McNeil's notes - cardio, resp, gi, nephro, most cancer, radiation, chemo, transplant, pharmacology, infectious diseases Flashcards Preview

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1

Patient with acute right-sided M.I., what is the best course of action in managing this patient?
a. Volume resuscitation with N/S.
b. Inotropes are not indicated.
c. There is decreased right diastolic pressure once the pulmonary artery pressure is decreased.
d. EKG is often not diagnostic.
e. You should increase the right after load.

a. Volume resuscitation

The initial therapy for hypotension in patients with right ventricular infarction should almost always be volume expansion.
- Braunwald: Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed., W. B. Saunders Company, p. 1181-1182.

a. Inotrops (yes if needed)
b. Reduce preload (opposite – want to increase preload)
c. IV fluid
d. Reduce afterload (yes, but most important is to give fluid to increase CO)

2

Post Operative MI, patients experiences cardiogenic shock. Which
is the best management?
a. Angioplasty
b. Intra-aortic balloon
c. Streptokinase
d. Decrease preload and afterload with an inotrope

a. Angioplasty

In the large randomized controlled SHOCK trial, investigators determined that patients with cardiogenic shock after acute myocardial infarction benefited if within 6 hours of the onset of shock they underwent an intervention that restored coronary blood flow, as opposed to medical stabilization and delayed intervention.[47] Two interventions used to restore coronary blood flow were immediate coronary artery bypass surgery and immediate percutaneous coronary interventions that included transluminal angioplasty and deployment of endoluminal stents to prevent reocclusion of the coronary artery.
- Townsend: Sabiston Textbook of Surgery, 18th ed.

3

Two days post major bowel surgery, a patient develops dyspnea, left-sided chest pain and ECG changes in lateral leads. Immediate treatment should include:
a) heparin
b) O2

- Most common time for post-op MI is day 2-3 due to reabsorption of 3rd space volume and therefore volume overload on the heart
- Diagnosis of acute MI is based on 2 of 3 of the following:
o history and physical
o ECG changes (ST segment elevation, T wave inversion, significant Q waves)
o cardiac enzyme elevation
- management goal is to minimize the amount of infarcted myocardium and prevent complications
- immediate measures include:
o O2, sublingual NTG, morphine (pain relief, sedation), ASA, B-blocker (if not contraindicated), ACE I
o anticoagulation therapy - IV heparin to prevent extension of clot/thrombus
o thrombolytic therapy - this patient would not be a candidate since only POD #2, but criteria for review are:
 CP for 30+ minutes
 ECG changes:
• 1mm ST elevation in 2 limb leads OR
• 1mm ST elevation in 2 adjacent precordial leads OR
• new onset LBBB
 presentation within 12h of symptom onset
- Reference: MCCQE

4

Signs of cardiac tamponade include all of the following EXCEPT
A. Narrow pulse pressure
B. Pulsus alternans
C. Wide pulse pressure
D. Hypotension
E. Distended neck veins

C. Wide pulse pressure
This is also asked with "Right atrial pressure greater than the Leftatrial pressure"
This question was often asked, and basically the answer is usually you do NOT see WIDE pulse pressure. Also Left atrial pressure is normally greater than the right, but in cardiac tamponade they can equalize as fluid accumulates.

5

One week after undergoing tooth extraction, a patient develops fever, increased white count and SOB. On exam, the patient has systolic murmur at left sternal border with hypotension and increased pulse pressure. The likely diagnosis is:
a. tricuspid endocarditis with tricuspid regurg
b. pulmonary valve endocarditis with regurg
c. mitral valve endocarditis with regurg
d. aortic valve endocarditis with regurg

- d. aortic valve endocarditis with regurg

The most common causes of an ejection systolic murmur are aortic stenosis and aortic sclerosis

The valves most commonly infected are left-sided valves, with approximately equal frequency between the mitral and aortic valves (see the following images). Vegetations on the mitral valve can extend onto the noncoronary and left cusps of the aortic valve, as they are contiguous, and double aortic and mitral valve replacements are not rare. Left-sided valve endocarditis is more frequent, even in drug addicts, than right-sided endocarditis,[3] although infections of the tricuspid and pulmonary valves are highly suspicious of intravenous drug abuse.

