14

long-acting nitrates

isosorbide mononitrate

Question 15

Prinzmetal angina (variant angina) due to:

Answer 15

coronary vasospasm, not linked to exertion

Question 16

Prinzmetal angina (variant angina) Treatment

Answer 16

Calcium channel blockers and nitrates to reduce vasospasm.

Question 17

Prinzmetal angina (variant angina)
Distinguished from unstable angina by

Answer 17

chronic, intermittent nature

Question 18

Prinzmetal angina (variant angina)
pain usually occurs

Answer 18

at a specific hour in the early morning.

Question 19

With Prinzmetal angina (variant angina), coronary vessels are

Answer 19

normal (no stenosis or plaques)

Question 20

With Prinzmetal angina (variant angina), ECG may show

Answer 20

transient ST elevations

Question 21

Coronary vasospasm can be seen in oncology patients being treated with

Answer 21

5-fluorouracil

Question 22

A 62-year-old smoker presents complaining of 3 episodes of severe chest heaviness this morning. Each episode lasted 3 to 5 minutes, but he has no pain now. He has never had this type of pain before.

Answer 22

Think: Unstable angina.

Question 23

A middle-aged woman comes to the emergency room (ER) with severe chest pain and ST elevations on ECG. She is rushed for a cardiac catheterization, which shows no obstruction in her coronary arteries.

Answer 23

Think: Variant angina (aka Prinzmetal angina/vasospasm).

Question 24

For Vasospastic (formerly Prinzmetal or variant) angina, ——— is a risk factor; (2) are not.

Answer 24

Tobacco smoking

hypertension and hypercholesterolemia

Question 25

For Vasospastic (formerly Prinzmetal or variant) angina, Triggers include (3)

Answer 25

cocaine, alcohol, and triptans

Question 26

Acute coronary syndrome (ACS) refers to patients in whom there is suspicion or confirmation of

Answer 26

acute myocardial ischemia (lack of blood flow to the heart) or MI (which is ischemia lasting long enough or severe enough that it leads to heart muscle damage)

Question 27

ACS events are classified according to changes on the ECG:

Answer 27

1. Non-ST-elevation changes: This category includes non-ST-elevation myocardial infarction (NSTEMI) and unstable angina. 2. ST-elevation changes

Question 28

Contrast the two types of ACS with Non-ST-elevation changes:

Answer 28

Both NSTEMI and unstable angina have chest pain and ECG changes, but unstable angina has no troponin elevation. Unstable angina is associated with increased frequency and/or severity of symptoms, symptoms at rest, or new onset of symptoms compared to stable angina, which has stable chronic symptoms.

Question 29

Family history for coronary artery disease is a ——— in men, and ——— in women.

Answer 29

first-degree relative with an MI before age 40 in men, and before age 55 in women.

Question 30

Stable angina vs Unstable angina vs NSTEMI vs STEMI: Pain occurrence

Answer 30

Stable angina: on exertion Unstable angina: mild exertion or at rest NSTEMI: at rest STEMI: at rest

Question 31

Stable angina vs Unstable angina vs NSTEMI vs STEMI: troponin level

Answer 31

Stable angina: no elevation Unstable angina: no elevation NSTEMI: elevated STEMI: elevated

Question 32

Stable angina vs Unstable angina vs NSTEMI vs STEMI: infarction

Answer 32

Stable angina: none Unstable angina: none NSTEMI: Subendocardial STEMI: Transmural

Question 33

Stable angina vs Unstable angina vs NSTEMI vs STEMI: ecg changes

Answer 33

Stable angina: none Unstable angina: Possible ST depression and/or T-wave inversion NSTEMI: ST depression and/or T-wave inversion STEMI: ST elevation, pathologic Q waves

Question 34

——— is the cardiac biomarker most commonly used clinically given its specificity for myocardium.

Answer 34

Troponin I

Question 35

If you suspect ACS in patients, all patients should have “serial enzymes” drawn, which consists of

Answer 35

sending cardiac biomarkers every 6 to 8 hours for a 24-hour period

Question 36

Myoglobin vs CK-MB vs Troponin T/I: onset (hrs)

Answer 36

Myoglobin: 1-4 CK-MB: 3-12 Troponin T/I: 3-12

Question 37

Myoglobin vs CK-MB vs Troponin T/I: peak (hrs)

Answer 37

Myoglobin: 6-8 CK-MB: 18-24 Troponin T/I: 18-24

Question 38

Myoglobin vs CK-MB vs Troponin T/I: duration:

Answer 38

Myoglobin: 24 hours CK-MB: 3-4 days Troponin T/I: 7-10 days

Question 39

Myoglobin vs CK-MB vs Troponin T/I: specificity/utility

Answer 39

Myoglobin: nonspecific CK-MB: Its onset and peak are similar to troponin but it clears in 3 to 4 days as opposed to 7 to 10 seconds with troponin. Therefore, it is extremely useful in patients where reinfarction after an MI occurs or for restent thrombosis. Troponin T/I: Very sensitive and specific markers for cardiac muscle injury.

Question 40

Criteria for STEMI on EKG

Answer 40

2mm ST elevation or new LBBB (wide flat QRS)

Question 41

Patients presenting with ACS should be given ——— (unless contraindicated):

Answer 41

SNAP Statin – high-intensity statin Nitrate – sublingual or IV to control pain Aspirin – non-enteric-coated, preferably chewed, 162 to 325 mg P2Y12 inhibitors – clopidogrel or ticagrelor Morphine

Question 42

For patients presenting with ACS, ——— should be the last medication given. It may ——— and should only be given when a diagnosis of ACS is certain and the patient still has severe pain.

Answer 42

Morphine mask angina

Question 43

Troponin may also be slightly chronically elevated in

Answer 43

congestive heart failure (CHF)

Question 44

Troponin is ———, so levels may be elevated in the setting of ———

Answer 44

renally cleared renal insufficiency

Question 45

Supplemental oxygen will ——— in nonhypoxic patients with ACS.

Answer 45

not affect outcomes

Question 46

The symptoms associated with chest pain that have the highest relative risk for MI are (4)

Answer 46

radiation to upper extremity and association with diaphoresis, nausea, or vomiting

Question 47

Typical symptoms for any angina/MI:

Answer 47

Left-sided/substernal chest pressure (not usually pain) with radiation to the left shoulder, arm, or jaw. The patient may characterize this by putting a closed fist over the chest (Levine sign), shortness of breath, diaphoresis, nausea, or vomiting. Chest pressure is worse with activity and improves with rest or nitroglycerin sublingually.

Question 48

Atypical presentation of ACS: (list 6 sxs)

Answer 48

Up to one-third of patients with MI have no chest pain on presentation. Other symptoms patients will complain about are dyspnea, weakness, nausea, epigastric pain, palpitations, or syncope.

Question 49

Patients at risk for atypical ACS presentations are (2)

Answer 49

diabetics (may have neuropathy that blunts the sensation of pain) women

Question 50

Heparin effect on clotting:

Answer 50

does not dissolve already-present clots; rather, it prevents future ones from forming

Question 51

Prescription of Beta blockers after presentation for ACS? Contraindications? (3)

Answer 51

do not need to be given immediately, but rather, within the first 24 hours of ACS presentation acute heart failure, cardiogenic shock, and right ventricular MI

Question 52

Thrombolytics are not used in ———because 60% to 80% of the time the infarcted artery is not occluded.

Answer 52

unstable angina or NSTEMI

Question 53

Patients with ST elevations have better outcomes when ——— happens within ——— minutes of arrival. This is known as ———

Answer 53

revascularization 60 minutes door-to-balloon (DTB) time

Question 54

Patients treated with thrombolytics should still be transferred to a ———capable hospital, for ——— and in case ———

Answer 54

PCI angiography the thrombus reforms!

Question 55

Causes of ST elevation: (4)

Answer 55

• MI • Pericarditis • Left ventricular (LV) aneurysm • Early repolarization (young people)

Question 56

A 47-year-old man presents to the ER with left-sided chest pain at rest. He is a chronic smoker with a family history of diabetes and hypertension. On examination, he is found to have stable vitals. ECG showed new ST depressions in II, III, and aVF. ASA, Plavix, and nitrate were given, and the patient still complained of pain. Next step:

Answer 56

Start heparin drip and send patient for cardiac catheterization

Question 57

STEMI is typically caused by

Answer 57

complete occlusion of a coronary artery

Question 58

Txt STEMI:

Answer 58

Need urgent opening of the blockage in the coronary artery (revascularization). This can be done with 1) thrombolytics (medicines that break up clots: tenecteplase, alteplase, and reteplase) and/or 2) cardiac catheterization and stenting (PCI)

Question 59

In txt STEMI, ——— is superior to ———

Answer 59

Cardiac catheterization with PCI thrombolytics

Question 60

Contrindications for STEMI txt (cardiac catheterization with PCI/thrombolytics):

Answer 60

risks of bleeding, particularly in the brain, prior intracranial hemorrhage, stroke within 1 year, brain tumor, active internal bleeding, or suspected aortic dissection

Question 61

Unstable angina and NSTEM have similar pathogenesis, typically due to an ———. NSTEMI differs from unstable angina in that ———

Answer 61

incomplete occlusion of a coronary artery the lack of oxygen is severe enough to cause myocardial damage and enzyme leakage (unlike unstable angina, where there is no enzyme leakage)

Question 62

Treatment NSTEMI/unstable angina:

Answer 62

SNAP. Can treat with invasive treatment (cardiac catheterization) or conservatively (medications) based on risk factors (TIMI score). Ongoing chest pain and signs of cardiac dysfunction should prompt intervention.

Question 63

What is a TIMI score?

Answer 63

A scoring system used to evaluate the risks of patients with NSTEMI and determine if early invasive management (i.e., cardiac catheterization) is warranted. Each item is worth a point: • Age>65 • ≥ 3 CAD risk factors • Prior coronary stenosis > 50% • ST changes on ECG • ≥ 2 anginal episodes in 24 hours • Use of aspirin in prior week • Positive serum markers TIMI > 4: Patient should get invasive management.

Question 64

Cocaine can cause ——— changes with elevated ——— and ——— pain due to ———. Vasoconstriction, in addition to ——— and ———, can lead to a mismatch between oxygen supply and myocardial demand (do a urine drug screen if suspicious).

Answer 64

ECG cardiac enzymes chest severe vasoconstriction without plaque rupture or thrombus formation tachycardia hypertension

Question 65

If location of MI is anterior, involved artery and leads with ST elevation or q waves will be:

Answer 65

LAD V1-V4

Question 66

If location of MI is lateral, involved artery and leads with ST elevation or q waves will be:

Answer 66

Circumflex I, aVL, V4-V6 (Note: Lateral includes aVL)

Question 67

If location of MI is inferior, involved artery and leads with ST elevation or q waves will be:

Answer 67

RCA II, III, avF (Note: inferior includes aVF)

Question 68

If location of MI is right ventricle, involved artery and leads with ST elevation or q waves will be:

Answer 68

RCA V4 on R-sided EKG is 100% specific

Question 69

Lead ——— is the only standard ECG lead that looks directly at the right ventricle.

Answer 69

V1

Question 70

Significant timing elements for STEMI ECG changes over time:

Answer 70

ST elevation occurs “pretty much immediately” (minutes to hours) T wave inversion occurs “a little later”“6hrs-years” Pathological q waves markers of an old infarct “last pretty much forever”

Question 71

Txt STEMI to restore blood flow (Emergency reperfusion)

Answer 71

Cath lab (best) or *thrombolytics if no contraindications (and if catch within 6 hours or if can’t get them to cath lab)

Question 72

Contraindications for thrombolytic use in STEMI: (4)

Answer 72

Bleeding “Ever ever had” hemorrhagic stroke Recent ischemic stroke Recent closed head trauma (if fell off a horse and then had a MI - no thrombolytics!)

Question 73

Lead V1 is predominantly ——— in a normal ECG.

Answer 73

negative

Question 74

A tall R wave in V1 has its own differential: (7)

Answer 74

• RBBB • Posterior MI • Dextrocardia • Wolff-Parkinson-White • Duchenne muscular dystrophy • Right ventricular hypertrophy • And, of course, a normal variant

Question 75

——— is commonly referred to as dual antiplatelet therapy (DAPT). The duration of DAPT after ACS is still being investigated.

Answer 75

Aspirin with a P2Y12 inhibitor

Question 76

A 65-year-old woman with a history of CAD and drug-eluting stent (DES) placed 6 months ago presents with acute crushing chest pain. She says that she had stopped taking her Plavix 1 week ago for a dental procedure.

Answer 76

Think: Acute in-stent thrombosis. Next step: ECG (may show ST elevation; send for urgent cardiac catheterization).

Question 77

Medications to be continued indefinitely after ACS: (5)

Answer 77

Aspirin Beta blocker Angiotensin-converting enzyme (ACE) inhibitor in patients with resulting low cardiac function (decreased left ventricular ejection fraction [LVEF]). High-intensity statin (HMG CoA reductase inhibitor) Clopidogrel, prasugrel, or ticagrelor if a stent was placed. (Clopidogrel or ticagrelor for 12 months if no stent was placed.)

Question 78

Postinfarction complications: Ruptures usually occur within ———of a large MI; These can be in the —(3)—. These are very rare in the era of angiography with PCI

Answer 78

4 to 5 days free wall of the heart, the intraventricular septum, or the papillary muscle, which causes acute mitral regurgitation

Question 79

Postinfarction complications (Arrhythmias): (3)

Answer 79

VT usually within 48 hours (when the myocardium reperfuses) bradycardia (usually from inferior wall MI) atrioventricular block (can be from anterior wall or inferior wall MI)

Question 80

Postinfarction complications: Dressler syndrome usually occurs ——— after cardiac injury (MI or cardiac surgery). It is associated with —(3 sxs)—; likely a ——— process. Treat with —(2)—.

Answer 80

1 or 2 weeks fever, pericarditis, and sometimes pericardial or pleural effusions hypersensitivity NSAIDs and steroids

Question 81

A 58-year-old man who was discharged from the hospital after an MI 2 weeks ago presents with fever, chest pain, and generalized malaise. ECG shows diffuse ST-T wave changes.

Answer 81

Think: Dressler syndrome. Treat with NSAIDs.

Question 82

——— is the most common cause of anemia worldwide.

Answer 82

IDA

Question 83

IDA occurs due to decreased

Answer 83

iron stores resulting in decreased hemoglobin synthesis

Question 84

The most common causes of IDA are: (5)

Answer 84

blood loss menorrhagia in premenopausal women gastrointestinal blood loss hookworm infection in tropical areas malnutrition/malabsorption (e.g., bariatric surgery, Helicobacter pylori gastritis, celiac sprue) pregnancy

Question 85

Symptoms of IDA are: (7)

Answer 85

fatigue exertional dyspnea decreased exercise tolerance Koilonychias (spoon nails) pica (ingestion of clay or ice) glossitis (red, beefy, glossy, swollen tongue without papillae) cheilosis (crusting of angle of the mouth)

Question 86

A young man or postmenopausal woman with IDA needs

Answer 86

aggressive workup with colonoscopy and endoscopy to evaluate for colon cancer.

Question 87

Differential for low MCV includes: (4)

Answer 87

IDA thalassemia anemia of chronic diseases sideroblastic anemia

Question 88

For IDA, serum iron, transferrin or TIBC, ferritin, % transferrin saturation (TSAT) (serum iron/TIBC):

Answer 88

serum iron: decreased transferrin or TIBC: increased ferritin: decreased % transferrin saturation (TSAT) (serum iron/TIBC): very decreased

Question 89

Both ferritin and transferrin saturation are decreased in ———; however, ferritin is increased in ———

Answer 89

IDA anemia of chronic diseases

Question 90

For IDA, MCV and RDW:

Answer 90

- Microcytosis, that is, low mean corpuscular volume (MCV) less than 80 - High red cell distribution width (RDW) more than 15% (Anisocytosis-increased variation in red cell size)

Question 91

Management with IV iron formulations

Answer 91

can be dangerous! Make sure the patient is in a setting where nursing can monitor closely for reactions.

