Hemodynamics Flashcards
1
Q
- While camping, a 15-year-old boy is bitten by
a mosquito. At the site of the mosquito bite, his skin
turns red and a small but noticeable bump forms.
Which of the following terms best describes the
color change in the skin?
A. Lividity
B. Ecchymosis
C. Contusion
D. Congestion
E. Hyperemia
A
- Correct: Hyperemia (E).
The red discoloration of the skin is a sign of acute
inflammation due to the mosquito bite and occurs
due to dilation of blood vessels, an active process.
The correct term in this situation is hyperemia (E).
Congestion is a passive process, which results from
impaired venous return (D). Lividity is the postmortem
pooling of blood in the skin due to gravity (A). A contusion (i.e., bruise) is due to extravasation of
red blood cells into the tissue as a result of trauma
(C), and an ecchymosis is also due to extravasation of
red blood cells (B), as opposed to hyperemia, where
red blood cells should be essentially confined to the
blood vessels.
2
Q
- A 66-year-old male has a long-standing history
of congestive heart failure due to uncontrolled
hypertension and has had multiple admissions to the
hospital for treatment of pulmonary edema. During
his most recent admission, he sustains a fatal cardiac
dysrhythmia. Which of the following is likely to be
observed in this patient’s lungs at autopsy?
A. Dilated alveolar septal capillaries filled with red
blood cells
B. Fibrotic and thickened alveolar septal capillaries
C. Loss of alveolar septa, resulting in large airspaces
D. Congestion of centrilobular sinusoids
E. Diffuse macrovesicular steatosis of the liver
A
- Correct: Fibrotic and thickened alveolar septal
capillaries (B)
With congestive heart failure, a chronic process, causing
multiple episodes of pulmonary edema, chronic pulmonary congestion, characterized by fibrotic and thick alveolar septa and macrophages with hemosiderin
would be most characteristic of the clinical scenario
(B). For the most recent episode, dilated alveolar septal
capillaries filled with red blood cells would be appropriate;
however, it would not best describe the overall clinical scenario. For (C–E), see previous information.
3
Q
- A 71-year-old male with a history of poorly controlled
hypertension due to noncompliance with medications
is brought to the emergency room by his family
because of increasing shortness of breath. An X-ray of the chest reveals bilateral pleural effusions and enlargement
of the heart. Given these features, of the following,
which is the most likely causative mechanism for the
condition producing his shortness of breath?
A. Increased hydrostatic pressure
B. Increased vascular permeability
C. Decreased colloid osmotic pressure
D. Lymphatic obstruction
E. Sodium retention
A
- Correct: Increased hydrostatic pressure (A)
The fluid in the pleural cavities represents pulmonary
edema due to heart failure from the uncontrolled
hypertension. Although the other mechanisms listed
can lead to pulmonary edema, the most likely cause,
given the scenario, would be congestive heart failure.
Congestive heart failure will increase hydrostatic
pressure in the pulmonary vasculature, causing fluid
to leak into the surrounding space (A). For (B–E), see
previous information.
4
Q
- A 68-year-old male with poorly controlled
hypertension presents to the emergency room with
shortness of breath. A chest X-ray reveals bilateral
pleural effusions. An S3 gallop is heard and crackles
(rales) are present in both lung fields. Which of the
following pigments is most likely to be found within
macrophages in his lungs?
A. Bilirubin
B. Hemosiderin
C. Melanin
D. Lipofuscin
E. Calcium
A
- Correct: Hemosiderin (B).
This individual has a clinical scenario consistent with
congestive heart failure. In congestive heart failure,
a common histologic finding is heart-failure cells,
which are macrophages filled with hemosiderin that
are found in the alveolar airspaces (B). For (A, C–E),
see previous information.
5
Q
- A 56-year-old male presents to his physician
because of swelling in the right lower extremity distal
to the knee. He has a history of mild hypertension,
which is well controlled with medication. He also
reports no trauma to the extremity, and no skin infections
or other known sites of infection. On examination
edema is noted, with the circumference of the right calf
measuring 3 cm larger than the circumference of the
left calf. There is a palpable cord present. Of the following,
which aspect of the history, physical, or laboratory
testing would be most likely to indicate the cause?