Tricuspid valve endocarditis may occur in community-acquired infection, usually in intravenous drug addicts, or hospital-acquired infections from implanted devices. Isolated pulmonary valve endocarditis is rare (except in patients with congenital heart disease) and may cause confusing clinical symptoms

6

Which drug of the following if given to cardiac patient in non cardiac surgery will improve survival:
b. Metoprolol
c. Digoxin
d. ASA
e. Atropine

b. beta blocker

Perioperative B-blocker therapy and mortality after major noncardiac surgery reduced risk of in-hospital death among high risk, but not low risk patients.
- NEJM July 28, 2005
-article does not differentiate between atenolol and metoprolol
-extended release metoprolol reduces cardiac mortality but increases overall mortality

In patients scheduled for noncardiac surgery, including those at high risk, we recommend not starting perioperative beta blockade (Grade 1B). (See 'Patients not taking beta blockers' above.)
●In patients treated with long-term beta blockers for recommended indications, we suggest continuing beta blockade perioperatively (Grade 2B). (See 'Beta blockers' above.)

7

what is the mechanism of epinephrine during a cardiac arrest?

Answer given: increase cardiac inotropy

Epinephrine
Chronotropy 4+
Inotropy 4+
Vasoconstriction 4+
Vasodilatation 3+
- Piccini & Nilsson: The Osler Medical Handbook, 2nd ed.

8

Intraoperatively patient bradys down to 40 – drug to give

atropine

9

In hypertensive cardiomyopathy, which of the following is true regarding myocardial muscle cells?
a) there is an increase in the number of cells
b) the cells increase in size
c) the is an increase in both the size and number of cells

Histologically, individual muscle cells are hypertrophied, with a disorganized, characteristic whorled pattern.
- Marx: Rosen's Emergency Medicine, 7th ed.

10

Worst prognosis with severe CHF
a. hypotension
b. hypoxia

a. hypotension

The largest analysis[152] found that BUN, systolic blood pressure, heart rate, and age were the main multivariate predictors, and using a different statistical approach with dichotomous variables, suggests that the best single predictor was an elevated admission blood urea nitrogen (BUN ≤ 43 mg/dl), followed by low blood pressure (systolic blood pressure

11

All of the following are benefits of smoking cessation 6 weeks prior to surgery except
a. improved ciliary function
b. decreased airway reactivity
c. decreased co2 retention
d. increased secretion clearance
e. none of the above

Answer given: c. decreased co2 retention

Intermittent quitters had less loss of lung function at comparable cumulative cigarette doses than continuing smokers. Interestingly, the shorter-term improvement after quitting or the decrement after relapsing was significantly related to methacholine reactivity, [145] implying that acute airway inflammation contributes to the observed FEV1 fluctuations.
- Sethi JM - Clin Chest Med - 01-Mar-2000; 21(1): 67-86, viii

Cigarette smoking increases perioperative mortality probably because of the effects of smoking on both the cardiovascular and the respiratory systems.[100] Smokers may have increased levels of carboxyhemoglobin as a function of their brand of cigarette, how deeply they inhale, the number of puffs they take, and the level of ventilation present while they are smoking.[101] The level of carboxyhemoglobin in smokers usually ranges from 3% to 15%, and the major effects are to reduce the amount of hemoglobin available to bind with oxygen, thereby decreasing arterial oxygen content, and to shift the oxygen-hemoglobin saturation curve to the left. Smokers have a decreased oxygen delivery and an increased tissue oxygen extraction, manifested by a reduced mixed venous oxygen content.[102] Patients at greater risk for elevated carboxyhemoglobin levels are those who smoke avidly late at night and then undergo an early morning operation. Therefore, it is recommended that smokers stop smoking 12 to 18 hours preoperatively to allow sufficient time (three half-lives) for carboxyhemoglobin clearance.

Decreased CO2 retention. There were lots of references made to improving ciliary function, increasing secretion clearance and decreasing airway reactivity but I couldn't find anything about CO2 retention so I figured this is the answer.