Question 92

HIV patients on highly active antiretroviral therapy (HAART) can have ——— anemia due to ———

Answer 92

macrocytic azathioprine (AZT)

Question 93

Causes of megaloblastic macrocytic anemia (2) vs non-megaloblastic macrocytic anemia (4):

Answer 93

Megaloblastic macrocytic anemia: folate deficiency vitamin B12 deficiency Non-megaloblastic macrocytic anemia: liver dysfunction hypothyroidism drugs bone marrow disorders

Question 94

Causes of folate-deficiency anemia: (4)

Answer 94

Pregnant MAN: Pregnancy and lactation Malabsorption (celiac and Crohn disease) Alcoholism Nutritional (toast and tea elderly diet)

Question 95

Causes of macrocytosis:

Answer 95

FEeD THeM Folate and vitamin B12 deficiency Ethanol and liver disease Drugs (AZT, methotrexate) Thyroid (hypothyroidism) Hemolysis (reticulocytosis) Myelodysplastic syndrome

Question 96

Folate deficiency can be differentiated from vitamin B12 deficiency by the lack of

Answer 96

neurologic abnormalities

Question 97

Folic acid is absorbed in the ———, so conditions like ——— will lead to folate deficiency.

Answer 97

upper third of the small intestine short gut syndrome

Question 98

Lab findings in folate (vit b9) deficiency: (5)

Answer 98

High MCV Hypersegmented neutrophils seen on peripheral smear High homocysteine levels Low red blood cells (RBCs) Low serum folate levels

Question 99

Most common causes of vitamin B12 deficiency include: (4)

Answer 99

pernicious anemia (lack of intrinsic factor) lack dietary B12 intake (vegan diet or no-dairy diets) fish tapeworm (Diphyllobothrium latum) malabsorption (celiac, Crohn disease, bacterial overgrowth, and ileal resection)

Question 100

Average age of diagnosis of pernicious anemia is

Answer 100

60 or older in adults

Question 101

Causes of vitamin B12 deficiency

Answer 101

VITAMIN B Vegan diet Ileal resection Tapeworm Autoimmune (pernicious anemia-lack of intrinsic factor) Megaloblastic anemia Inflammation of terminal ileum Nitrous oxide Bacterial overgrowth

Question 102

Causes of normocytic normochromic (normal size, normal shape) anemia include: (3)

Answer 102

• Bone marrow problems (aplastic bone marrow, leukemia, myelodysplastic syndromes, etc.) • Destruction (hemolytic anemias) • Early nutritional anemias (iron, B12, folate)

Question 103

Methylmelonic acid levels in vit b12 deficiency vs folate deficiency:

Answer 103

vit b12 deficiency: high folate deficiency: normal

Question 104

A hallmark of vitamin B12 deficiency is ——— symptoms that present after the anemia; may include:

Answer 104

neurologic dementia or “megaloblastic madness”: (Subacute combined degeneration of the dorsal (sensory) and lateral (upper motor neuron) spinal cord columns from myelin deficiency; Symmetrical, affecting the legs and beginning with paresthesias and ataxia (loss of vibration and position sense) and progressing to weakness, spasticity, clonus, and hyperreflexia (upper motor neuron symptoms))

Question 105

Lab findings with vit B12 deficiency: (5)

Answer 105

high MCV hypersegmented neutrophils high homocysteine levels high methylmalonate in urine low serum B12 levels

Question 106

Pernicious anemia pathogenesis:

Answer 106

- The parietal cell in the stomach produces hydrochloric acid (HCl) and intrinsic factor (IF). Vitamin B12 needs hydrogen ions from HCl to bind to IF, which carries vitamin B12 to the terminal ileum, where it is absorbed. - In pernicious anemia, autoantibodies are made against the IF and/or the parietal cells, thus impairing the absorption of vitamin B12. As the parietal cells get destroyed, chronic gastritis and eventually gastric cancer can ensue.

Question 107

Pernicious anemia associated with: (3)

Answer 107

chronic gastritis, vitiligo (another autoimmune process), and gastric cancer

Question 108

In G6PD deficiency, causes of Hb precipitation within cells and hemolysis: (4)

Answer 108

infections diabetic ketoacidosis medications such as sulfa drugs (trimethoprim-sulfamethoxazole, primaquine), quinolones fava beans

Question 109

G6PD deficiency is an —(mode of inheritance)— that is more common in those with ——— ancestry

Answer 109

X-linked disease Mediterranean (Italians, Greeks, Arabs) and African

Question 110

ABCs of G6PD deficiency:

Answer 110

ABCDEFG Antimalarials Bactrim/bite cells Ciprofloxacin DKA InfEction Fava beans (can be Fatal without transfusion) G6PD deficiency

Question 111

Key finding on smear for G6PD deficiency:

Answer 111

reticulocytes, bite cells, and Heinz bodies (Cells with precipitated Hb have Heinz bodies, which are removed by the spleen, resulting in bite cells)

Question 112

Clinical features G6PD deficiency: (3)

Answer 112

- Acute hemolysis causing anemia, with sudden onset of jaundice (high indirect bilirubin) - Dark urine (hemoglobinuria) and abdominal and back pain can occur -Acute tubular necrosis can occur due to hemoglobinuria

Question 113

G6PD deficiency: lab findings for bilirubin, haptoglobin, in urine, on smear, and for Coombs test

Answer 113

(Evidence of intravascular hemolysis) increased indirect bilirubin decreased haptoglobin Urine: hemoglobinuria Smear: reticulocytes, bite cells, and Heinz bodies Negative Coombs tests (nonautoimmune).

Question 114

For G6PD deficiency: G6PD assay timing

Answer 114

Check the G6PD assay 3 weeks after an acute episode because in acute situations younger RBCs that still have the G6PD enzyme reveal a falsely high level. The G6PD deficiency causes a decreased half-life of enzyme, so older RBCs without G6PD die.

Question 115

A 31-year-old Italian male with back pain, dark urine, jaundice, and anemia after 2 days of ciprofloxacin. Dx and next steps?

Answer 115

Think: G6PD deficiency. Next step: Check peripheral smear, looking for “bite cells”; transfuse if severe anemia; and check renal function.

Question 116

Aplastic anemia is a:

Answer 116

Marrow failure resulting in pancytopenia from stem cell defect, which is usually from immune-mediated injury (idiopathic or after exposure to radiation, drugs, infections, or certain chemicals).

Question 117

Common causative viral infection for aplastic anemia:

Answer 117

parvovirus B19 (Also viral hepatitis)

Question 118

Drug causes for aplastic anemia:

Answer 118

chloramphenicol ( Also, benzene and dichlorodiphenyltrichloroethane (DDT))

Question 119

Pure red cell aplasia (anemia only) can be seen in ——— patients after ——— infection

Answer 119

sickle cell patients parvovirus B19 (erythema infectiosum/fifth disease)

Question 120

Key clinical presentation features of aplastic anemia:

Answer 120

- Anemia: Weakness, fatigue, and pallor - Thrombocytopenia and symptoms such as of mucosal bleeding and spontaneous bleeding - Neutropenia can lead to fevers and infections with typical organisms

Question 121

Findings for Diagnostic Workup of aplastic anemia:

Answer 121

- Low reticulocyte count and normal MCV - Bone marrow biopsy will show hypocellular marrow with lots of white fat cells

Question 122

Lab findings for anemia of chronic disease for RBCs, EPO, serum iron, transferrin/TIBC, ferritin, % transferrin saturation (serum iron/TIBC):

Answer 122

RBCs: microcytic or normocytic anemia EPO: normal serum iron: decreased transferrin/TIBC: decreased (unlike IDA; Evolutionary reasoning—pathogens use circulating iron to thrive. The body has adapted a system in which iron is stored within the cells of the body and prevents pathogens from acquiring circulating iron) ferritin: increased (acute phase reactant) % transferrin saturation (serum iron/TIBC): normal or decreased

Question 123

Lab findings for hematochromatosis for serum iron, transferrin/TIBC, ferritin, % transferrin saturation (serum iron/TIBC):

Answer 123

serum iron: increased transferrin/TIBC: decreased ferritin: increased % transferrin saturation (serum iron/TIBC): very increased

Question 124

Lab findings for pregnancy/OCP use for serum iron, transferrin/TIBC, ferritin, % transferrin saturation (serum iron/TIBC):

Answer 124

serum iron: normal transferrin/TIBC: increased ferritin: normal % transferrin saturation (serum iron/TIBC): decreased

Question 125

Normal MCV, ↑LDH, ↑indirect bilirubin, ↓haptoglobin: what are we worried about?

Answer 125

Hemolysis

Question 126

Normal MCV, ↑LDH, ↑indirect bilirubin, ↓haptoglobin: Sickle cell kid w/ sudden drop in Hct?

Answer 126

Aplastic Crisis. Sickle Crisis from hypoxia, dehydration or acidosis (In SCD, aplastic crisis can be caused by infection with Parvovirus B-19. Fifth disease, a normally benign childhood disorder associated with fever, malaise, and a mild rash. This virus infects RBC progenitors in bone marrow, resulting in impaired cell division for a few days. Healthy people experience, at most, a slight drop in hematocrit, since the half-life of normal erythrocytes in the circulation is 40-60 days. In people with SCD, however, the RBC lifespan is greatly shortened (usually 10-20 days), and a very rapid drop in Hb occurs. The condition is self-limited, with bone marrow recovery occurring in 7-10 days, followed by brisk reticulocytosis.)

Question 127

Sickle cell patients should always be on ———! Chronic hemolysis causes ——— loss and deficiency, ——— infection.

Answer 127

folate folate B19 infection (erythema infectiosum/fifth disease)

Question 128

In sickle cell disease, Hb S will polymerize in ——— conditions, which ——— causing:

Answer 128

hypoxic distorts the red cell into the classic crescent or sickle shape decreased deformability can cause hemolysis and vascular occlusion, causing crisis

Question 129

In SCD, acute vasoocclusive pain crisis (VOC) is caused by and typically manifests as:

Answer 129

Caused by: vascular sludging and thrombosis, which can lead to organ failure secondary to infarction, dehydration, fever, and leukocytosis Manifests as: acute-onset generalized pain in the back, extremities, chest and abdomen, and joints

Question 130

In SCD, acute chest syndrome: cause, presentation, and txt:

Answer 130

Caused by: occlusion of pulmonary vasculature by sickled cells and/or infection. Presentation: Hypoxia, chest pain, shortness of breath, infiltrates Txt: It is the most common cause of death in sickle patients and is an emergency requiring exchange transfusion with normal red cells. Treat with exchange transfusion.

Question 131

In SCD, key genitourinary emergency:

Answer 131

Priapism can occur acutely or chronically. This is a medical emergency, as permanent damage can occur.

Question 132

Chronic disease manifestations of SCD include: (7)

Answer 132

aseptic necrosis of the femoral head pigmented gallstones (increased bilirubin) hematuria renal papillary necrosis pulmonary hypertension high-output cardiac failure secondary hemochromatosis

Question 133

In SCD, there is an increased susceptibility to infections due to ——— This carries a higher risk of sepsis with ———

Answer 133

functional asplenism (due to repeated infarction) encapsulated organisms (Streptococcus pneumoniae, Salmonella osteomyelitis, and Haemophilus influenzae)

Question 134

In SCA, hemoglobin ——— will show Hb S

Answer 134

electrophoresis

Question 135

Blood smear of SCD will show: (2)

Answer 135

Howell–Jolly bodies (cytoplasmic remnants of nuclear chromatin that are normally removed by the spleen) sickled cells

Question 136

Blood tests in SCD will show: (2)

Answer 136

anemia evidence of hemolysis: Increased reticulocyte count, increased indirect bilirubin, and leukocytosis

Question 137

Indications for exchange transfusion in sickle cell disease: (5)

Answer 137

Stroke/TIA Acute chest syndrome Priapism Third-term pregnancy Intractable vasoocclusive crisis

Question 138

Signs of SCA:

Answer 138

SICKLE Splenomegaly/Sludging Infection Cholelithiasis/acute Chest syndrome Kidney (hematuria, papillary necrosis) Liver congestion/Leg ulcers Eye changes

Question 139

Management of acute crisis in SCD: (3)

Answer 139

Analgesia, hydration, folate (and antibiotics if signs of infection) (assess for transfusion need)

Question 140

Management of acute chest syndrome in SCD: (3)

Answer 140

Respiratory support, exchange transfusion, and empiric antibiotics for pneumonia.

Question 141

Long term management of SCD: (2)

Answer 141

Hydroxyurea acts by increasing the amount of fetal hemoglobin; may increase frequency of crisis H. influenzae and pneumococcal vaccines for prophylaxis

Question 142

A patient walks in with macrocytic anemia: MVC = 100 (nl 80-100), ↓retics, ↑homocysteine, nl methylmelonic acid

Answer 142

Folate deficiency anemia

Question 143

A patient walks in with macrocytic anemia: arrow shows?

Answer 143

Arrow: hypersegmented neutrophil

Question 144

A patient walks in with macrocytic anemia: MVC = 100 (nl 80-100), ↓retics, ↑homocysteine, ↑ methylmelonic acid

Answer 144

Vitamin B12 deficiency anemia (And might also give neurologic sxs)

Question 145

A patient walks in with macrocytic anemia: MVC = 100 (nl 80-100). Arrow? Dx?

Answer 145

Arrow: Acanthocytes (“spur cells”) Dx: Liver disease (another cause of macrocytic anemia)

Question 146

A patient walks in with microcytic anemia... MCV = 70 (nl 80-100), ↓Fe, ↑TIBC, ↓retic, ↑RDW, ↓ferritin: Dx?

Answer 146

Iron deficiency anemia

Question 147

A patient walks in with microcytic anemia... MCV = 70 (nl 80-100), ↓Fe, ↓TIBC, ↓retic, ↑RDW, nl or ↑ ferritin: Dx?

Answer 147

Anemia of chronic disease

Question 148

A patient walks in with microcytic anemia... MCV = 60 (nl 80-100): Dx?

Answer 148

thalassemia (MCV super low - thalassemia characterized by really low MCV) (Also note low RDW (little variation) - if genetic defect, all RBC affected by thalassemia; whereas, in another cause might be more retics, so greater variation in size of RBCs)

Question 149

——— infection is a significant cause of morbidity in patients with thalassemia and other iron overload syndromes (cirrhosis and hereditary hemochromatosis)

Answer 149

Yersinia enterocolitica

Question 150

A patient walks in with microcytic anemia... MCV = 70, ↑Fe, ↑ferritin, ↓TIBC: Dx?

Answer 150

Sideroblastic anemia (Isoniazid (inh) can cause sideroblastic anemia; isoniazid used for TB) (Will see ringed sideroblasts in bone marrow and basophilic stippling in peripheral smear)

Question 151

Lab findings in immune-mediated hemolytic anemia: antibodies, retics, MCV, indirect bilirubin, haptoglobin, LDH, Coomb’s test

Answer 151

- Presence of autoantibodies to one’s RBCs, resulting in hemolysis - Reticulocytosis (bone marrow pushes out immature RBCs) - normal MCV - Increased indirect bilirubin (by-product of lysed cells [globin]) - increased LDH (by-product of lysed cells) - Decreased haptoglobin (binds free hemoglobin released from lysed cells) - Direct Coombs test (presence of antibody on RBC surface) (Also Splenomegaly (site of clearance))

Question 152

Normal MCV, ↑LDH, ↑indirect bilirubin, ↓haptoglobin… Sudden onset after penicillins, ceph, sulfas, rifampin or Cancer: Dx? Destruction location? Antibody? Tx?

Answer 152

Dx: Warm Agglutinins. Destruction in spleen. Antibody: IgG. Tx w/ steroids 1st, then splenectomy.

Question 153

Warm hemolytic anemia: Immunoglobin, temperature, tx, seen with?

Answer 153

- IgG antibodies to different RBC antigens (e.g., Rh) (Do not usually fix complement (IgG))(“Warm weather is Good.”) - Active at body temperature - Treat with steroids. Transfuse if severe anemia. Splenectomy for steroid resistant. - Seen with chronic lymphocytic leukemia (CLL), leukemias, SLE, and other autoimmune diseases, and drugs (penicillin, sulfas, and antimalarials); Sixty percent of cases are idiopathic.

Question 154

PT—tests function of ———

Answer 154

common and extrinsic pathway (factors I, II, V, VII, and X). defect Žresults in increased PT (Play Tennis outside [extrinsic pathway]).

Question 155

INR (international normalized ratio) =

Answer 155

patient PT/control PT. 1 = normal, > 1 = prolonged. (Most common test used to follow patients on warfarin, which prolongs INR.)

Question 156

PTT—tests function of ———

Answer 156

common and intrinsic pathway (all factors except VII and XIII) Defect increases PTT (Play Table Tennis inside).

Question 157

TT—measures ———. Prolonged by —(4)—

Answer 157

the rate of conversion of fibrinogen Žto fibrin anticoagulants, hypofibrinogenemia, DIC, liver disease.

