A balanced ligamentous tension technique is a subtype of

MFR which treats somatic dysfunctions my moving the

segment in the direction of ease and restoring ligamentous
tensions. It is an indirect technique which uses the patient’s
breathing or muscular cooperation to overcome resistance
and release the lesion. Remember that the respiratory
motion of the sacrum occurs around the superior transverse
axis which is at level S2. During inhalation the sacral base
moves posteriorly. When the sacral base moves posteriorly
this is also known as counternutation. A good clinical pearl is
that the most common dysfunction of the sacrum in post-
partum patients is bilateral sacral flexion.

1
Diabetic Patient with HTN: suffering from an embolic stroke, which left untreated, could cause
cerebral ischemia and irreversible brain injury and possibly death. Strokes result in rapid loss of
brain function to many causes (lack of blood flow, obstruction, or hemorrhage). As a result, the
affected area corresponds to an inability to move one or more limbs on one side of the body
(hemiparesis) or the inability to understand or formulate speech. Risk factors for stroke include old
age, hypertension, previous incidences of stroke or transient ischemic attacks, diabetes,
hypercholesterolemia, smoking, and atrial fibrillation. The patient in this question has several of
these risk factors including older age, history of hypertension and diabetes. A couple of the many
American Heart Association/ American Stroke Association (AHA/ASA) inclusion guidelines for
thrombolytic therapy requires the incident occurring in under 3 hours and hemorrhagic stroke being
ruled out. The patient experienced these symptoms a half an hour ago and is exhibiting neurologic
deficits. Also, hemorrhagic stroke has been ruled out by CT scan. The best therapy of choice is
thrombolytic therapy aimed at breaking the clot. Tissue plasminogen activator (t-PA) is involved in
breaking down clots. These proteins catalyze the conversion of plasminogen to plasmin, which is
the major enzyme responsible for clot breakdown. Plasmin breaks down the fibrin clots that form
inside blood vessels in a process known as fibrinolysis. Bottom Line: History of hemorrhagic
stroke, intracerebral bleeding, and symptoms lasting >3 hours are some of the contraindications
for thrombolytic therapy. Thrombolytics work by converting plasminogen to plasmin, which
produces fibrinolysis.

: Clopidogrel works by specifically and irreversibly binding to the ADP receptor located on platelet
cell membranes. The blockade of this receptor inhibits platelet aggregation by inhibiting the
glycoprotein IIb/IIIa pathway, which functions as a receptor mainly for fibrinogen binding.
Activation of this receptor complex is vital for platelet aggregation and is important in cross-linking
of platelets by fibrin. Clopidogrel is indicated to prevent vascular ischemic events such as stroke,
but it is not intended to treat an already existing stroke. It is also indicated in patients with acute
coronary syndrome without and with ST elevation.

Inhibition of vitamin-K dependent synthesis of calcium-dependent clotting factors II, VII, IX, and
X describe the mechanism of action for warfarin. This drug also inhibits the formation of regulatory
factors protein C and S, which can lead to thrombosis. The precursors of these clotting factors
require carboxylation of their glutamic acid residues in order to become activated and bind to
phospholipid surfaces inside the vascular endothelium. The enzyme that carries out this
carboxylation of glutamic acid is gamma-glutamyl carboxylase. This reaction will only occur if the
enzyme is able to convert a reduced form of vitamin K to vitamin K epoxide at the same time,
through epoxide reductase.

 Heparin and its low molecular weight derivatives (enoxaparin, etc.) binds to the enzyme inhibitor
antithrombin III causing a conformational change that results in accelerated activity. This activated
antithrombin III molecule then inactivates thrombin and other proteases involved in blood clotting,
especially factor Xa. Heparin is effective in preventing deep vein thromboses and pulmonary
emboli in patients at risk, however its role in treating embolic stroke is limited.

 Aspirin works by irreversibly binding to the enzyme cyclooxygenase, which prevents the
production of prostaglandins and thromboxane synthesis. Inhibition of thromboxane synthesis
produces an inhibitory effect on platelet aggregation. For many people, aspirin may help prevent
strokes or further strokes from occurring. However, its role in treating an existing embolic stroke is
limited and a thrombolytic would be the best therapy to use in this scenario.