A. AST/ALT levels
B. CK-MB levels
C. BUN/creatinine levels
D. Family history of colon cancer
E. History of recent surgery
A
- Correct: History of recent surgery (E)
This patient has sustained a deep venous thrombosis.
Given the unilateral nature, edema due to liver failure, renal failure, or heart failure is less likely (A–C). Unilateral edema of a lower extremity could be due to venous or lymphatic obstruction. A neoplasm would be a rare cause for unilateral swelling of a lower extremity (D). Of the choices, only the history of recent surgery would be expected to reveal a potential cause for this deep venous thrombosis (E).
6
Q
- A 40-year-old male is brought to the emergency
department by his wife because of his shortness
of breath. He reports the onset of a cough two days
prior with increasing shortness of breath. On arrival
his temperature is 100.5°F (38.0°C), his heart rate is
135/min, and blood pressure is 88/55 mm Hg. Physical
examination is unremarkable except for tachycardia.
The patient is alert and oriented. His leukocyte
count is 18,000/μL, his pCO2 on arterial blood gas is
30 mm Hg, and serum lactic acid is slightly elevated
at 4 mmol/L. A plain chest radiograph shows a right
lower lobe infiltrate. What is the most likely diagnosis?
A. Acute pulmonary embolism
B. Septic shock
C. Cardiogenic shock
D. Anaphylactic shock
E. Acute myocardial infarction
A
- Correct: Septic shock (B)
The patient has multiple diagnostic criteria for sepsis,
including fever, a leukocyte count > 12,000/μL, heart
rate > 90/min, and CO2 < 32 mm Hg (B). All of these findings can also be seen in acute pulmonary embolism;
however, the finding of an infiltrate on the chest radiograph is consistent with pneumonia and would not be expected in acute pulmonary embolism (A). There is no
additional information to suggest cardiogenic shock,
anaphylaxis, or acute myocardial infarction (C–E).
7
Q
- A 76-year-old man is evaluated in the emergency
department for hypotension and dyspnea. His temperature
is 97.8°F (36.5°C), pulse 125/min, and blood pressure
88/58 mm Hg. Bilateral crackles are present in the
lung fields. Pedal edema is noted bilaterally. His extremities
are cool, and his urine output is minimal. A plain
chest radiograph reveals cardiomegaly and pulmonary
edema. What is the pathophysiology of his shock?
A. Septic shock
B. Anaphylactic shock
C. Cardiogenic shock
D. Hypovolemic shock
E. Distributive shock
A
- Correct: Cardiogenic shock (C)
The patient has all the signs and symptoms of cardiogenic
shock (C). The presence of signs and symptoms of volume overload such as pedal and pulmonary edema would not be expected in the other types of shock (A–B, D–E).
8
Q
- In the previous clinical scenario, of the following,
which is most likely the underlying cause of this
man’s shock?
A. Acute pulmonary embolism
B. Acute right ventricular myocardial infarction
C. Pulmonary hypertension
D. Aortic stenosis
E. Pericardial tamponade
A
- Correct: Aortic stenosis (D)
Aortic stenosis can produce cardiogenic shock and
left ventricular failure resulting in pulmonary edema
(D). The other causes listed are associated with right
ventricular failure and would not be expected to
cause pulmonary edema (A–C, E).
9
Q
- A 67-year-old man is brought to the emergency
department with hypotension and tachycardia.
He has had no urine output. Which of the following
additional findings would suggest hypovolemia
rather than sepsis as the underlying cause of this
man’s low urine output?
A. Low leukocyte count
B. Elevated leukocyte count
C. Hypernatremia
D. Hyperglycemia
E. Elevated serum lactic acid
A
- Correct: Hypernatremia (C)
Leukocyte count is frequently low in sepsis, due to
bone marrow suppression (A). A high leukocyte count
may be seen either in sepsis, due to the response to
an infection, or in hypovolemia and dehydration
because of the hemoconcentration that occurs (B).
Hyperglycemia could be seen in either septic shock
or hypovolemic shock, due to cortisol release in the
stress response (D). Elevated serum lactic acid levels
are a common finding in all forms of shock (E).