Question 158

Coagulation disorders can be due to clotting factor deficiencies or acquired factor inhibitors (most commonly against factor VIII). Diagnosed with a ———, in which ———

Answer 158

mixing study normal plasma is added to patient’s plasma. Clotting factor deficiencies should correct (the PT or PTT returns to within the appropriate normal range), whereas factor inhibitors will not correct.

Question 159

Normal MCV, ↑LDH, ↑indirect bilirubin, ↓haptoglobin… Cyanosis of fingers, ears, nose + recent Mycoplasma infx (walking pneumonia): Dx? Destruction location? Antibody?

Answer 159

Dx: Cold Agglutinins. Destruction occurs in the liver. Antibody: IgM mediated.

Question 160

Cold hemolytic anemia: Immunoglobin, temperature, tx, seen with?

Answer 160

- Immunoglobulin M (IgM) antibodies. (Fixes complement (IgM)) - Active at cool temperatures (dissociate at 30°C) such as in distal body parts (blue fingers and toes). - Treatment includes keeping warm; corticosteroids don’t work well. - Seen acutely with Mycoplasma and infectious mononucleosis (resolve spontaneously) and chronically with lymphomas and Waldenström macroglobulinemia. (Degree of hemolysis is variable.)

Question 161

Normal MCV, ↑LDH, ↑indirect bilirubin, ↓haptoglobin… Splenomegaly, +FH, bilirubin gallstones, ↑MCHC (mean cell hemoglobin concentration): Dx? Tx?

Answer 161

Dx Hereditary spherocytosis (AD loss of spectrin). Tx w/ splenectomy (Small, round RBCs with no central pallor.  decreased surface area/dehydration Ž -> increased MCHC Ž-> premature removal by spleen (extravascular hemolysis).

Question 162

Normal MCV, ↑LDH, ↑indirect bilirubin, ↓haptoglobin… Dark (pink/red) urine in AM, Budd-Chiari syndrome (venous thrombosis, “clots in IVC”): Dx? Defect in? Increased risk for?

Answer 162

Dx: Paroxysmal Nocturnal Hemoglobinuria. Defect in PIG-A. Lysis by complement. Incr risk for aplastic anemia (and acute leukemias)

Question 163

Normal MCV, ↑LDH, ↑indirect bilirubin, ↓haptoglobin… Sudden onset after primiquine, sulfas, fava beans: Dx? Lab findings? Avoid?

Answer 163

Dx: G6PDH def. Finding: Heinz bodies, Bite cells. Avoid oxidant stress.

Question 164

A patient walks in with thrombocytopenia…. 30 y/o F recurrent epistaxis, heavy menses & petechiae. ↓plts only: Dx? Tx?

Answer 164

Dx: ITP. Tx w/ prednisone 1st. Then splenectomy. IVIG if <10K. Rituximab

Question 165

Clinical features ITP: (2)

Answer 165

- Petechiae and purpura over the trunk and limbs can occur spontaneously and with minimal trauma - Mucosal bleeding can occur as well.

Question 166

Cause and work up of ITP:

Answer 166

Cause: Immune-mediated thrombocytopenia of unknown etiology. (Antibodies against a platelet surface antigen are developed, and the antibody–antigen complexes effectively decrease platelet count by being removed from circulation.) Work up: CBC will show low platelet counts. It is a diagnosis of exclusion; thus, absence of other factors to explain thrombocytopenia is also key. (Antiplatelet antibodies are not useful for the diagnosis)

Question 167

Tx ITP:

Answer 167

- Corticosteroids acutely to improve platelet count. - IVIG for severe cases. - Platelet transfusion if significant bleeding present. - splenectomy can be performed electively to reduce recurrence.

Question 168

Thrombocytopenia presents as ——— vs Factor deficiencies (e.g., hemophilia) present with ———

Answer 168

oozing from mucosal sites (gums) and petechiae (Petechiae = Platelet Problem) large bleeds (typically hemarthrosis)

Question 169

Differentiate between ITP, aplastic anemia, and MDS:

Answer 169

• ITP has normal RBCs, normal WBCs, only low platelets with giant (young) platelets on the peripheral smear. Usually don’t give platelets – treat with steroids or IVIG. • Aplastic anemia has low RBCs, low WBCs, and low platelets (all cell lines low). No dysmorphic cells on smear. • Myelodysplastic syndrome (MDS) can have any one or all lineages low. The smear can show dysplastic neutrophils (hypolobulated), and RBCs with ringed sideroblasts.

Question 170

Causes of thrombocytopenia, think PLATELETS:

Answer 170

Platelet disorders: TTP, ITP, DIC Leukemia Anemia Trauma Enlarged spleen Liver disease EtOH (alcohol) Toxins (benzene, heparins, aspirin, chemotherapy agents, etc.) Sepsis And RBCs with ringed

Question 171

Classic pentad for TTP—

Answer 171

RAT FaN Renal dysfunction Anemia (hemolytic) Thrombocytopenia Fever Neurologic dysfunction

Question 172

What are the two Thrombotic microangiopathies? Difference from DIC?

Answer 172

Thrombotic microangiopathies: TTP and HUS May resemble DIC, but do not exhibit lab findings of a consumptive coagulopathy (eg,  PT,  PTT,  fibrinogen), as etiology does not involve widespread clotting factor activation

Question 173

TTP vs HUS: Population

Answer 173

TTP: typically females HUS: typically children

Question 174

TTP vs HUS: pathophysiology

Answer 174

TTP: Inhibition or deficiency of ADAMTS13 (a vWF metalloprotease) Ž-> decreased degradation of vWF multimers Ž  -> increased large vWF multimers Ž m -> platelet adhesion and aggregation (microthrombi formation) HUS: Predominately caused by Shiga toxin–producing Escherichia coli (STEC) infection (serotype O157:H7), which causes profound endothelial dysfunction.

Question 175

TTP vs HUS: presentation

Answer 175

Both: Triad of thrombocytopenia (decreased platelets), microangiopathic hemolytic anemia (decreased Hb, schistocytes, increased LDH), acute kidney injury (increased Cr) TTP: Triad + fever + neurologic symptoms HUS: Triad + bloody diarrhea

Question 176

TTP and HUS vs DIC: labs

Answer 176

Normal PT and PTT helps distinguish TTP and HUS (coagulation pathway is not activated) from DIC (coagulation pathway is activated)

Question 177

TTP vs HUS: tx

Answer 177

TTP: Plasma exchange, glucocorticoids, rituximab HUS: supportive care

Question 178

TTP cause:

Answer 178

ADAMTS13 is the protease that normally cleaves these multimers, but is deficient in this condition. Usually caused by an immune process that clears ADAMTS13 after an infection, but some cases are genetic. Infection (especially HIV and Escherichia coli O157:H7), malignancy, drugs (antiplatelet agents, chemotherapy agents, contraceptives), autoimmune disorders, and pregnancy can cause TTP. (medical emergency with mortality approaching 90% if untreated)

Question 179

Classic pentad of TTP– not all have to be present:

Answer 179

Fever altered mental status (waxing and waning) renal dysfunction (hematuria, oliguria) thrombocytopenia (mild to severe) microangiopathic hemolytic anemia (RAT FaN)

Question 180

TTP Labs: (7)

Answer 180

- thrombocytopenia - microangiopathic hemolytic anemia - Schistocytes on peripheral smear - decreased haptoglobin - elevated LDH - elevated total bilirubin - Renal failure can occur due to microangiopathy

Question 181

For TTP Tx, do not ———

Answer 181

Do not transfuse platelets! It will continue to feed the TTP and will not halt the end-organ damage.

Question 182

TTP Tx:

Answer 182

Plasma exchange (plasmapheresis) (Do not transfuse platelets! It will continue to feed the TTP and will not halt the end-organ damage.)

Question 183

——— is the causative organism in a bloody diarrhea syndrome that has been associated with the subsequent development of HUS. HUS differs from TTP in ———.

Answer 183

E. coli O157:H7 severity and lack of neurologic symptoms

Question 184

DIC is an acquired ——— defect that results in:

Answer 184

coagulation consumption of coagulation factors, including fibrinogen, causing bleeding and thrombosis

Question 185

DIC usually secondary to exposure of blood to

Answer 185

procoagulants such as tissue factor (fetus, bacteria) and cancer procoagulant, resulting in depletion of clotting factors and microangiopathic hemolytic anemia

Question 186

DIC time course

Answer 186

can be acute and life threatening or can be chronic, as seen with malignancies

Question 187

Causes of DIC:

Answer 187

obstetric problems (retained dead fetus, abruptio placentae, second-trimester abortion, amniotic fluid embolism, preeclampsia) sepsis (particularly with gram- negatives, Rickettsia, hemolytic uremic syndrome [HUS], malaria) local tissue damage (snake bites, burns, frostbite) extensive trauma chronic illness such as malignancy or liver disease

Question 188

DIC: Key clinical feature

Answer 188

Diffuse, systemic bleeding (not from a single site). (Usually have some other severe underlying condition also (e.g., sepsis).)

Question 189

SPELL Etiology of DIC— How do you “SPELL” DIC?

Answer 189

Sepsis/Surgery/Snake bite Pregnancy (retained dead fetus, abruptio placentae, second-trimester abortion, amniotic fluid embolism, preeclampsia) Extensive trauma Liver disease/Leukemia Local tissue damage (snake bites, burns, frostbite)

Question 190

Labs DIC: fibrinogen, platelets, PT, aPTT, TT, D-dimers, peripheral smear?

Answer 190

Decreased fibrinogen thrombocytopenia elevated prothrombin time (PT) elevated activate partial thromboplastin time (aPTT) elevated thrombin time (TT) Presence of fibrin split products (elevated D-dimers) evidence of MAHA (microangiopathic hemolysis) (schistocytes) on peripheral smear

Question 191

Tx DIC:

Answer 191

Treat underlying cause (Platelets, fresh frozen plasma (FFP), and cryoprecipitate to control bleeding can support until underlying cause is under control)

Question 192

A 50-year-old woman who is in the ICU for sepsis has purpura and gingival bleeding on day 2 of her hospital stay and blood coming from her urinary catheter. PT and PTT are increased and fibrinogen is decreased. Dx? Next step?

Answer 192

Think: DIC. Next step: Transfuse FFP and cryoprecipitate.

Question 193

So your patient is peeing blood... Kiddo s/p hamburger and diarrhea w/ renal failure, MAHA and petechiae. Dx? Cause? Tx?

Answer 193

Dx: HUS. Cause: E.Coli O157H7 or shigella. Tx: Don’t tx w/ ABX (releases more toxin)

Question 194

So your patient is peeing blood... Cardiac patient s/p ticlopidine w/ renal failure, MAHA, ↓plts, fever and AMS. Dx? Tx? Key distinction?

Answer 194

Dx: TTP. (Ticlopidine associated with increased risk TTP) Tx w/ plasmapheresis. DON’T give platelets (will be an answer, don’t choose it! The process that is consuming the platelets and causing thrombocytopenia will just continue to consume any more platelets you throw in there.) Distinction: Can tell from DIC b/c PT and PTT are normal in HUS/TTP.

Question 195

A patient walks in with thrombocytopenia and this smear... what is in smear?

Answer 195

Schistocytes (“that’s scary”)

Question 196

A patient walks in with thrombocytopenia and this smear... If PT and PTT are ↑, fibrinogen ↓, D-dimer and fibrin split products ↑: Dx? Causes? Tx?

Answer 196

Dx: DIC Causes: Sepsis (LPS from gram - sepsis), rhabdo, adenocarcinoma, heatstroke, pancreatitis, snake bites (“don’t get bit by a snake”), OB stuff, *Tx of M3 AML* (Auer rods) Tx: FFP, platelet transfusion, correct underlying d/o (“not much works right? You gotta correct underlying factor. You can give FFP to replace fibrinogen. You can transfuse platelets. But unless you correct what started this whole thing, you are kinda toast”)

Question 197

A patient walks in with thrombocytopenia and this smear... If PT and PTT are nl: Dx? Causes? Tx?

Answer 197

Dx: HUS or TTP Causes: O157H7 (causes HUS), ticlopidine, quinine, cyclosporine, (some drug associated with TTP-most important ticlopidine), HIV, cancer Tx: Plasmapheresis. NO PLATELETS!

Question 198

Opening snap with diastolic rumble at left 4th interspace. Tall jugular venous A waves. What is at the left 4th interspace? Dx?

Answer 198

Left 4th: Tricuspid area Dx: Tricuspid stenosis (note diastolic murmur)

Question 199

Opening snap with diastolic rumble at left 4th interspace. Tall jugular venous A waves. Dx? Why are jugular venous A waves tall?

Answer 199

Dx: Tricuspid stenosis (note diastolic murmur) Tall b/c: if atria contracting against increased resistance, then a wave will be bigger (Jugular venous pulse (JVP) a wave=atrial contraction)

Question 200

Opening snap with diastolic rumble at left 4th interspace. Tall jugular venous A waves. Dx? How can we increase the intensity of this murmur?

Answer 200

Dx: Tricuspid stenosis (note diastolic murmur) Increase intensity: increased preload will make loader b/c if bringing more blood to heart (leg raise or give infusion of fluid or inspire (b/c inspiration will increase venous return (note that this is right sided heart murmur)))

Question 201

Opening snap with diastolic rumble at left 4th interspace. Tall jugular venous A waves. Dx? What would increase in afterload do to this murmur?

Answer 201

Dx: Tricuspid stenosis (note diastolic murmur) Increased afterload: would decrease murmur b/c less flow across stenotic valve

Question 202

Jugular venous pulse (JVP) a wave is prominent in

Answer 202

AV dissociation (cannon a wave) (Note: a wave—atrial contraction)

Question 203

Jugular venous pulse (JVP) a wave is absent in

Answer 203

atrial fibrillation (Note: a wave—atrial contraction)

Question 204

30 yo F presents with 3 day hx of polydipsia and polyuria. Blood glucose is 650 mg/dl (nl <140), Bicarb is 21 (nl 21-29), pH is 7.35 (nl 7.35-7.46). Diagnosis?

Answer 204

Hyperglycemic hyperosmolar syndrome (HHS) (Trying to trick u into choosing dka, but for dka would have ketosis. Also ph would not be 7.35 in dka- usually pretty low in dka)

Question 205

Define HHS

Answer 205

plasma osmolarity >320 mOsm/L plasma glucose level >600 mg/dL but a normal bicarbonate level normal PH no significant evidence of ketosis

Question 206

HHS occurs in ——— and is caused by:

Answer 206

Occurs in patients with type 2 DM (diagnosis is considered in any elderly patient with altered mental status and dehydration, particularly with known diabetes) Common causes include medication noncompliance, severe infection or sepsis, dehydration, diuretics, and glucocorticoids.

Question 207

Sxs of HHS?

Answer 207

- Altered mental status is a key symptom with signs of profound dehydration -Seizures and transient neurologic deficits may occur. (Patients usually have a period of symptomatic hyperglycemia before the syndrome develops. When fluid intake becomes insufficient, extreme dehydration ensues because of the hyperglycemia-induced osmotic diuresis.)

Question 208

30 yo F presents with 3 day hx of polydipsia and polyuria. Blood glucose is 650 mg/dl (nl <140), Bicarb is 21 (nl 21-29), pH is 7.35 (nl 7.35-7.46). Diagnosis? Pathophysiology? Risk factors?

Answer 208

Dx: HHS Pathophysiology/RFs: get stressed with infection or study for shelf- release a ton of cortisol- cortisol increases blood glucose levels and have relative insulin deficiency w/ type 2 dm so cannot utilize that increased blood glucose so can tip over edge

Question 209

Treat HHS?

Answer 209

Diagnosis and management of HHS are similar to DKA with intravenous fluids, continuous insulin drop, and potassium repletion. However, it’s even more important to adequately hydrate patients prior to starting an insulin drip.

Question 210

30 yo F presents with 3 day hx of polydipsia and polyuria. Blood glucose is 650 mg/dl (nl <140), Bicarb is 21 (nl 21-29), pH is 7.35 (nl 7.35-7.46). Diagnosis? Treatment?

Answer 210

Dx: HHS Tx: fluids and insulin

Question 211

Why do pt with type 2 dm not have ketosis?

Answer 211

They have some insulin and insulin inhibits glucagon (remember beta cells in middle of the islets, the alpha cells that secrete glucagon are on the outside, so insulin on it way out inhibits glucagon), so they don’t have lipolysis so no ketosis (glucagon promotes lipolysis; lipolysis and oxidation of free fatty acids Žyields increased ketone bodies)

Question 212

30 yo F presents with 3 day hx of polydipsia and polyuria. Blood glucose is 650 mg/dl (nl <140), Bicarb is 21 (nl 21-29), pH is 7.35 (nl 7.35-7.46). Diagnosis? How is Na balance?