1
Ulcerative colitis is an inflammatory bowel disease characterized by recurrent
episodes of inflammation limited to the mucosal layer of the colon. It involves
the rectum and may extend proximally in a continuous fashion. There are many
extraintestinal manifestations that are associated with the disease, including
pyoderma gangrenosum (PG), uveitis, primary sclerosing cholangitis, erythema
nodosum, toxic megacolon, and apthous ulcers. PG is characterized by a
superficial, non-healing, ulcerated lesion with purulent material; the lesion is
most often found on the lower extremities. extraintestinal processes associated
with ulcerative colitis, including primary sclerosing cholangitis and pyoderma
gangrenosum(PG). PG is a chronic slow healing or non-healing ulcer that is
most commonly seen on the lower legs. It is a rare, poorly understood,
noninfectious skin disease that occurs in a variety of inflammatory conditions,
including inflammatory bowel disease (IBD).

PG lesions are the second most common skin manifestation of ulcerative colitis,
although its incidence is less than 1%. Initially, PG lesions appear as
erythematous papules or pustules, often preceded by trauma. Subsequent
necrosis leads to the development of ulcerations that contain purulent, but
sterile, material. These lesions do not parallel IBD disease activity and are
treated with steroids and TNF antagonists.

Besides PG, there are many other extraintestinal disease processes that are
associated with IBD, as discussed below:
• Primary sclerosing cholangitis: This is a biliary tract disease that is
associated with ulcerative colitis in 70% of cases. It is an idiopathic disorder
characterized by inflammation, fibrosis, and strictures of bile ducts.
• Erythema nodosum: These consist of raised, tender, red or violet
subcutaneous nodules that are 1–5 cm in diameter. The lesions are most
commonly found over the anterior tibial area. Unlike PG, erythema nodosum
lesions do parallel disease activity of IBD and, therefore, resolve with IBD
treatment.
• Anterior uveitis: Ocular pain and redness are characteristic of anterior uveitis,
which is often described as "ciliary flush" due to the inflamed capillaries
surrounding the iris. The iris is often inflamed, giving the pupil a distorted
appearance. Urgent ophthalmologic evaluation is recommended.
• Toxic megacolon: Toxic megacolon is characterized by a colonic diameter ≥ 6
cm or cecal diameter > 9 cm and the presence of systemic toxicity. It has a high
mortality rate, requiring emergent surgical evaluation. It often occurs as a result
of fulminant colitis, where the inflammatory process extends beyond the mucosa
to involve the muscle layers of the colon.
• Apthous ulcers: These are superficial ulcerations that involve the mucosal
surfaces. They are more common in Crohn disease, but are also seen in
ulcerative colitis. Affected patients may initially present with apthous stomatitis
with corresponding cobblestoning and inflammation of the surrounding mucosa.

Arterial ulcers occur as a result of poor circulation, often in the setting of

peripheral arterial disease (PAD), which occurs in older patients. These ulcers
are painful, well-demarcated lesions with a punched-out appearance and
surrounding erythema. PAD findings include diminished distal pulses,
claudication, loss of hair on extremities, and poor capillary refill.

Cellulitis is a skin infection described as red, hot, and tender skin with an
indistinct erythematous border. It often occurs in the setting of a loss of the
skin barrier, such as in breaks in the skin from an injury or concurrent infections.
Although skin flora are the most common infectious agents
(Staphylococcus and Streptococcus), patients with diabetes have an increased
risk of polymicrobial infections.

Irritable bowel syndrome (IBS) is an idiopathic, symptom-based diagnosis

characterized by chronic abdominal pain, discomfort, bloating, and altered bowel
habits. It is a clinical diagnosis and is not the same as IBD, which includes
ulcerative colitis and Crohn disease. IBS is a diagnosis of exclusion and is not
associated with extraintestinal manifestations.

Erythema nodosum consists of raised, tender, red or violet subcutaneous

nodules that are 1–5 cm in diameter and are most commonly found over the
anterior tibial area. 4% of patients with active ulcerative colitis have erythema
nodosum

1
Table 1

1
Table 1

1
Chronic myelogenous leukemia is due to a chromosomal translocation of
t(9;22), which is known as the Philadelphia chromosome.
- gene product BCR-ABL1, which is a constitutively active tyrosine kinase.
Thus, it is the target for the drug imatinib. Chronic myelogenous leukemia
is suspected in a patient with the systemic complaints of fatigue, malaise,
sweating, weight loss, and hepatosplenomegaly. Laboratory findings
reveal an elevated white blood cell count with an associated mild anemia,
thrombocytosis, and basophilia. The "gold standard" for the diagnosis of
CML is either the demonstration of the Philadelphia chromosome [t(9;22)
translocation] or the BCR-ABL1 fusion gene or mRNA product. Treatment
is with imatinib.

Burkitt's lymphoma is derived from germinal B cells.

