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Hemodynamic Disorders and Shock -CIL
Mechanisms of Disease
May 5, 2003
10am
Lori Wasson, D.O.
Scribe-Heather Volkman
I.
II.
Introduction
- Dr. Wasson went over her powerpoints for this lecture, as well as,
questions from the Robbins Review book.
Powerpoints
- A 25-year-old IV drug abuser presents with high fever, chills and rigors.
On examination he is found to have a murmur in the tricuspid valve
area. His face and extremities look flushed and blood pressure is 90/60.
Laboratory examination reveals an elevated leukocyte count with
polymorphonuclear leukocytosis. Blood culture shows growth of gramnegative bacteria. He is treated with intravenous antibiotics. His blood
pressure continues to fall and urinary output declines to 100 mL/24 hr.
He died 3 days later.
i. Acute infectious process due to fever, chills, rigor, and elevated
WBC count
ii. Septic shock
iii. Look at view of vegetations on tricuspid valve
iv. What might be the consequences of infective endocarditis with
formation of vegetations on the right side of the heart? --embolism
to the lung, causing infarction if it gets to the end arterioles –the
bacteria on the vegetations might cause an abcess—septicemia due
to gram negative rods
v. Look at view of acute (renal) tubular necrosis (ATN)
--it is pale due to low perfusion of kidneys
vi.
Why did this patient develop shock? –gram negative rods
due to LPS activated macrophages which secreted IL-1 and TNF
(look at figure in book for LPS) resulting in hypotension and
hypoperfusion
vii. Look at high power of ATN—viable tubes next to necrotic tubes (at
autopsy, can determine shock if viable next to necrotic tubes in
kidney)
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-
What might happen if the infected vegetation breaks loose from the valve
and lodges in distant organs? (aortic valve) –systemically, most likely
place, resulting in infarction or abcess
Rheumatic heart disease results in mitral valve stenosis with vegetations
that are not infected (aseptic)
i. What complications might arise from this lesion? –mitral stenosis --can become infected and can embolize systemically –pulmonary
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III.
Questions from Powerpoints
-
-
IV.
edema and hypertension –the mitral valve, chordae tendinae, or
papillary muscles can rupture resulting in septicemia and
ventricular failure
ii. Look at view of infective endocarditis at medium power
How is fibrin formed? And What are the categories of coagulant proteins?
i. Coagulation cascade with end of thrombin converting fibrinogen to
fibrin.
ii. Three types of coagulant proteins (fibrin, active coagulation factors
(V,VIII), and cofactors)
iii. Look at infective endocarditis at high power –have necrosis and
microorganism
--Could this person develop a cerebral infarct? What would the
appearance of such an infarct of the brain? ---yes, liquifactive
necrosis and abscess formation
iv.
Look at nonbacterial endocarditis picture --lots of fibrin
note: non-bacterial endocarditis will not go on to become an abscess,
however, infective endocarditis can become an abscess is breaks off
Question 1: A 21 year old female sustains multiple injuries, including
fractures of the right femur, right tibia, and left humerous. The fractures
are stabilized after surgery and she is in stable condition. However, 2 days
after admission, she becomes severely dyspneic. What happened?
--she did not develop a PE (pulmonary embolism) due to time frame
--fat embolus, is the correct answer
Question 2: A 76 year old female fell and fractured she left femoral
trochanter. After 2 weeks in the hospital, she left leg is swollen,
particularly her lower leg below the knee. She experiences pain on
movement of this leg, and there is tenderness to palpation. Which of the
following complications is most likely to occur after these events? -PE
--What happened? a DVT (deep vein thrombosis)
--Will it cause gangrenous infection of foot? --no (from arterial
circulation)
--note: most PEs comes from veins above the knee
Questions from Review Book
- Question 1: answer—vasoconstriction is the first thing that happens, then
after a few minutes the platelets aggregate (adhesion then activation)
- Question 2: answer—liver (also, lung)—due to dual circulation
- Question 4: answer---congestive heart failure (also tricuspid valve
stenosis)
- Question 5: answer—immobilization
- Question 6: answer—damage to endothelium (most likely causeatherosclerosis)
- note: very common cause of hypercoagulable state—factor V mutation
(Leiden mutation)
- Question 7: answer—t-PA (most common drug used now) (most are not
using urokinase or streptokinase)
- note: t-PA should be given within 30 minutes of acute MI due to irreversible
injury and hardened clot (criteria: ST segment elevation, etc) (diabetics can
have silent MI and days later be diagnosed with MI—not candidate for t-PA)
- Question 8: answer—acute pulmonary congestion—therefore, congestion
of alveolar capillaries with transudate in the alveoli (low protein) (not
purulent or exudative)
- note: even if the congestion is chronic, don’t assume exudative effusion
unless given information about fever or infection (even though increased risk
due to chronic effusion)
-note: effusion can be exudative or transudative
- Question 9: answer—tissue nitrogen emboli (disease—the bends)
- Question 10: answer—lymphatic obstruction due to tumor cells in dermal
lymphatics –inflammatory carcinoma (note: fine-needle aspirate is used to
biopsy and retrieval of cells)
- Question 26: she did not like terminology in this question answer--lymphedema due to lymphatic obstruction
- Question 13: answer—factor V Leiden mutation (most common cause of
hypercoagulable state)
- note: a woman with recurrent miscarriages and recurrent DVT--lupus
anticoagulant or anti-phospholipid antibody syndrome (interchangeable)