Answer 212

Dx: HHS Na balance: hyperosmolar hyponatremia b/c have ton of glucose, it’s pulling water out of cells so artificially lowers blood sodium levels

Question 213

30 yo F presents with 3 day hx of polydipsia and polyuria. Blood glucose is 650 mg/dl (nl <140), Bicarb is 21 (nl 21-29), pH is 7.35 (nl 7.35-7.46). Diagnosis? How is the total body potassium?

Answer 213

Dx: HHS Total body K: Low, but potassium measured on lab may be high or normal; don’t be fooled by high potassium in pt with DKA or HHS- want to supplement potassium

Question 214

30 yo F presents with 3 day hx of polydipsia and polyuria. Blood glucose is 650 mg/dl (nl <140), Bicarb is 21 (nl 21-29), pH is 7.35 (nl 7.35-7.46). Initial Dx? What is your dx if the patient becomes altered/comatose with rapid treatment?

Answer 214

Initial Dx: HHS Dx if the patient becomes altered/comatose with rapid treatment: cerebral edema; remember sodium mnemonic- from low to high your pons will die, from high to low your brains will blow (can extend hypernatremia mnemonic to hyperglycemia) - so never correct glucose too quickly

Question 215

Type 1 vs type 2 DM: Primary defect

Answer 215

Type 1: Autoimmune T-cell–mediated destruction of β cells  Type 2: increased resistance to insulin, progressive pancreatic β-cell failure

Question 216

Type 1 vs type 2 DM: insulin necessary in tx?

Answer 216

Type 1: always Type 2: sometimes

Question 217

Type 1 vs type 2 DM: age (exceptions common)

Answer 217

Type 1: <30 Type 2: >40

Question 218

Type 1 vs type 2 DM: association with obesity

Answer 218

Type 1: no Type 2: yes

Question 219

Type 1 vs type 2 DM: genetic predisposition

Answer 219

Type 1: Relatively weak (50% concordance in identical twins), polygenic Type 2: Relatively strong (90% concordance in identical twins), polygenic

Question 220

Type 1 vs type 2 DM: association with HLA system

Answer 220

Type 1: Yes, HLA-DR4 and -DR3 (4 – 3 = type 1) Type 2: No

Question 221

Type 1 vs type 2 DM: severity of glucose intolerance

Answer 221

Type 1: Severe Type 2: Mild to moderate

Question 222

Type 1 vs type 2 DM: insulin sensitivity

Answer 222

Type 1: high Type 2: low

Question 223

Type 1 vs type 2 DM: ketoacidosis

Answer 223

Type 1: common Type 2: rare

Question 224

Type 1 vs type 2 DM: beta cell in islets

Answer 224

Type 1: decreased Type 2: variable (with amyloid deposits)

Question 225

Type 1 vs type 2 DM: Serum insulin level

Answer 225

Type 1: decreased Type 2: initially increased, but decreased in advanced disease

Question 226

Type 1 vs type 2 DM: Classic sxs of polyuria, polydipsia, polyphagia,weight loss

Answer 226

Type 1: common Type 2: sometimes

Question 227

Type 1 vs type 2 DM: histology

Answer 227

Type 1: islet leukocytic infiltrate Type 2: Islet amyloid polypeptide deposits

Question 228

DKA vs HHS: pathogenesis

Answer 228

HHS: Profound hyperglycemia Ž resulting in excessive osmotic diuresis Žresulting in dehydration and increased serum osmolality. Classically seen in older patients with type 2 DM and limited ability to drink. Insulin present, ketones deficient. DKA: Insulin noncompliance or  increased requirements due to  stress (eg, infection) Žleads to lipolysis and oxidation of free fatty acids Žwhich yields ketone bodies (β-hydroxybutyrate > acetoacetate). Insulin deficient, ketones present.

Question 229

DKA vs HHS: signs and sxs

Answer 229

HHS: Thirst, polyuria, lethargy, focal neurologic deficits, seizures. DKA: DKA is Deadly: Delirium/psychosis, Kussmaul respirations (rapid, deep breathing), Abdominal pain/nausea/vomiting, Dehydration. Fruity breath odor due to exhaled acetone.

Question 230

DKA vs HHS: labs

Answer 230

HHS: Hyperglycemia (often > 600 mg/dL), increased serum osmolality (> 320 mOsm/kg), normal pH (no acidosis), no ketones. Normal/increased serum K+, decreased intracellular K+. DKA: Hyperglycemia, increased H+, decreased HCO3 – (anion gap metabolic acidosis), increased urine and blood ketone levels, leukocytosis. Normal/increased serum K+, but depleted intracellular K+ due to transcellular shift from decreased insulin and acidosis. Osmotic diuresis leads to K+ loss in urine Ž and total body K+ depletion.

Question 231

DKA vs HHS: complications

Answer 231

HHS: Can progress to coma and death if untreated. DKA: Life-threatening mucormycosis, cerebral edema, cardiac arrhythmias.

Question 232

DKA vs HHS: tx

Answer 232

HHS and DKA: IV fluids, IV insulin, and K+ (to replete intracellular stores). Glucose may be required to prevent hypoglycemia from insulin therapy.

Question 233

Define DKA:

Answer 233

Metabolic acidosis due to ketoacid accumulation secondary to severely depressed insulin levels. (Severe insulin deficiency causes the body to switch from metabolizing carbohydrates to metabolizing and oxidizing lipids. Usually precipitated by a lapse in insulin treatment, acute infection, major trauma, or stress.)

Question 234

Urine ketones only tests for

Answer 234

acetoacetic acid

Question 235

DKA pathogenesis:

Answer 235

Insulin deficiency causes hyperglycemia, which induces an osmotic diuresis (severe dehydration). Profound dehydration, sodium loss, and potassium loss occur. The body believes there is no glucose because the cells aren’t getting any, which triggers the oxidation of free fatty acids from adipose tissue. The liver converts these free fatty acids into an alternative energy source: ketones (acetoacetic acid and beta-hydroxybutyric acid), which causes the metabolic ketoacidosis.

Question 236

Respiration in DKA

Answer 236

There is respiratory compensation for this metabolic acidosis (fast breathing [i.e., Kussmaul], blowing off CO2)

Question 237

Breath odor in DKA?

Answer 237

Acetone is produced from spontaneous decarboxylation of acetoacetic acid. The acetone is disposed of by respiration, and its odor is present on the patient’s breath (fruity odor).

Question 238

Sxs DKA

Answer 238

Polyuria and polydipsia, nausea, vomiting, and vague abdominal pain. Lethargy and fatigue are later components and may progress to coma. Signs of dehydration are present, and patients may be hypotensive and tachycardic. Kussmaul respirations (rapid deep breaths) may be present, and acetone (fruity) odor on the patient’s breath.

Question 239

DKA is characterized by the lab findings triad of:

Answer 239

• Hyperglycemia: Usually between 350 and 500 mg/dL and rarely more than 800 mg/dL. Higher glucose levels are more consistent with HHS • Anion gap metabolic acidosis (pH <7.30 and bicarb <18) • Ketones: Both in the blood and in the urine.m

Question 240

Common underlying causes of DKA are:

Answer 240

Infection: Commonly a urinary tract infection, cellulitis, pneumonia, viral URIs, viral gastroenteritis. Always send a CBC and consider chest radiographs. Pancreatitis: Consider getting a serum amylase and lipase if the patient has symptoms. Ischemia: DKA can be a sign of a myocardial infarction or stroke, since patients with diabetes are at high risk for cardiovascular disease. ECG and ruling out myocardial infarction should be considered.

Question 241

The effect of hyperglycemia is well known for its ——— of serum sodium levels. The most commonly used correction factor is obtained by ———

Answer 241

lowering Adding 1.6 mEq of sodium for each 100 mg/dL of glucose above normal (ie, a 1.6 mEq/L decrease in serum sodium for every 100 mg/dL increase in glucose concentration)

Question 242

Electrolyte disturbances in DKA:

Answer 242

a. Pseudohyponatremia (not real hyponatremia) is due to a normal response to the osmotic shifts of severe hyperglycemia. The sodium reading in the lab value does not accurately represent what the true sodium is. The “corrected” sodium concentration is obtained by adding 1.6 mEq of sodium for each 100 mg/dL of glucose above normal. b. Potassium: Can be low due to glucose osmotic diuresis but is more commonly normal or high even though total body stores are low. This is because insulin usually shifts potassium from the extracellular space to the intracellular space. Because DKA is an insulin-deficient state, all the intracellular potassium moves into the bloodstream. c. Phosphate: Is often high as well due to a similar process as potassium.

Question 243

When calculating the anion gap in DKA, use the ——— Na

Answer 243

actual Na, not the corrected Na

Question 244

Tx for DKA:

Answer 244

• Intravenous fluids: DKA patient usually has severe volume deficits • Insulin: Regular insulin is used with a bolus followed by continuous insulin infusion. Patients are also not allowed to eat during treatment. • Replace potassium • Correct acidosis: Fluids and insulin help correct the underlying cause of the acidosis; however, some patients whose pH drops below 6.9 need bicarbonate infusions to help correct the acidosis more quickly.

Question 245

When treating DKA transition to subcutaneous insulin occurs:

Answer 245

only after anion gap has closed!

Question 246

When treating DKA: If initial potassium is low (<3.3 mEq/L):

Answer 246

HOLD insulin and give potassium to avoid severe hyponatremia

Question 247

A woman presents with a recurrent vaginal candidiasis that is refractory to treatment. Think? Next step?

Answer 247

Diabetes mellitus. Next step: Get a finger stick for blood glucose. (With type 1 DM: Usually presents with symptomatic hyperglycemia or DKA; sxs include polyuria, polydipsia, weight loss, dehydration, and fatigue; Blurred vision and recurrent infections as disease progresses)

Question 248

Latent autoimmune diabetes of adulthood (LADA): Define?

Answer 248

looks like type 1 DM in older patients; Think when DKA appears in a thin adult

Question 249

The required treatment for type 1 DM patients is

Answer 249

insulin (both long and short acting), administered by subcutaneous injection (Most oral hypoglycemics have no role in management because these patients have no functioning pancreatic beta cells)

Question 250

A patient presents with persistent morning hyperglycemia, despite steadily increasing his evening NPH insulin dose. He also complains of frequent nightmares. His wife brings him in because she witnessed him having a seizure in the middle of the night. Think? Next step?

Answer 250

Somogyi effect. Next step: Check 3 am blood glucose.

Question 251

Define the Somogyi effect, it workup, and resolution:

Answer 251

Nighttime hypoglycemia followed by a dramatic increase in fasting glucose levels and increased plasma ketones. If the Somogyi effect is suspected, patients should check their blood glucose around 3 am because hypoglycemia at this time confirms the diagnosis. The morning hyperglycemia is a rebound effect. Replacement of intermediate-acting insulin with long-acting insulin at bedtime can help this effect (try to avoid peaking of insulin effect in the middle of the night), as can a reduced long-acting insulin dose (basal).

Question 252

Dx of dm type 2 based on:

Answer 252

FBGL > 126 x 2 or 2hr OGTT > 200 or random glc > 200 + sxs (polyuria, polydipsia, blurred vision) (First aid says: Requires any one of the following: Random glucose >200 mg/dL in the presence of symptoms or HbA1c equal or above 6.5% is diagnostic or Asymptomatic patients require a fasting glucose of >126 mg/dL on 2 separate occasions Use of glucose tolerance test: If patients have fasting glucose levels of >100 mg/dL and <126 mg/dL, an ogtt is indicated. A positive ogtt is a plasma glucose >200 mg/dL at 2 hours after ingesting glucose in solution.

Question 253

Pt presents with nausea, vomiting, abdominal pain, Kussmaul respirations, coma, and BGL=400. Dx? Workup findings? Tx?

Answer 253

Dx: DKA Workup: Ketones in blood (& urine), AGMA, hyperkalemia Tx: High volume NS (normal saline) + insulin bolus & drip. Add K once peeing. Add glc <200

Question 254

Pt presents with polyuria, polydipsia, profound dehydration, confusion and coma w/ BGL = 1000. Dx? Tx?

Answer 254

Dx: HHS Tx: High volume fluid & electrolytes. May require insulin.

Question 255

MC cause of death in dm?

Answer 255

Cardiovascular disease

Question 256

47 yo F with a history of “relentless DM” presents with a 1 week history of a necrotic, erythematous skin lesion. Diagnosis? Skin lesion is?

Answer 256

Dx: glucagonoma (Skin lesion is Necrolytic migratory erythema)

Question 257

47 yo F with a history of “relentless DM” presents with a 1 week history of a necrotic, erythematous skin lesion. Diagnosis? Endocrine “syndrome” association?

Answer 257

Dx: glucagonoma Endocrine syndrome association: MEN1

Question 258

47 yo F with a history of “relentless DM” presents with a 1 week history of a necrotic, erythematous skin lesion. Diagnosis? Tx?

Answer 258

Tx: Surgery, but if surgery not an option give octreotide (analog of somatostatin) (If ever blank out on bad endocrine disorder- octreotide is almost always a safe option)

Question 259

Inheritance of MEN syndromes?

Answer 259

All MEN syndromes have autosomal dominant inheritance (The X-MEN are dominant over villains)

Question 260

Key components of each MEN syndrome:

Answer 260

MEN 1: 3Ps MEN2A: 2Ps, 1M MEN2B: 1P, 2Ms MEN 1: - Pituitary tumors (prolactin or GH) - Pancreatic endocrine tumors—(Zollinger-Ellison syndrome, insulinomas, VIPomas, glucagonomas) - Parathyroid adenomas MEN2A: - Parathyroid Hyperplasia - Medullary Thyroid Carcinoma - Pheochromocytoma MEN2B: - Pheochromocytoma - Medullary Thyroid Carcinoma - Mucosal Neuromas

Question 261

MEN 1: key features and association

Answer 261

- Pituitary tumors (prolactin or GH) - Pancreatic endocrine tumors—Zollinger-Ellison syndrome, insulinomas, VIPomas, glucagonomas (rare) - Parathyroid adenomas Associated with mutation of MEN1 (tumor suppressor, codes for menin, chromosome 11), angiofibromas, collagenomas, meningiomas

Question 262

MEN 2A: key features and association

Answer 262

- Parathyroid hyperplasia - Medullary thyroid carcinoma: neoplasm of parafollicular C cells; secretes calcitonin (prophylactic thyroidectomy required) - Pheochromocytoma (secretes catecholamines) Associated with mutation in RET (protooncogene, codes for receptor tyrosine kinase, chromosome 10)

Question 263

MEN 2B: key features and association

Answer 263

- Medullary thyroid carcinoma: neoplasm of parafollicular C cells; secretes calcitonin - Pheochromocytoma (secretes catecholamines) - Mucosal neuromas (oral/intestinal ganglioneuromatosis) Associated with marfanoid habitus; mutation in RET gene

Question 264

What is true of total thyroid hormone and free thyroid hormone levels in the setting of OCP use?

Answer 264

total thyroid hormone: high free thyroid hormone: normal (Like in pregnancy)

Question 265

Thyroid produces:

Answer 265

triiodothyronine (T3) and thyroxine (T4), iodine-containing hormones that control the body’s metabolic rate

Question 266

Bound vs unbound thyroid hormone activity?

Answer 266

Thyroxine-binding globulin (TBG) binds most T3/T4 in blood. Bound T3/T4 = inactive Only free hormone is active (T3 binds nuclear receptor with greater affinity than T4)

Question 267

Increased TBG with: ƒ 

Answer 267

pregnancy and OCP use (estrogen yields increased TBG) Žresulting in greater total T3/T4

Question 268

Decreased TBG with:

Answer 268

steroid use and nephrotic syndrome

Question 269

5′-deiodinase role?