- translocation between the c-MYC oncogene on chromosome 8, and the
Ig heavy chain gene on chromosome 14. This results in the t(8;14)
translocation. The endemic African form most commonly presents as a jaw
or facial bone tumor. The non-endemic form usually has an abdominal
presentation with accompanying ascites. Presenting symptoms can include
those related to bowel obstruction or gastrointestinal bleeding.
Lymphadenopathy is generally localized. Treatment includes combination
chemotherapy of cyclophosphamide, vincristine, doxorubicin, and
methotrexate. Also, the addition of rituximab can be beneficial.

Ewing Sarcoma most commonly arises in the long bones of the

extremities. This includes the femur, tibia, fibula, humerus, and the
pelvis. Patients with Ewing Sarcoma typically present with localized pain
or swelling of a few weeks or months duration. Constitutional signs such
as fever, fatigue, weight loss, or anemia, can be present. The diagnostic
work-up begins with plain radiographs. Ewing Sarcoma involving bone
typically presents as a poorly marginated destructive lesion with a
moth-eaten appearance. Ewing Sarcoma is characterized by chromosomal
translocations of the Ewing sarcoma (EWS) gene on chromosome 22 with
chromosome 11, resulting in the translocation t(11;22).

Follicular lymphoma is the second most common lymphoma in the United

States. It most frequently presents in female middle-aged Caucasians. It
arises from germinal center B-cells. Patients with follicular lymphoma
usually present with painless peripheral lymphadenopathy, often with a
history of lymph node enlargement. Cytogenetic analysis of the tumor cells
reveals expression of CD 10, CD 19, and CD20. They test negative for

1
history of lymph node enlargement. Cytogenetic analysis of the tumor cells
reveals expression of CD 10, CD 19, and CD20. They test negative for
CD5 and CD23. Molecular genetics can confirm the presence of the
t(14;18) chromosomal translocation involving the BCL-2 gene. The
diagnosis of follicular lymphoma is with a lymph node biopsy.

Acute promyelocytic leukemia is characterized by the translocation

t(15;17). The alpha retinoic acid receptor gene (RARA) on chromosome 17
translocates with the PML gene on chromosome 15. The translocation
results in the PML/RARA fusion gene. Treatment is with all-trans retinoic
acid, which activates genes to lead to terminal differentiation of
promyelocytes. Acute promyelocytic leukemia is associated with
disseminated intravascular coagulation. A characteristic folded, bilobed
nucleus is found in the promyelocytes. Coarse azurophilic granules and
multiple Auer rods are also present on histological examination.

Sickle cell disease is an autosomal recessive disorder that commonly

affects African-Americans. It is due to a point mutation that results in the
substitution of valine in the place of glutamic acid at the 6th amino acid
position of beta globin, causing abnormal sickling of red cells at low oxygen
concentrations. Sickle cell disease patients are at risk of having an aplastic
crisis, often associated with parvovirus B19 infection, during which time
erythropoiesis is suppressed. aplastic crisis as a result of a
recent parvovirus B19 infection, evident by decreased hemoglobin and
hematocrit and a decrease in the reticulocyte count. Parvovirus B19
causes erythema infectiosum, also known as Fifth disease, a normally
benign childhood disorder initially presenting after an incubation period of
5-15 days with fever, headache, and nausea, followed by a malar, or
"slapped cheek," rash 2-5 days later. This malar rash is commonly seen in
children, and is erythematous with circumoral pallor. Adults, especially
women, will often present with arthralgias of the knees, wrists, and small
joints of the hands, in either the presence or absence of a rash. The virus
infiltrates the bone marrow where it has a strong affinity and cytotoxicity
for erythroid progenitor cells and can prevent erythropoiesis.
This can cause a self-limiting aplastic anemia and transient bone marrow
suppression in healthy individuals. In children with hemoglobinopathies,
such as sickle cell disease, severe anemia can occur. This commonly
manifests with pallor, weakness, fatigue and a recent history of viral
infection. Lab studies will show a decrease in hemoglobin and hematocrit
and a decrease in the reticulocyte count due to both chronic hemolysis
secondary to sickle cell disease (or other hemoglobinopathies)

2
and a decrease in the reticulocyte count due to both chronic hemolysis
secondary to sickle cell disease (or other hemoglobinopathies)
and decreased production of new red cells due to infection.

A mild macrocytosis is occasionally observed. Treatment is usually with IV

fluids, oxygen, and pain management, although blood transfusion may be
necessary. Erythropoiesis and reticulocyte production usually occurs within
2 to 14 days following infection.

Excess bilirubin production due to increased hemolysis can cause

pigmented gallstone formation in patients with sickle cell disease. This
would present with right upper quadrant pain, nausea, vomiting, and
possibly shoulder pain (referred pain due to diaphragm irritation).