Hypernatremia occurs when there is severe loss of
free water (dehydration), a situation that would be
consistent with hypovolemic shock but not septic
shock (C).
10
Q
- A 76-year-old man is found dead at home.
Microscopic examination of samples of the liver and
lung reveals centrilobular hemorrhagic necrosis of
the liver and hemosiderin-laden macrophages in the
lungs. Of the following, what additional finding at
autopsy would be most likely?
A. Pleural effusion
B. Aortic dissection
C. Deep venous thrombosis
D. Disseminated intravascular coagulation
E. Pericardial tamponade
A
- Corect: Pleural effusion (A)
Centrilobular hemorrhagic necrosis of the liver (“nutmeg
liver”) and hemosiderin-laden macrophages in the lungs are manifestations of chronic passive congestion, which is seen in chronic heart failure. Of the choices, pleural effusions are most characteristic of congestive heart failure (A). The other options (B–E) would not be expected as routine autopsy findings in congestive heart failure.
11
Q
- A 60-year-old female status post right radical
mastectomy and right axillary lymph node dissection
develops chronic edema of the right arm. Which
of the following is the cause of her edema?
A. Increased plasma oncotic pressure
B. Renal sodium retention
C. Increased interstitial protein
D. Increased vascular permeability
E. Decreased plasma albumin
A
- Correct: Increased interstitial protein (C)
The lymphatic system returns proteins back to the
intravascular space that have been forced out of the
arterial capillary system and into interstitial space by
hydrostatic pressure. Up to 50% of serum proteins are
transported via the lymphatic route each day (C). For
(A–B, D–E), see previous information.
12
Q
- A 79-year-old male nursing home resident with
dementia is admitted to the hospital for failure to
thrive. According to his primary caregiver he has taken
very little fluids or food over the preceding three weeks.
On admission his serum sodium is 165 mmol/L, and he
subsequently receives a large amount of free water in
the form of intravenous D5W over a two-hour period.
Shortly after finishing the fluids he becomes unresponsive.
He dies after a brief attempt at resuscitation. Blood
for a chemistry panel is drawn during resuscitation,
with laboratory testing revealing the serum sodium to
be 124 mmol/L. Examination of the brain at autopsy is
most likely to reveal which of the following findings?
A. Liquefactive necrosis
B. Acute thrombosis of the middle cerebral artery
C. Narrowed sulci and distended gyri
D. Passive venous congestion
E. Diffuse axonal injury
A
- Correct: Narrowed sulci and distended gyri (C)
This patient sustained cerebral edema due to
overcorrection of hypernatremia. The finding of
narrowed sulci and distended gyri is the classic
description of the edematous brain (C). Liquefactive
necrosis would be seen in acute infarction, as
would middle coronary artery thrombosis; however,
the clinical scenario gives no indication of stroke (A,
B). Passive venous congestion would be expected in
strangulation or in central venous thrombosis (D).
Diffuse axonal injury is seen in trauma (E).
13
Q
- A 58-year-old man with a history of deep
venous thrombosis following right total knee replacement
is recovering from multiple injuries sustained
in a motor vehicle collision. His injuries include
fractures to both tibial plateaus. He is on subcutaneous
unfractionated heparin for prevention of deep
venous thrombosis. On his 6th hospital day his platelet
count dropped from 250,000/μL to 110,000/μL. He
is otherwise recovering well with no complications,
and a lower extremity Doppler is performed, which
is negative for deep venous thrombosis. Which of the
following additional tests would be most helpful in
determining the cause of his thrombocytopenia?
A. PT and PTT
B. Anti-platelet factor 4 antibody
C. Protein C activity
D. Protein S activity
E. Factor Xa level
A
- Correct: Anti-platelet factor 4 antibody (B)
The > 50% drop in the platelet count is suggestive of
heparin-induced thrombocytopenia, and his prior
treatment for deep venous thrombosis would likely
have meant prior exposure to heparin. Heparin induced
thrombocytopenia is caused by antibodies to heparin-platelet factor-4 complexes (B). Coagulation studies (PT, PTT, Factor Xa level) are unlikely to be helpful as these tests mainly assess coagulation rather than platelet function (A, E). Protein C and S levels would be indicated in the workup for recurrent deep venous thrombosis, or for unprovoked deep venous thrombosis in patients under age 50 (C, D).