Answer 269

converts T4 (the major thyroid product) to T3 in peripheral tissue (5, 4, 3)

Question 270

Peripheral conversion of T4 to T3 is inhibited by

Answer 270

glucocorticoids, β-blockers, and propylthiouracil (PTU)

Question 271

Reverse T3 (rT3) is

Answer 271

a metabolically inactive byproduct of the peripheral conversion of T4 and its production is increased by growth hormone and glucocorticoids

Question 272

Functions of thyroid peroxidase include

Answer 272

oxidation, organification of iodine, and coupling of monoiodotyrosine (MIT) and diiodotyrosine (DIT)

Question 273

Thyroid peroxidase inhibited by

Answer 273

PTU and methimazole

Question 274

Key sxs hyperthyroidism

Answer 274

Heat intolerance, sweating, palpitations (hyperthyroidism is a common cause of atrial fibrillation), weight loss, and tremor, Nervousness, anxiety, weakness, fatigue, diarrhea, and hyperdefecation

Question 275

Patients may experience ——— nails from excess thyroid hormone

Answer 275

onycholysis (Plummer nails) where the nail raises up away from the nail bed

Question 276

Causes of large tongue (macroglossia):

Answer 276

• Acromegaly • Myxedema • Amyloidosis

Question 277

Hyperthyroidism epidemiology and pathophysiology:

Answer 277

Epi: Ten times more common in women than in men; Graves disease most common cause Pathophys: High levels of free thyroid hormones increase levels of cellular metabolism, cause a state of hypermetabolism, and amplify catecholamine signals

Question 278

A 45-year-old woman presents to the emergency department due to agitation and altered mentation. The patient was in her usual state until a few hours ago when she started having severe nausea, vomiting, and diarrhea. Medical history is remarkable for long-standing Graves disease and gastroesophageal reflux disease. Last week, the patient had an upper respiratory infection that resolved without treatment. The patient has been partially compliant in taking her medications, which include omeprazole and propylthiouracil. Temperature is 40°C (104.0°F), pulse is 150/min and irregular, and blood pressure is 150/100 mmHg. On physical examination, the patient is stuporous and her skin is moist. Laboratory tests show elevated liver enzymes, mild hyperglycemia, and leukocytosis. IV propranolol is initiated. Which of the following additional medications should also be administered to this patient? A. Hydrocortisone B. Heparin C. Ceftriaxone D. Aspirin E. Dantrolene

Answer 278

A. Hydrocortisone This patient is presenting with acute onset of nausea, vomiting, diarrhea, arrhythmia, and very high fever. In the light of the known noncompliance with medications and long-standing Graves disease, the most likely dx is a thyroid storm. Thyroid storm is a rare, life-threatening condition typified by severe clinical manifestations of thyrotoxicosis. The condition is caused by longstanding untreated/undertreated hyperthyroidism (e.g., Graves disease, toxic multinodular goiter, toxic adenoma). Treatments include: Beta blockers (to control adrenergic sequelae and inhibit the conversion of T4 to T3), thionamides (PTU and methimazole) - to block new hormone synthesis (PTU also blocks conversion of T4 to T3 in the periphery), lodine solution (to block the release of thyroid hormone and inhibit new hormone synthesis; given after the thionamide), glucocorticoids (to reduce conversion of T4-to-T3, vasomotor stability)

Question 279

Thyroid storm prognosis:

Answer 279

Mortality is high (20% to 50%) even with the correct treatment

Question 280

Sxs thyroid storm

Answer 280

Exaggerated manifestation of hyperthyroidism with fever and CNS, CV, GI sxs: Overactivated sympathetic NS causes most of sxs, including fever, tachycardia, diarrhea, abdominal discomfort, and exhaustion High-output CHF and volume depletion can occur Continuum of CNS alterations (from agitation to confusion when moderate to stupor or coma with or without seizures when most severe) Jaundice is a late and ominous manifestation.

Question 281

Causes thyroid storm

Answer 281

Acute stress event, infection, trauma, surgical procedures, DKA, MI, CVA, PE, labor, withdrawal of antihyperthyroid meds, iodine administration, thyroid hormone ingestion, or idiopathic causes

Question 282

Txt thyroid storm

Answer 282

• Primary stabilization is the most important first step, with focus on airway protection, oxygenation, circulation (pulse/BP), continuous cardiac monitoring, IV hydration • Beta blocker therapy (propranolol) is given to block adrenergic effects and block peripheral conversion of T4 to T3 • Treat fever with acetaminophen and cooling blanket (not aspirin, which displaces T4 from thyroid-binding protein) • Address the thyroid hormone itself with PTU or methimazole to block synthesis of new thyroid hormone and iodine to decrease release of preformed thyroid hormone • Corticosteroids are also given to prevent peripheral conversion of T4 to T3 and to treat “relative” adrenal failure occurring due to a high metabolic rate • Treat any precipitating factors

Question 283

When treating thyroid storm, never give iodine (Lugol or potassium iodine) until

Answer 283

after the thionamide has started to take effect

Question 284

Never send any thyroid storm patient for a procedure involving iodine contrast before

Answer 284

giving a thionamide (propylthiouracil or methimazole)

Question 285

Burch and Wartofsky score used to evaluate

Answer 285

the likelihood of thyroid storm based on presentation

Question 286

Graves disease (and Hashimoto thyroiditis) are sometimes associated with

Answer 286

other autoimmune diseases (type 1 diabetes mellitus, vitiligo, myas- thenia, pernicious anemia, collagen diseases)

Question 287

Tx thyroid storm:

Answer 287

Question 288

Sxs thyroid storm

Answer 288

Question 289

Lab values in thyroid storm

Answer 289

low TSH and high free T4 and/or T3 concentrations (may also reveal mild hyperglycemia, mild hypercalcemia, abnormal LFTs, leukocytosis or leukopenia)

Question 290

A 47-year-old woman presents to the emergency department due to altered mental status. She is accompanied by her partner, who reports that the patient was in her usual state before having severe nausea and vomiting during dinner. Medical history is remarkable for long-standing Graves disease, but the patient has been non-compliant with medications. Last week, she had an upper respiratory infection that was resolved without treatment. Temperature is 40°C (104.0°F), pulse is 155/min and irregular, and blood pressure is 155/100 mmHg. On physical examination, the patient is agitated and in severe distress. The patient’s skin is moist, and a large goiter is noted. Laboratory tests show an elevated T3 and T4, low TSH, elevated liver enzymes, mild hyperglycemia, and leukocytosis. The patient is administered IV propranolol, propylthiouracil, and hydrocortisone. An hour later, the doctor adds a potassium iodide-iodine (Lugol's) solution to the treatment. This medication has which of the following immediate effects? - Inhibition iodide organification - Inhibition of hormone release - Inhibition of the conversion of T4 to T3 - Thyroglobulin synthesis - Inhibition of iodide uptake into thyroid follicular cells

Answer 290

Inhibition of hormone release This patient is presenting with acute onset of nausea, vomiting, diarrhea, arrhythmia, and very high fever. In light of the medication noncompliance and long-standing Graves Disease, the most likely diagnosis is thyroid storm. In healthy individuals, exposure to excess iodine inhibits the organification of iodide and diminishes hormone biosynthesis, a phenomenon known as the Wolff-Chaikoff effect. Iodine also acutely (hours) inhibits hormone secretion by inhibiting thyroglobulin proteolysis. Iodine solution is indicated for preoperative preparation before thyroidectomy in Graves disease, for adjunctive therapy in Graves disease, and for the treatment of thyroid storm. Administration without antithyroid drugs can precipitate iodine-induced hyperthyroidism by serving as substrate for new hormone production by autonomous regions within the thyroid gland. Therefore, it is generally administered at least an hour after starting antithyroid drugs.

Question 291

Describe the Wolff-Chaikoff effect

Answer 291

protective autoregulation; sudden exposure to excess iodine temporarily turns OFF thyroid peroxidase Žleading to decreased T3/T4 production

Question 292

A 50-year-old woman comes to the clinic due to insomnia and anxiety over the past few months. The patient’s last menstrual period was 1 year ago, but she denies hot flashes or vaginal dryness. The patient notes that her hair has become fine lately, and she has been losing weight without intention. On physical examination, a non-tender, diffuse goiter is noted. Laboratory tests show low TSH and high free T3 and T4 serum levels. The physician suspects that the patient’s condition is due to the most common cause of hyperthyroidism. Which of the following is the most specific finding for this condition? - Exophthalmos - Atrial fibrillation - Myxedema - Onycholysis - Elevated creatine kinase levels

Answer 292

Exophthalmos Graves disease is an autoimmune condition caused by autoantibodies to the TSH receptor, which leads to increased thyroid hormone synthesis. The classic presentation includes ophthalmopathy, a large non-nodular thyroid, and signs of hyperthyroidism. Exophthalmos, periorbital and conjunctival edema, restriction of eye movement, and discrete infiltrative dermopathy (pretibial myxedema) are findings unique to Graves disease. (Note: Myxedema describes non-pitting edema. Although myxedema can be caused by Graves disease (pretibial myxedema), it can also be caused by hypothyroidism (generalized myxedema).)

Question 293

A 40-year-old woman comes to the clinic due to anxiety and eye pain for the past few months. The patient also discloses a 10 lb (4.5 kg) weight loss over the past 2 months without changes in her diet. Medical history is unremarkable, and she does not use caffeine, alcohol, or illicit drugs. Temperature is 37.0°C (98.6°F), pulse is 110/min, and blood pressure is 135/85 mmHg. On physical examination, the patient's skin is moist, and a diffuse goiter is noted. Examination of the eyes reveals mild exophthalmos and conjunctival erythema. Which of the following is most likely involved in the pathogenesis of this patient’s eye condition? - T4 hormone - Glycosaminoglycans deposition - Sympathetic hyperactivity - Thyroid-stimulating hormone - T3 hormone

Answer 293

Glycosaminoglycans deposition Graves orbitopathy is mediated by activation of the TSH receptors and T cells in the retro-ocular space, which results in inflammation and accumulation of glycosaminoglycans. This patient is presenting with classic signs of hyperthyroidism including goiter, tachycardia, diaphoresis, and weight loss. In addition, the patient has exophthalmos, which is a characteristic finding in patients with Graves disease.

Question 294

A 38-year-old woman came to the office due to anxiety and palpitations for the past 2 months. She also notes a 6 lbs (2.7 kg) weight loss over this time period without changes in her diet. The patient is generally healthy; medical history is unremarkable. She does not consume caffeine, alcohol or illicit drugs. Temperature is 37.0°C (98.6°F), pulse is 115/min, and blood pressure is 125/85 mmHg. On physical examination, the patient’s skin is moist, and a fine hand tremor is noted. The thyroid gland is diffusely enlarged and nontender. Laboratory tests are obtained and shown below: Which of the following is the most likely diagnosis? - TSH-secreting pituitary adenoma - Ingestion of exogenous thyroid hormone - Toxic adenoma - Graves disease - Subacute thyroiditis

Answer 294

TSH-secreting pituitary adenoma TSH-secreting pituitary adenoma is a rare cause of secondary hyperthyroidism. Patients may present with classic signs of hyperthyroidism, in addition to visual field defects, menstrual disturbances, galactorrhea, and headaches. Laboratory tests typically show normal/high serum TSH concentrations and elevated serum total and free T4 and T3 concentrations, as well as elevated alpha subunit of glycoprotein hormones.

Question 295

Older patient presenting with new-onset atrial fibrillation and weight loss =

Answer 295

classic apathetic Graves disease: Check TSH! (In elderly patients presentation is less classic. Apathy can be present without the common hyperactivity signs (apathetic hyperthyroidism). Cardiovascular features may be prominent, and hyperthyroidism may not be suspected initially.)

Question 296

Symptoms SPECIFIC to Graves disease:

Answer 296

Exopthalmos, thyroid bruit, pretibial myxedema

Question 297

Finding for radioactive iodine uptake on a radionuclide imaging (I-123) in Graves’ disease

Answer 297

Elevated and diffuse uptake

Question 298

Tx Graves’ disease:

Answer 298

- Antithyroid therapy is first-line treatment (Surgery and ablation can be considered after the patient is euthyroid. But antithyroid therapy alone can lead to remission) • Usually accomplished with methimazole (MMI). MMI is as effective as PTU when administered at one-tenth of the PTU dosage. • PTU inhibits peripheral T4 to T3 conversion but is more toxic (liver failure). Beta blockers (adjunctive therapy) Radioactive iodine ablation therapy (I-131) can produce the same effects as surgery without the surgical complications, but commonly results in hypothyroidism (may be delayed over time). Radiation thyroiditis commonly appears within 7 to 10 days after therapy and is associated with accelerated release of thyroid hormone into the blood. Rarely, this results in thyrotoxic crisis. Thyroidectomy is still used for younger patients or when ablation therapy is unsuccessful. Delayed complications include hypoparathyroidism (can be life threatening) and hypothyroidism.

Question 299

Methimazole contraindication

Answer 299

First-trimester pregnancy – use PTU

Question 300

Side effects Methimazole:

Answer 300

Granulocytopenia/agranulocytosis (If patient develops fever or sore throat, check CBC); Liver injury; Rash

Question 301

Indications for PTU

Answer 301

PTU has fallen out of favor and is only used in rare circumstances: first-trimester pregnancy, thyroid storm (some), reaction to Methimazole

Question 302

When monitoring patients on methimazole, dose changes are initially based on

Answer 302

Dose changes are initially based on free T4 changes and not TSH (TSH levels lag thyroid hormone levels to normalize)

Question 303

A 31-year-old man comes to the physician complaining of neck pain for the past week. The pain is located mainly in the neck, but states that it travels to the jaw at times. He experienced episodes of palpitations and anxiety-attacks for several weeks, which resolved spontaneously one week ago. Past medical history is significant for Crohn disease, which is well-managed with diet. The patient’s father had thyroid cancer at the age of 77. Temperature is 37.0°C (98.6°F), pulse is 82/min, blood pressure is 124/88 mm Hg, and BMI is 20 kg/m2. Palpation of the neck causes severe pain for the patient. The thyroid gland is asymmetrically enlarged. Laboratory studies show the following: ESR high TSH high Anti-thyroid peroxidase Negative Anti-thyroglobulin antibody Negative A biopsy of the thyroid gland is performed and shows diffuse infiltration with lymphocytes and giant cells forming noncaseating granulomas, as well as disruption and collapse of thyroid follicles. Further evaluation of this patient will most likely reveal which of the following? - Family history of thyroid cancer - Recent flare-up of Crohn disease - A recent viral infection - Biopsy showing vasculitic disease - Positive serology for thyroid-peroxidase autoantibodies

Answer 303

A recent viral infection Subacute granulomatous thyroiditis (de Quervain thyroiditis) is an inflammatory condition that occurs after a viral infection. The inflammation damages thyroid follicles, resulting in transient hyperthyroidism, followed by hypothyroidism, before returning to a euthyroid state. This patient had a previous episode of hyperthyroidism (e.g., palpitations, anxiety attacks), followed by an extremely tender neck mass, elevated ESR) signs and symptoms of hypothyroidism, and biopsy findings showing granulomatous inflammation of the thyroid. These findings are suggestive of subacute granulomatous thyroiditis (de Quervain thyroiditis). Although the exact mechanism is not yet established, subacute granulomatous thyroiditis is presumed to be caused by a viral infection. There are classically 3 stages to this condition, which are: 1) hyperthyroidism due to the extra thyroid hormones released by the damaged follicles, 2) hypothyroidism, and 3) return to a euthyroid state. Biopsy findings in the early phases will show neutrophils and destruction of follicles with colloid depletion, followed by formation of granulomas that surround the follicles. On clinical examination, the most common and consistent finding is severe neck pain, which can often radiate to the lower face, causing jaw pain. Since the underlying cause of this condition is inflammation, laboratory studies typically show an elevated ESR. The majority of cases resolve spontaneously after several weeks.

Question 304

A 41-year-old woman comes to the physician complaining of excessive fatigue for the last 2 weeks. She states that 1 month ago, she had experienced episodes of palpitations and diarrhea, but those symptoms have now resolved. Past medical history is significant for type I diabetes mellitus, which is treated with insulin. She also has been taking a laxative several times a week to help with new-onset constipation, which started 3 weeks ago. Temperature is 36.5°C (97.7°F), pulse is 48/min, blood pressure is 124/88 mm Hg, and BMI is 22 kg/m2. Physical examination shows cold, dry skin and thinning hair on the scalp. There is 1+ non-pitting edema on both lower extremities. Which of the following additional findings is likely present in this patient? - Diffuse uptake of radioactive iodine on thyroid scintigraphy - Positive antimicrosomal antibodies - Human leukocyte antigen DQ8 positivity - Decreased thyroid stimulating hormone levels - Positive TSH-receptor antibodies

Answer 304

Positive antimicrosomal antibodies Hashimoto thyroiditis is the result of an autoimmune-mediated lymphocytic inflammation and destruction of the thyroid tissue. Diagnosis is based on thyroid function tests, as well as the presence of certain antibodies, such as anti-thyroid peroxidase (anti-microsomal) and anti-thyroglobulin. This middle-aged female is presenting with constipation, dry skin, thinning hair, and non-pitting edema in the lower extremities. She most likely has hypothyroidism. Taking into account the history of a previously diagnosed autoimmune condition (e.g. type I diabetes mellitus) as well as prior symptoms of hyperthyroidism (e.g. episodes of palpitations and diarrhea), she most likely has chronic autoimmune thyroiditis (Hashimoto thyroiditis). Hashimoto thyroiditis is the leading cause of hypothyroidism in the United States; it is autoimmune-mediated, and thus it tends to occur in patients with other underlying autoimmune conditions such as type I diabetes mellitus and vitiligo. Although the etiology is not fully understood, there is autoimmune-mediated lymphocytic inflammation and destruction of the thyroid tissue. This destruction of the follicular cells results in release of preformed thyroid hormones, which usually presents as an initial phase of hyperthyroidism. Patients subsequently progress to hypothyroidism as the thyroid parenchyma is destroyed and fibrosed. Treatment is primarily with levothyroxine to replete the thyroid hormone deficiency.