12

You are called to see a patient after a blood gas that was ordered by the clinical clerk shows a PaO2 of 40mmHg. After 20 min of 100% O2 by face mask a CBC reveals a hematocrit of 0.65 and a repeat blood gas reveals values of 7.30/40/60/26 with a saturation of 88% on an FiO2 of 1.0. The likely diagnosis is:
a. polycythemia rubra vera
b. pulmonary fibrosis
c. COPD
d. Intrapulmonary shunt
e. Carbon monoxide poisoning

Answer given: b. pulmonary fibrosis

Carbon monoxide poisoning: “ arterial blood gases reveal metabolic acidosis, a normal PO2, decreased O2 saturation (by direct co-oximetry measurement rather than a calculated or pulse oximetry value) and a normal or slightly decreased PCO2”
- Harrison’s 13th ed

Polycythemia Vera: Normal arterial oxygen saturation (>92%)
- Ferri: Ferri's Clinical Advisor 2010, 1st ed.

DDX Polycythemia
Absolute
a) autonomous erythroid proliferation (polycythemia rubra vera)
b) secondary erythroid proliferation
I – Autonomous or inappropriate increase in erythropoiten eg neoplasm, renal lesions, familial
2- Secondary increase in erythropoiten
i – hypoxia (decrease PO2) – eg high altitude, alveolar hypoventilation, pulmonary disease, cardiac left to right shunt
ii – abnormal hemoglobin function (normal PO2) – eg high affinity genetic variants, congenital methemoglbinemia, carboxyhemoglobin (smoker’s polycythemia)
c) Hormonal stimulus to erythropoesis eg cushing sydrome, androgen or corticosteroid administration
Relative (reduced plasma volume, normal cell mass) eg dehydration, stress erythrocytosis
- Harrisons pg 180

Any pulmonary disease which produces chronic hypoxia may lead to erythrocytosis

13

Woman in third trimester of pregnancy is jaundiced which test would show hepatocellular damage
a) increased alk phos
b) increased unconjugated bili
c) increased conjugated bili
d) increased GGT
e) decreased urobilinogen

D. we agreed GGT is the answer at review week

Also known as intrahepatic cholestasis of pregnancy. Usually occures in thrid trimester but may develop any time after the 7th week of gestation. Clinical features include: pruritis and jaundice. Clinical and laboratory abnormalities include: elevated alkaline phosphatase (but during pregnancy, this is usually due to placental source rather than hepatic), elevated bilirubin (conjugated > unconjugated) and elevated GGT.

a) increased alk phos (post-hepatic and other sources)
b) increased unconjugated bili (pre-hepatic)
c) increased conjugated bili (hepatic and post-hepatic)
d) increased GGT (cholestatic but also from liver)
e) decreased urobilinogen (no conjugated bilirubin)

GGT is another enzyme found in hepatocytes and released
from the bile duct epithelium. Elevation of GGT is an early
marker and also a sensitive test for hepatobiliary disease. Like
AP elevation, however, it is nonspecific and can be produced by
a variety of disorders in the absence of liver disease. Increased
levels of GGT can be induced by certain medications, alcohol
abuse, pancreatic disease, myocardial infarction, renal failure,
and obstructive pulmonary disease. For this reason, elevated
GGT levels are often interpreted in conjunction with other
enzyme abnormalities. For example, a raised GGT level with
increased AP level supports a liver source.
Schwartz

14

A 58 y.o. M with cirrhosis presents with an UGI bleed. Initial resuscitation measures are carried out. What is the MOST helpful adjunct to treatment?
A. Synthetic vasopressin
B. Somatostatin (Octreotide)
C. Ranitidine
D. NG tube

- Somatostatin infusion

****if patient did not have a history of liver failure the diagnosis of duodenal or gastric ulcer is more likely , and treatment with PPI. PPI stablize the clot but does not speed clot resolution *******

Patients with evidence of liver disease (by history, physical examination, or laboratory data) who have active upper gastrointestinal bleeding should be started on pharmacologic therapy (e.g., intravenous octreotide) to lower portal venous pressure and stop the bleeding as soon as possible and then undergo urgent endoscopy.
- Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.