14
Q
- A 37-year-old female with a history of deep
venous thrombosis during her first pregnancy and
two spontaneous abortions is evaluated in the emergency
department. Forty minutes prior to arrival she
experienced the sudden onset of weakness of the
right face, right arm, and right leg. Neurologic examination
reveals flaccid paralysis of the right side of the
body with expressive aphasia without visual field
defect. Magnetic resonance imaging (MRI) of the
brain and basic lab work including complete blood
count, prothrombin time (PT), and activated thromboplastin
time (aPTT) are ordered in the emergency
department. The treating physician administers
tissue plasminogen activator (t-PA) to the patient
according to hospital protocol in the treatment of
acute stroke. Which of the following is true regarding
the mechanism of t-PA?
A. t-PA prevents platelet activation by inhibiting
GpIIb-IIIa complex.
B. t-PA prevents platelet activation by inhibiting
GpIb receptors.
C. t-PA increases the degradation of fibrin.
D. t-PA binds anti-thrombin III, leading to thrombin
inactivation.
E. t-PA binds and inactivates clotting factors.
A
- Correct: t-PA increases the degradation of
fibrin. (C)
t-PA converts plasminogen to plasmin, which in turn
cleaves fibrin, releasing fibrin degradation products
(C). By this mechanism, t-PA prevents further deposition
of thrombin and thus clot propagation. GpIb and GpIIb-IIIa are platelet membrane glycoproteins present on the platelet surface that promote platelet aggregation (A, B). Inhibition of GpIIb-IIIa is the mechanism of action of eptifibatide (Intergrilin) (A). There is no drug currently available that inhibits GpIa. Heparin, not t-PA, activates anti-thrombin III (D). (E) is incorrect because t-PA acts by promoting fibrinolysis, not by inactivating clotting factors.
15
Q
- Ristocetin is an antibiotic, which is no longer
in use, that causes platelet agglutination by facilitating
binding of von Willebrand’s factor (vWF)
to GpIb. Two tests used in the workup of von Willebrand’s
disease are the ristocetin cofactor assay and
the ristocetin-induced platelet aggregation (RIPA).
The ristocetin cofactor assay measures the ability of
formalin-fixed (i.e., dead) control platelets to agglutinate
in the patient’s plasma. The ristocetin-induced
platelet aggregation test involves adding ristocetin
to a sample of the patient’s platelet-rich plasma.
Which results on the ristocetin cofactor assay and
the RIPA would be consistent with Bernard-Soulier’s
syndrome?
A. Normal agglutination on ristocetin cofactor assay
and normal agglutination on RIPA
B. Normal agglutination on ristocetin cofactor assay
and hypoactive agglutination on RIPA
C. Hypoactive agglutination on ristocetin cofactor
assay and normal agglutination on RIPA
D. Hypoactive agglutination on ristocetin cofactor
assay and hypoactive agglutination on RIPA
E. Hyperactive agglutination on ristocetin cofactor
assay and normal agglutination on RIPA
A
- Correct: Normal agglutination on ristocetin
cofactor assay and hypoactive agglutination on
RIPA (B)
Ristocetin induces platelet aggregation in a von Willebrand factor (vWF) dependent mechanism by promoting
the binding of vWF to GpIb. The ristocetin cofactor assay is an indirect measurement of von Willebrand’s factor, which uses control platelets and measures the amount of ristocetin induced platelet agglutination. In von Willebrand’s disease, caused by a deficiency of the vWF, platelet agglutination would be hypoactive on both the ristocetin cofactor assay and the RIPA (D). Bernard-Soulier’s disease is caused by a genetic deficiency of glycoprotein Ib (GpIb) on platelets. In Bernard-Soulier’s disease ristocetininduced platelet agglutination would be normal on the ristocetin cofactor assay (which uses control
platelets) and hypoactive on the RIPA (which uses the patient’s own, in this case defective, platelets) (B). For (A, C, E), see previous information.