Question 305

Queen Anne sign (sign of Hertoghe)?

Answer 305

In hypothyroidism, the loss of outer one-third of the eyebrows.

Question 306

Patients with subclinical hypothyroidism are more likely to develop overt disease if

Answer 306

positive antibodies

Question 307

Patient difficult to wean from ventilator with no other obvious cause, think?

Answer 307

Think hypothyroidism

Question 308

A 35-year-old female with symptoms of hyperthyroidism and a recent flu presents with neck pain and an elevated ESR. Think:

Answer 308

Subacute thyroiditis. Next step: Check thyroid function tests.

Question 309

A 75-year-old female presents with progressive obtundation and nonarousal. Core temperature is 35°C; cold, doughy skin; delayed deep tendon reflex in the relaxation phase. Urine analysis with many leukocytes and gram-negative rods. Think:

Answer 309

Myxedema coma.

Question 310

No single test can diagnose myxedema coma or thyroid storm: Think of as a spectrum of ——— with ——— as most concerning.

Answer 310

severe hypothyroidism/hyperthyroidism altered mental status (AMS) and hypothermia/hyperthermia

Question 311

——— are given empirically in myxedema coma before T4 is given due to a concern that:

Answer 311

Corticosteroids associated Addison disease exists; Giving only T4 could precipitate an addisonian crisis

Question 312

Thyrotoxic patient (weight loss, palpitations, heat intolerance, etc.) with a TENDER thyroid: Think

Answer 312

subacute thyroiditis, not Graves disease

Question 313

Hashimoto disease: Even though called thyroiditis, you often don’t see patients during———; epidemiology of Hashimoto thyroiditis?

Answer 313

the hyperthyroid phase Epi: Most common cause of hypothyroidism in the United States is Hashimoto thyroiditis

Question 314

A patient who comes in with fever, anxiety, and a painful neck should be worked up for? Labs? Next step tx?

Answer 314

thyroiditis (pain!) Labs: Thyroid function tests will show decreased TSH with increased T4 but decreased uptake on iodine scan Next step: Prescribe a NSAID or steroid

Question 315

Consider evaluating thyroid function tests in any patient with ——— lab finding

Answer 315

hypercholesterolemia

Question 316

Hypothermia is often missed by tympanic thermometers. Use a ——— if hypothermia is suspected

Answer 316

rectal probe

Question 317

———- is a common precipitant of myxedema coma; ——— is recommended for all affected patients

Answer 317

Infection panculture and empiric antibiotic therapy with broad-spectrum antibiotics

Question 318

——— have predictive value for progression to overt hypothyroidism or development of drug-induced thyroid dysfunction

Answer 318

Thyroid peroxidase autoantibodies (TPO Ab)

Question 319

The thyroid in Hashimoto and silent thyroiditis is ——— which distinguishes it from other forms of thyroiditis

Answer 319

nontender

Question 320

Presentation of silent thyroiditis

Answer 320

Usually occurs postpartum; presents similar to subacute thyroiditis except there is no tenderness of the gland (painless thyroiditis)

Question 321

Slowly enlarging, rock-hard mass in the anterior neck. Tight, stiff neck. Dx?

Answer 321

Riedel thyroiditis Must differentiate from thyroid cancer; Hypothyroidism may occur if advanced

Question 322

Riedel thyroiditis described as a ——— thyroid

Answer 322

“woody” thyroid: Tremendously firm and nonmobile

Question 323

Differential Dx for Hashimoto, subacute, or silent thyroiditis?

Answer 323

The hyperthyroid stage of Hashimoto, subacute, or silent thyroiditis may mimic Graves disease

Question 324

Differential Dx for Riedel thyroiditis?

Answer 324

must be differentiated from thyroid cancer

Question 325

Subacute thyroiditis can be mistaken for

Answer 325

oropharyngeal or tracheal infections or for suppurative thyroiditis

Question 326

Presentation of supperative thyroiditis

Answer 326

Fever with severe neck pain; Focal tenderness of involved portion of the gland; Usually a bacterial infection, but fungi and parasites have also been implicated; Immunocompromised hosts, or those with retained thyroglossal duct (IV antibiotics and abscess drainage, if present, should be performed)

Question 327

Radioactive iodine uptake (RAIU) can be useful to distinguish Graves disease (——— RAIU) from subacute thyroiditis (——— RAIU) in a thyrotoxic patient

Answer 327

increased decreased

Question 328

Presentation of hypothyroidism following viral URI is suggestive of

Answer 328

subacute thyroiditis

Question 329

Presentation of hypothyroidism after penetrating injury to the neck is suggestive of

Answer 329

suppurative processes

Question 330

Postpartum hypothyroidism presentation is suggestive of

Answer 330

silent thyroiditis

Question 331

Do not ———give drugs in thyroiditis

Answer 331

PTU or methimazole (mechanism in thyroiditis is release of preformed hormone from an inflamed gland, not overproduction of hormone by the gland)

Question 332

A 14-year-old girl comes to the emergency department because of worsening fatigue, nausea and vomiting for the past day. For the past week she has been receiving outpatient treatment of intravenous gentamicin for an infectious exacerbation of her longstanding bronchiectasis. She has type 1 diabetes and self-manages her insulin administration. She is afebrile, pulse is 92/min, respirations are 16/min, saturation is 96% on room air, and blood pressure is 142/86. An arterial blood gas shows pH 7.1, PaCO2 22 mmHg, PaO2 85 mmHg, and HCO3 14 mEq/L. Further blood results show an elevated serum blood urea nitrogen (BUN), creatinine and urea. Which of the following is the most likely diagnosis? -Intrinsic acute kidney injury -Chronic kidney disease -Pre-renal acute kidney injury -Acute pyelonephritis -Post-renal acute kidney injury

Answer 332

Intrinsic acute kidney injury Acute tubular necrosis (ATN) is the most common cause of intrinsic acute kidney injury, usually it results from an ischemic or toxic event. ATN has three phases, initiation, maintenance and recovery. This patient is suffering from an intrinsic AKI which is characterized by an acute, and often reversible reduction in GFR. The most common cause of Intrinsic AKI is ATN, which results from an acute ischemic and/or toxic event, which results in damage to the tissue parenchyma and impaired kidney function. In this patient, she has been receiving gentamicin, a known nephrotoxic medication that can cause ATN. Initiation, maintenance, and recovery are the 3 phases of ATN. The initiation phase is characterised by damage and necrosis to renal tubular cells, and there is an acute decrease in GFR to very low levels, with a sudden increase in serum creatinine and blood urea nitrogen (BUN) concentrations. The maintenance phase is characterized by sustained damage to renal tubular cells, and there is a continual, sustained reduction in GFR for up to 1-2 weeks with a concomitant rise in creatinine and BUN. Complications related to uremia often occur in this phase. During the recovery phase function is restored with re-epithelialization of tubules. Urine volume will increase and BUN/serum creatinine will return to normal. (Pre-renal acute kidney injury is characterized by normal kidneys that respond to hypoperfusion by decreasing the glomerular filtration rate. Although this patient is vomiting, it is much more likely that the nephrotoxic medication she is receiving is causing an intrinsic acute kidney injury, resulting in vomiting via a metabolic acidosis.) (Acute pyelonephritis is a bacterial invasion of the renal parenchyma leading to neutrophilic infiltration, possible scarring, and tissue damage. The patient is afebrile and has no specific signs or symptoms of pyelonephritis, such as flank pain or hematuria. )

Question 333

A 62-year-old man comes to the clinic for follow up after a hospital admission a month ago. During that admission he presented to the emergency department with left shoulder pain. He was discharged the following day with a diagnosis of "musculoskeletal pain" and was began on ibuprofen. He says he has been feeling fatigued since his discharge. His medications are low-dose aspirin, simvastatin, glipizide, and atenolol. He is afebrile, pulse is 57/min, respirations are 16/min, and blood pressure is 133/56 mm Hg. Urinalysis shows hyaline casts, and is negative for red or white blood cells. His creatinine level is 2.8 mg/dL, 4 weeks ago it was 1.3 mg/dL. Which of the following is the most likely diagnosis? -Rhabdomyolysis -Goodpasture syndrome -Acute interstitial nephritis -Acute kidney injury -Nephrotic syndrome

Answer 333

Acute kidney injury Acute kidney injury is a common adverse renal event caused by NSAIDs. Patients with underlying chronic kidney disease, volume depletion, heart failure, and those of an older age are at the most risk. Patients will have an increased plasma creatinine. NSAIDs, which includes ibuprofen and aspirin, are a class of medications used for analgesic and anti-inflammatory benefits. Adverse renal events occur in approximately 1-5% of patients taking NSAIDs, and result from a reduced renal production of prostaglandins, leading to reversible renal ischemia, reduced GFR, and acute kidney injury. Patients with underlying chronic kidney disease, volume depletion, heart failure, and those of an older age are more reliant on prostaglandin-mediated vasodilation of the afferent arteriole, and are therefor at a higher risk of NSAID induced reduction in GFR. Patients are found to have an increased plasma creatinine, usually incidentally as part of evaluation of an unrelated problem. Urinalysis is usually negative for hematuria and proteinuria. Significant proteinuria may indicate an NSAID-induced glomerular lesion. Urine may contain hyaline casts, and if acute tubular necrosis has developed, granular casts. White blood cells are not seen in acute kidney injury and are suggestive of acute interstitial nephritis. Treatment is based on stopping the offending agent, in this case the ibuprofen. If hypovolemia was present then volume resuscitation would also be warranted. Renal replacement therapy is very rarely required.

Question 334

Goodpasture syndrome is a rare autoimmune condition characterized by ———. Patients usually present with ———.

Answer 334

rapid destruction of the kidneys and lungs (IgG antibodies produced against the glomerular basement membrane result in damage via a type II hypersensitivity reaction) hemoptysis and hematuria

Question 335

Rhabdomyolysis can cause ——— failure, ——— levels are typically elevated. The disease is characterized by ———.

Answer 335

renal creatine kinase myalgia and red or brown coloured urine (myoglobinuria)

Question 336

Definition acute kidney injury:

Answer 336

- Increase in serum creatinine by ≥0.3 mg/dL within 48 hours - Increase in serum creatinine by ≥1.5 times baseline if known over 7 days - Urine volume <0.5 mL/kg/h for 6 hours (oliguria)

Question 337

Definition of pre-renal AKI:

Answer 337

AKI in which kidney glomerular and tubular functions remain intact but there is impaired kidney perfusion.

Question 338

Causes of pre-renal AKI:

Answer 338

• Absolute decrease in blood volume: hemorrhage or volume depletion (gi losses (N/V/D), kidney losses (polyuria, diuretic)) • Reductions in kidney perfusion due to edematous states: CHF (cardiorenal syndrome) low-flow state or Cirrhosis (hepatorenal syndrome) • Drugs that affect glomerular hemodynamics: Decrease afferent arteriolar dilatation (NSAIDs or calcineurin inhibitors) or Decrease efferent arteriolar constriction: ACE inhibitors or ARBs

Question 339

Key lab values with pre-renal AKI:

Answer 339

BUN: Cr ratio >20:1 (BMP) urine sodium<20 mEq/L FeNa: - <1% – pre-renal. - 1%–2% – pre-renal or acute tubular necrosis (ATN). - > 2% – ATN • FeUrea: - <35% – pre-renal. - 35%–50% – pre-renal or ATN. - >50% – ATN. Urine osmolality >500 mOsm/kg or urine osmolality greater than plasma osmolality (In pre-renal acute renal failure the kidney is responding to poor renal perfusion by retaining sodium and water ( --> low urine sodium and a concentrated urine with high osmolality).)

Question 340

Define fractional excretion of sodium and it’s clinical significance:

Answer 340

Fractional excretion of sodium is the amount of sodium that leaves the body through urine compared to the amount filtered and reabsorbed by the kidney. (Ie, FENa is calculated in two parts—figuring out how much sodium is excreted in the urine, and then finding its ratio to the total amount of sodium that passed through (aka "filtered by") the kidney) FENa can be useful in the evaluation of acute kidney failure in the context of low urine output. Low fractional excretion indicates sodium retention by the kidney, suggesting pathophysiology extrinsic to the urinary system such as volume depletion or decrease in effective circulating volume (e.g. low output heart failure). Higher values can suggest sodium wasting due to acute tubular necrosis or other causes of intrinsic kidney failure. The FENa may be affected or invalidated by diuretic use, since many diuretics act by altering the kidney's handling of sodium.

Question 341

For assessing pre-renal AKI vs ATN, ——— is the most widely used but it is not accurate when patients are using ———. In those cases, you can use ———.

Answer 341

FeNa diuretics FeUrea

Question 342

Treatment for cardiorenal syndrome

Answer 342

Diuretics (relieve venous congestion to improve kidney perfusion and improve cardiac output if in cardiogenic shock)

Question 343

Treatment for heptaorenal syndrome syndrome

Answer 343

Some evidence for midodrine and octreotide to improve kidney perfusion and combat splanchnic vasodilation, though definitive treatment is liver transplant.

Question 344

Tx pre-renal AKI from hypovolemia

Answer 344

Intravenous fluids. Find and reverse the underlying cause. Pre-renal AKI reverses relatively quickly with fluids in hypovolemia. Prolonged pre-renal AKI can lead to tubular damage.

Question 345

A patient is being treated for an infection with penicillin and now presents with acute kidney injury several days after the initiation of antibiotic therapy. The urine sediment reveals numerous white blood cells and white blood cell casts. Think:

Answer 345

Acute interstitial nephritis and stop the antibiotic.

Question 346

Definition of renal AKI:

Answer 346

AKI in which there is injury to part of the kidney parenchyma

Question 347

Your patient is found down after several days and has acute kidney injury, hyperkalemia, and a mark- edly elevated creatinine kinase (CK) level. Think:

Answer 347

Rhabdomyolysis

Question 348

Types of renal AKI

Answer 348

1. Glomerular diseases: Nephritic and nephrotic syndromes 2. Interstitial diseases: Acute interstitial nephritis 3. Tubular disease: ATN

Question 349

Acute interstitial nephritis is classically, described with

Answer 349

Presence of fever, rash, eosinophilia, and eosinophiluria (but these features are not commonly seen)

Question 350

Causes of AIN

Answer 350

- Autoimmune diseases: Sjögren disease, sarcoidosis - Medications: β-lactam antibiotics, NSAIDs, PPIs

Question 351

ATN causes

Answer 351

• Ischemic: Hypotension from any cause leads to impairment of kidney perfusion and tubular necrosis. • Sepsis: Mediated by both hypotension and inflammation and cytokine-induced injury. • Toxic: - Contrast: IV contrast for CT scan and cardiac catheterization. - Antibiotics: Aminoglycoside antibiotics, vancomycin commonly. - Rhabdomyolysis: Myoglobinuria (look for elevated creatine kinase levels). - Severe hemolysis causing hemoglobinuria.

Question 352

Labs with renal AKI

Answer 352

- BUN: Cr ratio 10:1 or 15:1. - Urine sodium >20 mEq/L or FeNa>1% or FeUrea >35%. - Urine sediment: Tubular injury: Muddy brown granular casts. Interstitial injury: WBCs, WBC casts.

Question 353

Don’t order a test to look for ——— to confirm acute interstitial nephritis (AIN), as this test has both low sensitivity and specificity

Answer 353

urine eosinophils

Question 354

Definition postrenal AKI:

Answer 354

AKI from the obstruction of urinary outflow tracts. (Urine flows from kidney to ureters to bladder then to urethra)

Question 355

Causes of postrenal AKI:

Answer 355

-Ureter Obstruction: Retroperitoneal fibrosis; Obstructing kidney stones -Bladder: Neurogenic bladder (i.e., diabetic nephropathy, paralysis, anticholinergics, antihistamines); Bladder, urologic, or cervical tumor. Urethra: Malpositioned Foley catheter; Benign prostatic hypertrophy (BPH), prostate cancer.