Somatostatin and octreotide have been studied in patients with ulcer-related upper gastrointestinal bleeding. A meta-analysis revealed a reduction in the rate of rebleeding in 1829 patients treated with somatostatin or octreotide, but mortality was not improved.[114] It is this author's opinion that these agents may be useful in some patients (e.g., those with severe bleeding who are awaiting endoscopy or surgery or those in whom other drug therapy is not possible) but are not indicated routinely.
- Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.

15

Patient with bleeding esophageal varices is started on vasopressin. What side effect should you watch for?
a. Coronary vasoconstriction
b. Decreased small bowel motility
c. Bronchial dilatation
d. Peripheral vasodilation

Answer: a. Coronary vasoconstriction

Vasopressin is an alternative pharmacotherapeutic agent but is used less frequently because of significant complications (including myocardial ischemia and infarction, ventricular arrhythmias, cardiac arrest, mesenteric ischemia and infarction, and cutaneous ischemic necrosis). In patients with vascular disease or coronary artery disease, vasopressin should be used with caution in an ICU setting with cardiac monitoring. The infusion should be reduced or terminated if chest pain, abdominal pain, or arrhythmias develop. Concomitant infusion of nitroglycerin may reduce undesirable cardiovascular side effects of vasopressin therapy and may provide more effective control of bleeding. Nitroglycerin is administered only if the systolic BP is greater than 100 mm Hg, at a dose of 10 mu g/minute IV, increased by 10 mu g/minute q10-15min until the systolic BP falls to 100 mm Hg or a maximum dose of 400 mu g/minute is reached.
- Washington Manual

In addition, vasospastic side effects are seen in approximately 25% of patients receiving vasopressin, with the risk of myocardial infarction being of greatest concern.
- Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 6th ed., p.1299.

16

#1 cause of massive upper GI bleed

The most common causes of UGIB include the following (in approximate descending order of frequency) [3-5,8,9]:

●Gastric and/or duodenal ulcers
●Esophagogastric varices
●Severe or erosive esophagitis
●Severe or erosive gastritis/duodenitis
●Portal hypertensive gastropathy
●Angiodysplasia (also known as vascular ectasia)
●Mass lesions (polyps/cancers)
●Mallory-Weiss syndrome
●No lesion identified (10 to 15 percent of patients)

17

2L of diarrhea will result in all except:
a- decrease effective circulatory volume
b- decrease urine Na
c- increase thirst
d- increase ADH
e- decrease serum Cl

e. decreased serum Cl

Can easily answer this by process of elimination.

Remember: basically every fluid past the stomach is "high in bicarb"

Metabolic acidosis with normal anion gap results from a loss of fluid with a bicarbonate concentration greater than chloride concentration, the addition of acids with chloride as their associated anion, or the transient dilution of extracellular bicarbonate with nonbicarbonate solutions. To maintain electroneutrality, the decrease in serum bicarbonate is associated with a proportionate increase in the serum chloride level. For example, in diarrhea, bicarbonate loss is greater than chloride loss; thus, hyperchloremia develops.
- Shannon: Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose, 4th ed.

18

Most sensitve test for pancreatitis
a-serum lipase
b-serum amylase
c- urine amylase

a. lipase

Although serum lipase is derived from pancreatic acinar cells, it rises slightly earlier than amylase, 4-8 hours after the onset of acute pancreatitis, and peaks earlier, at 24 hours ( Steinberg, 1985 ). The serum lipase also lasts longer in the serum, 8-14 days. For these reasons, serum lipase is more sensitive and specific than the serum amylase.
- McPherson & Pincus: Henry's Clinical Diagnosis and Management by Laboratory Methods, 21st ed.

19

Pancreatitis causes all of the following except:
a) makes the patient delusional
b) fat necrosis
c) pleural effusion
d) dyspnea
e) pain

a) makes the patient delusional

The typical symptoms of acute pancreatitis are abdominal pain, nausea, and vomiting.
Examination of the skin may reveal tender areas of induration and erythema resulting from subcutaneous fat necrosis
- Goldman: Cecil Medicine, 23rd ed.