Question 356

Key diagnostic step and tx with post-renal AKI:

Answer 356

Palpate the lower abdomen to look for a distended bladder on physical exam. A bedside ultrasound can also confirm the presence of a distended bladder and lead to a quick diagnosis of obstructive uropathy. Treatment is placement of a Foley catheter.

Question 357

Diagnostic Workup for post-renal AKI:

Answer 357

- Physical exam: Lower abdominal palpation to look for distended bladder - Renal ultrasound is the image of choice because of the speed of obtaining it. But CT scan is also reasonable, especially if nephrolithiasis is a concern and can better delineate masses. - Hyperkalemia is common due to the development of a type 4 renal tubular acidosis (RTA) in postrenal AKI.

Question 358

Approaches to relieving obstruction in post-renal AKI

Answer 358

Foley: If the obstruction is at the level of the bladder or distal to it, place a Foley catheter Percutaneous nephrostomy (cannulation of renal pelvis resulting in flow of urine directly from kidney into an external bag) if obstruction is above bladder or unable to bypass with Foley catheter

Question 359

After relief of the obstruction in post-renal AKI, look out for:

Answer 359

postobstructive diuresis (mild to severe polyuria) (High urine output after obstruc- tion relief is described as postob- structive diuresis. Urine output should be replaced with hypotonic fluid (ie, 0.45% NaCl - half normal saline), to prevent volume depletion. Electrolytes should be monitored and replaced often.)

Question 360

NSAIDs may cause ——— in kidneys. This is characterized by:

Answer 360

acute interstitial nephritis with an interstitial inflammatory infiltrate pyuria, hematuria, white cell casts, proteinuria, and a rise in the plasma creatinine concentration.

Question 361

Nephrotic syndrome is a nonspecific disorder in which the kidneys are damaged, causing

Answer 361

them to leak large amounts of protein resulting in significant proteinuria, hypoalbuminemia, hypercholesterolemia and increased clot formation

Question 362

EA Prev 1 of 4 Next Settings A 28-year-old man is reviewed on the surgical ward because of oliguria for 12 hours. The patient had an emergency splenectomy 1 day ago for a ruptured spleen after being involved in a motor vehicle accident. Temperature is 36.8°C (98°F), pulse is 87/min, respirations are 18/min, and blood pressure is 102/64 mm Hg. Examination shows a midline laparotomy scar and marked abdominal hematoma. Laboratory tests show low haemoglobin and elevated serum creatinine. Which of the following is the most likely diagnosis? -Acute tubular necrosis -Bladder calculi -Acute tubulointerstitial nephritis -Acute glomerulonephritis -Renal vasculitis

Answer 362

Acute tubular necrosis ATN is a condition commonly related to episodes of significant hypotension leading to renal hypoperfusion, leading to necrosis of proximal convoluted tubule epithelium. Muddy brown casts in the urine are virtually pathognomonic. This patient has ATN, secondary to renal ischemia that resulted from his injury/hemorrhage. A history significant for recent hypotension, surgery, or volume depletion is an important factor that may help make this diagnosis. Hypotension causes decreased blood flow to the kidney, which eventually results in infarction of the proximal convoluted tubule epithelium, which then sloughs off, resulting in "muddy brown casts" and a decrease in the GFR (glomerular filtration rate). This manifests as oliguria. Other causes of ATN include direct toxic injury to the epithelium of the proximal convoluted tubular. These toxins may include free hemoglobin or myoglobin (e.g. post crush injury), antibiotics (e.g. aminoglycosides), statins (e.g. atorvastatin), or cytotoxic drugs (e.g. cisplatin). Intoxication with ethylene glycol or "anti-freeze" can also cause acute tubular necrosis. (Renal vasculitis is an important diagnostic consideration in patients with oliguria, however this patient has an obvious inciting event that led to his condition. Also note that the history does not suggest an autoimmune condition or chronic disease state that might suggest renal vasculitis.) (Acute glomerulonephritis usually develops following an infection, as in Poststreptococcal Glomerulonephritis (PSGN). This patient's history is not suggestive of this diagnosis.) (Bladder calculi can cause blockage of the urethra and oliguria. However, this leads to pain, most commonly beginning in the flank or lower back and often radiating to the groin. Other associated symptoms include: nausea, vomiting, fever, blood in the urine, pus in the urine, and painful urination.)

Question 363

A 38-year-old woman comes to the emergency department for evaluation of altered mental status that began five hours ago. She is accompanied by her husband. Past medical history is notable for asthma and diffuse scleroderma. On arrival, her temperature is 37.6°C (99.7°F) and blood pressure is 183/121 mmHg. On physical examination, the patient is oriented to self but neither time nor place. Diffuse thickening of the skin is observed, and contractures are present in the bilateral fingers. Laboratory testing is obtained, and results are as follows: Hemoglobin low Leukocyte Count normal Platelet Count low Blood Urea Nitrogen high Creatinine, Serum high Which of the following is the next best step in the management of this patient’s condition? -Initiation of propranolol therapy -Long-term dialysis -Initiation of methotrexate therapy -Initiation of prednisone therapy -Initiation of captopril therapy

Answer 363

Initiation of captopril therapy Scleroderma renal crisis is characterized by severe hypertension and acute renal failure. It can present with hypertensive encephalopathy, heart failure, and arrhythmias. Laboratory testing will reveal an elevated blood urea nitrogen, elevated creatinine, and low platelet count. ACE-inhibitors are the first-line treatment option. This patient is having a scleroderma renal crisis, which is characterized by severe hypertension and acute renal failure. Over 90% of patients with scleroderma renal crisis have blood pressures exceeding 150/90 mmHg. Renal failure can present with elevated blood urea nitrogen and creatinine levels. In addition, patients can present with hypertensive encephalopathy, heart failure, and arrhythmias. The pathophysiology of scleroderma renal crisis is unclear; however, it is believed that the renin-angiotensin-aldosterone system (RAAS) plays an important role. Scleroderma is known to cause damage to small arteries within the kidneys, which subsequently undergo hypertrophy, resulting in relative ischemia. In severe cases, damage to the renal blood vessels can trigger thrombosis, occluding the glomerular capillaries. This causes rapid deterioration in renal function, resulting in scleroderma renal crisis. Of note, the thrombosis can lead to a low platelet count on laboratory testing, as well as the presence of schistocytes on peripheral blood smear. Angiotensin-converting (ACE) inhibitors are the first-line treatment for scleroderma renal crisis. Dialysis can be used in an acute setting in patients with significant kidney injury; however, long-term dialysis is indicated only in patients who develop end-stage renal disease as a result of the injury.

Question 364

Define CHF

Answer 364

failure of the heart to pump blood effectively to the tissues (CHF is also known as heart failure with reduced ejection fraction (HFrEF), as opposed to heart failure with preserved ejection fraction (HFpEF))

Question 365

Key results of left heart failure vs right heart failure:

Answer 365

Left heart failure causes pulmonary venous congestion and compromised systemic circulation. Right heart failure causes systemic venous congestion.

Question 366

The most common cause of right heart failure is

Answer 366

chronic left heart failure

Question 367

Define Congestive Heart Failure with Preserved Ejection Fraction (HFpEF; Formerly Known as Diastolic Dysfunction)

Answer 367

CHF with a normal ejection fraction; the problem occurs during filling (diastole) due to cardiac wall stiffness. HFpEF is a poorly understood condition.

Question 368

HFpEF: Epi? Sxs? Associated with? Tx?

Answer 368

Epi: Accounts for 40% to 60% of heart failure; More common in women Signs/symptoms of heart failure with normal ejection fraction (>50%) Associated with hypertension, left ventricular hypertrophy (LVH), dilated cardiomyopathy, and ischemia Most therapies with proven benefit for HFrEF have not been proven to have a mortality benefit in HFpEF. Treat hypertension, use diuretics for congestion, and control heart rate if in atrial fibrillation.

Question 369

Left Heart Failure: key sxs

Answer 369

dyspnea, orthopnea (dyspnea that worsens when lying down), paroxysmal nocturnal dyspnea (dyspnea that wakes patient from sleep), cough (usually nonproductive), nocturia, weight gain from fluid retention

Question 370

Left Heart Failure: key exam signs

Answer 370

rales (ie crackles), S3 gallop, jugular venous distention, tachycardia, peripheral edema

Question 371

Describe pathophysiology/common cause of S3 and S4

Answer 371

Both S3 and S4 have similar pathophysiology; they are caused by rapid deceleration of blood going from the left atrium to the left ventricle. In the case of S3, the blood decelerates due to a congested LV from CHF, whereas in S4 it decelerates due to a hypertrophied LV

Question 372

Describe the sound of S3 vs S4

Answer 372

They are both low-pitched sounds that are therefore best heard with the bell while listening at the apex. S3 is heard immediately after S2, whereas S4 is heard immediately prior to S1. S3 comes and goes with changes in volume status and is therefore an important tool for evaluating volume overload, whereas S4 generally does not come and go.

Question 373

On their own, crackles or edema are not statistically significantly associated with CHF, so always check for

Answer 373

an S3 gallop and elevated neck veins

Question 374

Right Heart Failure: Key sxs:

Answer 374

right upper quadrant pain (due to hepatic congestion), dyspnea, abdominal swelling (ascites), weight gain (fluid retention)

Question 375

Right Heart Failure: Key signs

Answer 375

hepatomegaly, hepatojugular reflex, JVD, ascites, cirrhosis, abnormal liver function tests (congestive hepatopathy), peripheral edema

Question 376

——— is the most specific SXS of heart failure. ——— is the most specific SIGN.

Answer 376

Orthopnea S3

Question 377

The initial evaluation of left-sided heart failure should include an evaluation of ischemia as the cause using

Answer 377

angiography or perfusion imaging

Question 378

Key causes of left sided HF

Answer 378

Question 379

A 26-year-old man presents with SOB, PND, orthopnea, and pleuritic chest pain for 1 week. He had an URI 1 week prior to onset of symptoms. Dx? Workup? Tx?

Answer 379

Dx: Viral myocarditis (type of dilated cardiomyopathy) Workup: ECG shows diffuse ST-segment elevation and PR-segment depression. Treat with NSAIDs. Steroids have not been shown to change outcomes.

Question 380

Key causes of right HF

Answer 380

Question 381

Decreased LVEF is a sign of a cardiomyopathy; ——— necessary to diagnose the syndrome of heart failure.

Answer 381

symptoms

Question 382

Heart failure with a normal ejection fraction still requires evidence of

Answer 382

ventricular dysfunction

Question 383

New York Heart Association (NYHA) Functional Classification of Heart Failure

Answer 383

Class I: No limitation Class II: Slight limitations (symptoms with ordinary efforts) Class III: Marked limitation (comfortable at rest, symptoms with minimal efforts)

Question 384

——— can cause acute right ventricular failure by producing an acute increase in afterload.

Answer 384

Pulmonary embolism

Question 385

Workup findings in HF: chest X-ray

Answer 385

Chest x-ray can show enlargement of cardiac silhouette, pulmonary vascular congestion with redistribution to upper lobes, and effusion

Question 386

B-type (brain) natriuretic peptide: Released from? Diagnostic for?

Answer 386

Released from ventricular myocytes in response to tension BNP blood test used for diagnosing HF

Question 387

——— is the gold standard for diagnosing right or left heart failure

Answer 387

Echocardiogram

Question 388

Workup findings in HF: BNP

Answer 388

Brain natriuretic peptide (BNP) is elevated in CHF with fluid retention

Question 389

Virtually all patients with new-onset heart failure should have a workup for ———, including:

Answer 389

CAD stress testing and usually a cardiac catheterization

Question 390

——— are the only drug indicated in patients with a decreased LVEF without symptoms of heart failure

Answer 390

ACE inhibitors

Question 391

First-line therapy HF

Answer 391

• ACE inhibitors: Decrease afterload and preload. They decrease symptoms, improve survival, and decrease hospitalization. • Diuretics: Use in NHYA class II to IV for fluid retention. Helps to reduce preload, improve symptoms, but does not change mortality. Use loop diuretics like furosemide or bumetanide to produce natriuresis and diuresis, not thiazide diuretics. • Beta blockers: For NYHA class II to III (decrease symptoms, improve survival). Only metoprolol, carvedilol, or bisoprolol are approved for heart failure in the United States. • Spironolactone (potassium-sparing diuretics): Low dose, use in NYHA class III to IV because it improves survival. Concomitant use of ACE inhibitors can make potassium go very high, so monitor closely. • Eplerenone: Similar to spironolactone, but fewer side effects (namely gynecomastia). • Implantable cardioverter-defibrillator (ICD): Should be implanted in any patient who has had VT or fibrillation. As primary prevention in patients with CHF, ICD has been shown to improve survival in select patients. First, pharmacologic therapy must be maximized prior to consideration for ICD.

Question 392

Second-line therapy HF

Answer 392

• Neprilysin inhibition (sacubitril) with angiotensin receptor neprilysin blocker (ARNI): Shown to improve symptoms, reduce hospitalizations, and improve survival in patients who remain symptomatic on ACE inhibitors or can’t tolerate them. • Angiotensin receptor blockers (ARBs): If ACE inhibitors are not well tolerated (e.g., cough). • Nitrate–hydralazine combination: Improves symptoms and survival. High rate of intolerance and lower effect on mortality make this therapy a second line to ACE inhibitors. It is often used in patients who cannot tolerate an ACE inhibitor or ARB. • Cardiac resynchronization therapy: Reserved for patients who are in class III heart failure despite maximal therapy. Essentially a pacemaker that times the contractions of both ventricles for maximum efficiency and has to been shown to improve survival. • Digoxin: Add for NYHA class III to IV in patients in atrial fibrillation (for symptomatic relief only; does not improve survival but reduces hospitalization).

Question 393

ICD implantation in heart failure patients may not prevent

Answer 393

sudden cardiac death

Question 394

A 74-year-old caucasian man comes to the clinic for a planned review. His past medical history is significant for New York Heart Association (NYHA) Stage II heart failure. His current medications include lisinopril 20 mg, furosemide 20 mg, potassium chloride 10 mg twice daily, rosuvastatin 10 mg, and low dose aspirin. He also supplements his medications with fish oil several days a week. Given his class of heart failure, which of the following medications could be added to his heart failure treatment to optimize mortality benefits? - Atenolol 50mg daily - Digoxin 0.125 mg daily - Amlodipine 10mg daily - Isosorbide dinitrate/hydralazine 20 mg /37.5 mg - Metoprolol succinate 12.5 mg daily

Answer 394

Metoprolol succinate 12.5 mg daily Patients with congestive heart failure should receive either an ACE inhibitor or an angiotensin receptor blocker, and one of the following beta-blockers: bisoprolol, carvedilol, or sustained-release metoprolol succinate. According to current guidelines, patients with congestive heart failure (CHF) should receive a beta-blocker and an angiotensin antagonist in the form of either an angiotensin converting-enzyme inhibitor or an angiotensin receptor blocker (ARB). When selecting these medications, recall that only three distinct beta-blockers have been proven to reduce all-cause and cardiac-specific mortality in patients congestive with heart failure. These include the following: (1) bisoprolol, (2) carvedilol, and (3) sustained-release metoprolol succinate. Long-term randomized controlled trials have only demonstrated mortality benefits for heart failure patients with the use of ACE inhibitors, angiotensin receptor blockers, and these select beta-blockers. Neither digoxin nor other subtypes of beta-blockers have demonstrated such a benefit.