Tachypnea and shallow respirations may be present if subdiaphragmatic inflammatory exudate causes painful breathing. Dyspnea may accompany pleural effusions, atelectasis, congestive heart failure, or ARDS.
- Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.

Chronic pancreatitis indicates some degree of progressive and permanent damage to the pancreas, usually visualized as calcifications on radiographs and CT scans (Figs. 49-27 and 49-28 [27] [28]). This damage often leads to diabetes and pancreatic insufficiency, resulting in malabsorption with chronic diarrhea.
- Rakel: Textbook of Family Medicine, 7th ed.

Periostitis, nodular skin lesions, and synovial fat necrosis may develop as a result of lipases released during pancreatitis.
- Kliegman: Nelson Textbook of Pediatrics, 18th ed

Similarly asked question with choice diarrhea: answer is diarrhea (The question is likely ACUTE PANCREATITIS (which does not have diarrhea))

20

Hepatic dysfunction gives all except?
a. Decreased glucose
b. Increased bilirubin
c. Increased PT
d. Increased BUN
e. Altered circulating glucose profile

Glycogenesis, glycogen storage, glycogenolysis, and the conversion of
galactose into glucose all represent hepatic functions. Hypoglycemia is a rare accompaniment of extensive hepatic disease, but the amelioration of diabetes in patients with hemochromatosis is considered an indication of neoplastic change. The more common effect of hepatic disease is a deficiency of glycogenesis with resulting hyperglycemia. A hepatic enzyme system is responsible for the conversion of galactose into glucose, and abnormal galactose tolerance tests are seen in hepatitis and active cirrhosis.

Because urea is synthesized in the liver, hepatic dysfunction decreases urea production and, therefore, BUN concentration.
- Miller: Miller's Anesthesia, 7th ed.

21

Saliva is ineffective in digestion because
a) amylase deactivated by stomach ph
b) too small amount

Answer given: a) amylase deactivated by stomach ph

The function of saliva is to begin chemical digestion, for lubrication of the food, and for protection. Saliva contains mostly water and electrolytes, as well as amylase, lipase, mucin, immunoglobins and lysosymes. Amylase begins breakdown of carbohydrates and lipase begins breakdown of fats (but this is not significant).

22

Lower esophageal sphincter is affected by all of the following except:
a) caffeine
b) smoking
c) alcohol
d) impaired peristalsis of the esophagus

Peristaltic contractions alone do not generate enough force to open up the LES
- Townsend: Sabiston Textbook of Surgery, 18th ed.

23

63 year old male heavy drinker & smoker present with 8 week history of difficulty in swallowing and weight loss. The most appropriate next step is:
a. Esophagoscopy and biopsy
b. 24h PH study
c. motility study
d. CT Scan
e. OR

Esophagoscopy and biopsy

24

All of the following are cause of ileus except :
a. Hyperkalemia
b. Hypokalemia
c. Early post op
d. Intra abdominal sepsis
e. All of the above

- Hyperkalemia

Drugs
Narcotics, phenothiazines, diltiazem, anticholinergic agents, clozapine
Electrolyte abnormalities
Hypokalemia, hyponatremia, hypomagnesemia, hypermagnesemia, hypocalcemia, hypercalcemia
Intestinal ischemia
Mesenteric arterial embolus or thrombosis, mesenteric venous thrombosis, chronic mesenteric ischemia
Intra-abdominal inflammation
Appendicitis, diverticulitis, perforated duodenal ulcer
Iatrogenic
Laparotomy, laparoscopy
Retroperitoneal inflammation or hemorrhage
Lumbar compression fracture, acute pancreatitis, pyelonephritis
Infection
Intra-abdominal or systemic sepsis

Thoracic diseases
Lower rib fractures, lower lobe pneumonia, myocardial infarction
- Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.