Question 395

A 72-year-old man comes to the office because he's been having progressively worsening shortness of breath over the past six months, but no fevers or cough during that time. Rales are heard in all lung fields. He has a chest X-ray which shows peribronchial cuffing and a prominent left-sided heart shadow, and an echocardiogram which shows concentric hypertrophy of the left ventricular wall. Which of the following is most likely to be the underlying cause of these symptoms and findings? - Emphysema - Tricuspid valve regurgitation - Alcohol abuse - Silicosis - Hypertension

Answer 395

Hypertension Hypertension commonly leads to left ventricular hypertrophy, which can progress to congestive heart failure. Antihypertensive therapy can induce some regression of left ventricular hypertrophy. This patient has left ventricular hypertrophy (LVH) on echocardiogram, a common finding in patients with hypertension. LVH is associated with cardiovascular complications, including decreased left ventricular ejection fraction and congestive heart failure. Congestive heart failure can cause symptoms like pulmonary edema and dyspnea, which were both seen in this patient. Other sequelae of LVH include aortic root dilation, ventricular arrhythmias, and even sudden cardiac death. LVH causes myocardial ischemia which is the underlying mechanism for the cardiac complications. This happens because there is more muscle tissue which increases the demand for blood, and there's a relative reduction in capillary density and ability for arteriole dilation in the thickened muscle which reduces supply. Antihypertensive therapy with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can lead to some regression of LVH. (Emphysema is a chronic obstructive pulmonary disease that usually leads to pulmonary hypertension and subsequent cor pulmonale and right-sided heart failure. Typical symptoms of right-sided heart failure include elevated jugular venous distention, congestive hepatomegaly, and peripheral edema.) (Tricuspid valve regurgitation is a right-sided heart lesion that is more likely to cause right-sided heart failure. Typical symptoms of right-sided heart failure include elevated jugular venous distention, congestive hepatomegaly, and peripheral edema.) (Silicosis is a type of a restrictive lung disease which can cause pulmonary hypertension and subsequent cor pulmonale and right-sided heart failure. Typical symptoms of right-sided heart failure include elevated jugular venous distention, congestive hepatomegaly, and peripheral edema.) (Alcohol abuse can lead to dilated cardiomyopathy, which typically affects both left and right ventricular function. Dilated cardiomyopathy often presents with an enlarged cardiac silhouette, but it has a pattern of eccentric hypertrophy, rather than concentric hypertrop)

Question 396

Tx HFpEF:

Answer 396

Unlike HFrEF, there is limited evidence to support a specific drug regimen, as no drugs have been proven to change mortality. 1. Diuresis: Generally done with loop diuretics (important to remember that HFpEF patients with stiff, small left ventricles are preload dependent, so it is important to avoid overdiuresis) 2. Control HTN 3. Heart rate control in patients with atrial fibrillation

Question 397

Cardiac resynchronization is effective for patients with

Answer 397

LV dysfunction and a wide QRS complex on ECG (>150 ms with a left bundle branch morphology)

Question 398

Clinical features of acute decompensated HF

Answer 398

- Pulmonary edema is characterized by dyspnea with hypoxia as it progresses. Chest roentgenogram (X-ray) shows pulmonary congestion - Congestive hepatopathy is low-level hepatic ischemia and consequent dysfunction from impaired venous outflow. Traditionally described as mild transaminitis without significant bilirubinemia. - Renal dysfunction typically as a result of impaired venous outflow, or the “cardiorenal” syndrome

Question 399

Causes of ADHF

Answer 399

-myocardial ischemia, -arrhythmias (VT, supraventricular tachycardia [SVT] with fast ventricular rates), -infection, -valvular disease, -medication and dietary noncompliance

Question 400

Initial Management ADHF:

Answer 400

• Oxygen: Supplemental oxygen should be provided to improve hypoxia,and in cases of severe respiratory distress, bilevel positive airway pressure (BiPAP) can be used and even intubation if needed. • Diuretics: Must be given immediately. They both relieve congestion and reduce afterload. Commonly used diuretics are furosemide, torsemide, and bumetanide. • Afterload reduction: In patients with normal or elevated blood pressure who are not responding initially to diuretics, further afterload reduction may be needed. Nitroglycerin infusions are often used. Is the patient’s tissue perfusion impaired? Are they cold or warm? • Inotropes: In patients with signs of cardiogenic shock (e.g., cold extremities ) ADHF will often require an inotrope to augment myocardial contractility.

Question 401

Patients with ADHF not responding to loop diuretics may benefit from ——— to increase venous capacitance and improve renal function.

Answer 401

IV nitrates

Question 402

When treating ADHF: Hold ——— when using inotropes and watch for ———.

Answer 402

beta blockers arrhythmias

Question 403

Commonly used iontropes in tx ADHF (in patients with signs of cardiogenic shock (e.g., cold extremities))

Answer 403

a. Dobutamine – increases contractility with vasodilation. b. Norepinephrine – increases contractility with vasoconstriction. c. Milrinone – similar to dobutamine, but expensive; useful in patients chronically on a beta blocker.

Question 404

A 6-year-old boy is brought to his pediatrician's office by his parents because of blister formation on his buttocks for the past 3 days. His mother reports seeing enlarged blisters on his buttocks that appear to be filled with fluid. His temperature is 37.1°C (98.8°F); pulse is 72/min; respirations are 18/min, and blood pressure is 95/60 mm Hg. Physical examination shows the following image: Which is the following toxins is most likely responsible for this patient's condition? - Toxic shock syndrome toxin-1 - Streptolysin S - Exfoliative toxin A - Pyrogenic exotoxin - Streptolysin O

Answer 404

Exfoliative toxin A Bullous impetigo is caused by exfoliative toxin A released from Staphylococcus aureus. Bullous impetigo should be treated with oral antibiotics.

Question 405

——— is the most common contagious bacterial skin infection in children. The most common organism implicated in this infection is ——— and the second most common organism is ———.

Answer 405

Impetigo Staphylococcus aureus group A beta-hemolytic Streptococcus pyogenes

Question 406

The most common form of impetigo is the——— characterized as ———.

Answer 406

non-bullous form papules and vesicles with a honey-crust appearance

Question 407

Bullous impetigo results from ———-. Physical examination shows ———.

Answer 407

Staphylococcus aureus species which produces exfoliative toxin A fragile bullae filled with yellow fluid (Staphylococcal scalded skin syndrome (SSSS) is also caused by an exfoliative toxin produced by Staphylococcus aureus. Exfoliative toxins are spread hematogenously from a localized source and can cause epidermal damage at distant sites. Meanwhile, bullous impetigo causes localized infection and cultures of the blisters will grow Staphylococcus aureus)

Question 408

Exfoliative toxins produced by Staphylococcus aureus cause:

Answer 408

Staphylococcal scalded skin syndrome (SSSS) and bullous impetigo

Question 409

C

Question 410

C

Question 411

A 45-year-old man comes to the emergency department and is undergoing coronary artery bypass grafting for the treatment of ischemic heart failure with reduced ejection fraction. He has no allergies to medications. At the beginning of the case, his cardiac index is 1.8 L/min/m2. Which of the following medications is most appropriate to provide myocardial support for this patient? Phenylephrine Dexmedetomidine Glycopyrrolate Fenoldopam Dobutamine

Answer 411

Dobutamine Ischemic heart failure causes low cardiac output, which should be treated with inotropic agents like dobutamine rather than chronotropic agents that can worsen myocardial ischemia. This patient is undergoing coronary artery bypass grafting for the treatment of ischemic heart failure and is characterized by a low cardiac output. Patients with diminished cardiac output secondary to ischemic heart disease are most appropriately treated by vasoactive agents that provide myocardial support through increased inotropy. Dobutamine, a β-adrenergic agonist at β1 receptors, is commonly used as a first-line therapy to treat patients with heart failure, as it acts primarily by inotropic rather than chronotropic effects. Chronotropic agents, such as dopamine, should be avoided as first-line treatment for patients with low cardiac output, as they can increase myocardial oxygen demand and worsen ischemia.

Question 412

Inotropic vs chronotropic?

Answer 412

inotropic (increases contractility), vs chronotropic (increases heart rate)

Question 413

Describe the FAST exam:

Answer 413

Focused assessment with sonography in trauma (commonly abbreviated as FAST) is a rapid bedside US performed as a screening test for blood around the heart (hemopericardium) or abdominal organs (hemoperitoneum) after trauma. )There is also the extended FAST (eFAST) which includes some additional US views to assess for pneumothorax)

Question 414

A 56-year-old man comes to the hospital for an open resection of a gastrinoma. He has a 20-year history of gastroesophageal reflux disease, a 15-year history of type 2 diabetes mellitus, and a 10-year history of congestive heart failure. Current medications include pantoprazole, metformin, glyburide, lisinopril, and metoprolol. He has a history of severe allergy to propofol, for which thiopental is given as an anesthetic induction agent. After thiopental administration, the patient's cardiac output drops severely, necessitating the use of vasopressors and inotropes. Which of the following medications is the most likely precipitating factor in the patient's sudden decrease in cardiac output? -Metformin -Pantoprazole -Metoprolol -Lisinopril -Glyburide

Answer 414

Metoprolol Congestive heart failure and β blockers can blunt the normal physiologic response of tachycardia to compensate for hypotension. These patients may experience a profound drop in cardiac output on the administration of barbiturates, which cause vasodilation and hypotension. Barbiturates such as thiopental can be used for anesthetic inductions. These medications lower blood pressure by depressing the medullary vasomotor center, causing global vasodilation and peripheral pooling of blood. Physiologically, the baroreceptor response to hypotension elicits a reflex tachycardia that maintains normal cardiac output. In addition, the central vagolytic effect of barbiturates is a minor factor in this compensatory response. If the baroreceptor response is blunted, a profound decrease in cardiac output can occur with barbiturate administration, as the patient's systemic hypotension is not compensated by increased heart rate. In particular, congestive heart failure and β-adrenergic blockers such as metoprolol can interfere with the physiologic compensation. Due to lack of a compensatory response, these patients can suffer a severe drop in cardiac output when given barbiturates.)

Question 415

A 60-year-old man comes to the emergency department because of severe shortness of breath. He has become progressively dyspneic over the past month and he can no longer walk to the bathroom without stopping to catch his breath. Patient says he stopped some of his home medications because he "couldn't stand going to the bathroom so much". Patient's medical history is contributory for congestive heart failure. His temperature is 37.8°C (100°F), pulse is 120/min, respirations are 28/min, and blood pressure is 145/90 mm Hg. Physical examination shows jugular venous pulsations on the ear and well perfused lower extremities, with 3+ pitting edema bilaterally. An S3 sound and wheezes in all lung fields are heard on auscultation. ECG shows sinus tachycardia and chest x-ray is shown below. Which of the following is the most appropriate next step in management? -Ipratroprium -Metoprolol -Nitroglycerin -Furosemide -Dobutamine

Answer 415

Metoprolol Nitroglycerin is used to decrease preload and alleviate symptoms in acute decompensated congestive heart failure (CHF) exacerbation. CHF is related with pulmonary edema (PE), which is fluid accumulation in the air spaces and parenchyma of the lungs that leads to impaired gas exchange causing respiratory failure. Pulmonary edema (PE) is fluid accumulation in the air spaces and parenchyma of the lungs. It leads to impaired gas exchange and causes respiratory failure. It can be a cardiogenic pulmonary edema (CPE) or a noncardiogenic pulmonary edema (NCPE). PE leads to fatal respiratory distress or cardiac arrest due to hypoxia, and is characterized by dyspnea, hemoptysis, hyperhidrosis, anxiety, and pallor. Diagnose is made with low oxygen saturation, disturbed arterial blood gas readings, and chest X-ray, which shows fluid in the alveolar walls, Kerley B lines (short lines perpendicular to the pleural surface that extend one to two centimeters into the lung and represent the thickening of the pulmonary interstitium), increased vascular shadowing, upper lobe diversion, and pleural effusions, among others. Managment is with tracheal intubation, mechanical ventilation, supplementary oxygen, and treatment of the underlying cause. Loop diuretics are administered, often together with morphine or diamorphine to reduce respiratory distress. Specific vasodilators are used (intravenous glyceryl trinitrate or ISDN), continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BIPAP/NIPPV), for reducing the need of mechanical ventilation. In acute decompensated congestive heart failure (CHF) exacerbation, the underlying cause is treated. Nitroglycerin is used to decrease preload and alleviate symptoms. (Furosemide is a loop diuretic that reduces a person's total volume status over the course of hours to days. However, in the absence of prior preload or afterload reduction, furosemide is associated with worsening hemodynamic function.) (Dobutamine is a catecholamine inotropic agent which is used to increase cardiac output in patients who have congestive heart failure and signs of poor organ perfusion. However, inotropic therapies are also associated with tachyarrhythmias, increased myocardial oxygen demand, and increased rates of mortality.)

Question 416

Tiotropium and Ipratropium use?

Answer 416

a competitive inhibition of muscarinic receptors and it is used in chronic obstructive pulmonary disease (COPD) to prevent bronchoconstriction

Question 417

A 25-year-old previously healthy woman comes to the emergency department because of 2 days of mild nausea and vomiting. She denies recent sick contacts or eating anything out of the ordinary. She has maintained good oral intake of food and fluids over the past two days, but has noticed increasing malaise and a dull pain on her right side. She endorses mild dysuria and urinary frequency for the past 2 days. Medical history is negative for kidney stones. Her temperature is 38.3°C (101.0°F), pulse is 101/min, respirations are 18/min, and blood pressure is 108/68 mm Hg. Physical examination shows no definite costovertebral angle tenderness on percussion or palpation. Urine dipstick is positive for leukocyte esterase and hematuria. Urinalysis shows white blood cell casts. Which of the following is the most likely diagnosis? -Pyelonephritis -Transitional cell carcinoma -Acute cystitis -Kidney stones -Complicated UTI

Answer 417

Pyelonephritis Pyelonephritis can present mildly as a low-grade fever (which distinguishes it from cystitis alone), with or without costovertebral angle tenderness (CVAT), and signs of cystitis (i.e. dysuria, urinary frequency, urinary urgency), or more severely with rigors, chills, nausea, and vomiting. This patient has an infection of the renal parenchyma, calyces, and renal pelvis called pyelonephritis. Fever is often the differentiating clinical sign that distinguishes pyelonephritis from cystitis. Pyelonephritis can present mildly as a low-grade fever with or without costovertebral angle tenderness (CVAT) and signs of cystitis (i.e. dysuria, urinary frequency, urinary urgency). More severe infections present with high spiking fevers, rigors, nausea, vomiting, and flank/loin pain which can progress to severe sepsis. Renal papillary necrosis can rarely occur leading to an obstructive uropathy. Acute pyelonephritis is often caused by an ascending urinary tract E. coli infection that results in neutrophilic infiltration of the renal interstitium on histology. White blood cells also flood the tubules, form casts, and are seen on urinalysis. Chronic pyelonephritis occurs after repeated bouts of acute pyelonephritis and eventually the kidney tubules fill with eosinophilic casts, referred to as thyroidization of the kidney (because they resemble thyroid follicles on histology).

Question 418

Define multifocal atrial tachycardia? Associations?

Answer 418

Irregularly irregular rate and rhythm with at least 3 distinct P wave morphologies, due to multiple ectopic foci in atria. Associated with COPD, pneumonia, HF.

Question 419

Cardiac myxomas: Epi? Location? Presentation? Histo?

Answer 419

Epi: Most common 1° cardiac tumor in adults (Adults make 6 myxed drinks) Location: 90% occur in the atria (mostly left atrium). Presentation: Myxomas are usually described as a “ball valve” obstruction in the left atrium (associated with multiple syncopal episodes). IL-6 production by tumor Žconstitutional symptoms (eg, fever, weight loss). May auscultate early diastolic “tumor plop” sound (mimics mitral stenosis). Histology: gelatinous material, myxoma cells immersed in glycosaminoglycans

Question 420

Sick sinus syndrome: define

Answer 420

Age-related degeneration of SA node. ECG can show bradycardia, sinus pauses, sinus arrest, junctional escape beats.

Question 421

Most common cause paroxysmal supraventricular tachycardia? Presentation? Tx?

Answer 421

Most often due to a reentrant tract between atrium and ventricle, most commonly in AV node. Commonly presents with sudden onset palpitations, lightheadedness, diaphoresis. Treatment: terminate reentry rhythm by slowing AV node conduction (eg, vagal maneuvers, IV adenosine), electrical cardioversion if hemodynamically unstable. Definitive treatment is catheter ablation of reentry tract.

Question 422

Key sxs acute gastroenteritis:

Answer 422

Diarrhea (may start 1 to 2 days into start of illness) and vomitting

Question 423

Acute gastroenteritis: 3 key pieces of history

Answer 423

Atypical food intake, recent travel, sick contacts

Question 424

Classic pattern of pain with appendicitis

Answer 424

periumbilical pain followed by migration of pain to the right lower quadrant (Diffuse abdominal tenderness is possible (as in the case of peritonitis due to a ruptured appendix))

Question 425

Non pain sxs of appendicitis

Answer 425

Anorexia, nausea and vomiting, fever

Question 426

C

Answer 426

Pelvic examination revealing a bluish color of the vaginal wall and cervix

Question 427

C

Answer 427

history of STI alone or with pelvic inflammatory disease

Question 428

Unruptured ectopic pregnancy classically presents with

Answer 428

C

Question 429

Ruptured ectopic pregnancies are a surgical emergency. On physical exam, ——— suggests intraperitoneal bleeding and ——— correlates with the degree of blood loss

Answer 429

C