With severe hypothyroidism (i.e., myxedema), paralytic ileus and intestinal pseudo-obstruction can occur.
- Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 8th ed.;

Causes of Ileus
o Postlaparotomy
o Metabolic and electrolyte derangements (e.g., hypokalemia, hyponatremia, hypomagnesemia, uremia, diabetic coma)
o Drugs (e.g., opiates, psychotropic agents, anticholinergic agents)
o Intra-abdominal inflammation
o Retroperitoneal hemorrhage or inflammation
o Intestinal ischemia
o Systemic sepsis
- Townsend: Sabiston Textbook of Surgery, 16th ed

25

What is the cause of hyponatremia in liver disease?

A variety of factors can contribute to the development of hyponatremia in patients with cirrhosis. The most important factor is systemic vasodilation, which leads to activation of endogenous vasoconstrictors including antidiuretic hormone (ADH); ADH promotes the water retention that is responsible for the fall in serum sodium.
(uptodate)

26

Which form of hypertension is associated with low renin?
A. Renal artery stenosis
B. Primary hyperaldosteronism
C. CHF
D. Cirrhosis

B. Primary hyperaldosteronism

My simplified way to see it is that the kidneys produce renin when they aren't getting enough bloodflow in order to get more blood. So anything that would limit renal flow would cause increased renin. Primary hyperaldosteronism causes hypertension so kidneys are getting plenty of blood therefore don't need to secrete renin.

As diagnostic tests for quantifying the components of the renin-angiotensin-aldosterone system have become available, the syndrome of primary hyperaldosteronism (PAL) is now identified by hypertension, suppressed plasma renin activity (PRA), and high urine and plasma aldosterone levels.
- Wein: Campbell-Walsh Urology, 9th ed.

Decreased renin levels are found in the following conditions:
a Primary aldosteronism (98% of cases)
b Unilateral renal artery stenosis
c Administration of salt-retaining steroids
d Congenital adrenal hyperplasia with 17-hydroxylase deficiency
e Liddle's syndrome

Hyperaldosteronism > Increased sodium resorption at distal convoluted tubule > decreased renin release

27

Which of the factors below do not stimulate renin release by the kidney?
a) Epinephrine
b) Norepinephrine
c) Dopamine
d) Thromboxane A2
e) Leukotrienes

D and E

Renin is released in shock/hypoperfusion to the kidney.
- Stimulates: Catecholamines , also ACTH
- Does not stimulate: Thromboxane A2, Leukotrienes

28

Which of the following causes of polyuria is associated with a high urine specific gravity?
A. Diabetes Mellitus
B. SIADH
C. Acute non-oliguric renal failure
D. ATN

A. Diabetes Mellitus (increased, glucosuria and dehyrdation)


B. SIADH (increased retain H2O and concentrate urine)
C. Acute non-oliguric renal failure (decreased, lose both h20 and Na, osmols dilutes)
D. ATN (same as C)

Urine osmolality is determined by the number of particles in the urine (eg, urea, sodium, potassium), while the specific gravity is determined by both the number and size of the particles in the urine .

Notes: DI (high urine output – low specific gravity)

29

Which of the following drugs does not cause ARF?
a) NSAID.
b) ACE inhibitor.
c) Aminoglycosides.
d) Semi-synthetic penicillins.
e) Corticosteriods.

Answer: Corticosteroids.

30

Lab values in ATN, which is true:
a) Urine osmolality 600
b) Urine Na 80
c) FeNa

Answer: Urine Na of 80

Basically the kidney isn't able to concentrate urine

a) Urine osmolality 600 (250-300 is plasma) - so able to concentrate
b) Urine Na 80 (the answer)
c) FeNa 3% in ATN)
d) WBC casts and pyuria (AIN)

Test Prerenal Parenchymal
Urine osmolarity (mOsm) >500 250–350
U/P osmolality >1.5 20 40
FENa 3%
- Greenfield

FeNa is the fractional excretion of Na+. It is the most reliable for distinguishing prerenal azotemia from ATN (a measure of the kidney’s concentrating ability)

Hyaline casts: Low urine flow, concentrated urine, or an acidic environment can contribute to the formation of hyaline casts, and, as such, they may be seen in normal individuals in dehydration or vigorous exercise