Sickled red blood cells cause microvascular infarcts in vascular beds

throughout the body. Over time, multiple infarcts in the spleen result in
functional asplenia. This makes sickle cell disease patients particularly
susceptible to infections with encapsulated organisms (Streptococcus
pneumoniae, Klebsiella pneumoniae, Haemophilus influenza type
B, Neisseria meningitidis, Salmonella, group B streptococcus).

Progressive narrowing of cerebral blood vessels increases the risk of

stroke in patients with sickle cell disease. Stroke, usually ischemic, affects
up to 11% of sickle cell children by age 20 years. Up to 25% of patients will
have a stroke by age 45 years, with adults more commonly presenting with
hemorrhagic stroke.

The renal medulla is particularly prone to vasoocclusion in sickle cell

patients. This may cause hyposthenuria, in which the kidneys cannot fully
concentrate urine leading to nocturia and polyuria. Infarcts, papillary
necrosis, and progression to end stage renal disease can occur

This patient most likely has iron deficiency anemia due to chronic blood
loss from her uterine fibroids.

Laboratory findings for iron deficiency anemia include decreased iron,

decreased ferritin, and increased total iron binding capacity. This is
because the liver responds by increasing transferrin (the protein that carries

3
decreased ferritin, and increased total iron binding capacity. This is
because the liver responds by increasing transferrin (the protein that carries
iron in the blood); thus, the capacity to bind iron increases.

This image shows the classic finding of spoon nails (koilonychia) in a

patient with iron deficiency anemia. Image used with permission. By CHeitz
- https://www.flickr.com/photos/coreyheitzmd/15023020192, CC BY 2.0,
https://commons.wikimedia.org/w/index.php?curid=74757229.

Elevated ferritin is associated with the anemia of chronic disease.

Answer C: Increased total bleeding time is associated with

thrombocytopenia and von Willebrand disease.

Answer D: Disseminated intravascular coagulation (DIC) is associated with

low fibrinogen and deranged coagulation studies.

Answer E: Prolonged PT is associated with warfarin, end-stage liver failure,

and DIC.

4
Labs

iron deficiency anemia: decreased iron, decreased ferritin, and increased total iron
binding capacity. This is because the liver responds by increasing transferrin (the
protein that carries iron in the blood); thus, the capacity to bind iron increases.

.
Elevated ferritin is associated with the anemia of chronic disease.

Increased total bleeding time is associated with thrombocytopenia and von

Willebrand disease.

Low fibrinogen and deranged coagulation studies Disseminated intravascular

coagulation (DIC) l

Prolonged PT is associated with warfarin, end-stage liver failure, and DIC.

1
Stats

1
Rubeola, or measles,
- caused by a paramyxovirus and like the virus associated
with mumps,
- single-stranded, negative-sense RNA virus
- 3 Cs of cough, coryza, and conjunctivitis.
- Small irregular red spots with central gray specks, called
Koplik spots, appear on the buccal mucosa. These spots
often resolve before the appearance of the rash. The rash is
a maculopapular rash that spreads from the head toward
the feet. A high fever is present. After rash development,
patients with measles often present with
lymphadenopathy and pharyngitis. Thrombocytopenia
and leukopenia are common CBC findings. In some
children, measles can result in complications
including diarrhea, pneumonia, or encephalitis (many of
these other symptoms are due to secondary infections).

Erythema infectiosum, commonly known as fifth disease,

is caused by parvovirus B19, a linear, single-stranded
DNA virus. If present, the fever is typically low-grade. The
rash is often described as “slapped cheek” as the child’s
cheeks are erythematous. A pruritic, maculopapular rash
starts on the arms and spreads to the trunk and legs in a
lacy, reticular pattern. The rash worsens with fever and sun
exposure. While mild in children, congenital infection can
result in fetal hydrops and death.

Mumps is caused by a paramyxovirus which is an

enveloped, single-stranded, negative-sense RNA virus. The
prodrome is nonspecific (low-grade fever, headache,
malaise). Parotid gland swelling occurs. Patients have local
parotid tenderness and sometimes an earache before
the swelling occurs. Painful testicular swelling (orchitis)
can occur in males.

Roseola is caused by the double-stranded HHV-6 and

HHV-7 viruses. The prodrome is an acute onset of high
fever (> 40ºC), which lasts without other symptoms
for 3 to 4 days. As the fever breaks, a maculopapular rash
appears. The rash begins on the trunk and spreads to the
face and extremities. The rash is usually gone after 24
hours. Febrile seizures can occur due to the acute onset of
high fever.

Rubella (German/3-day measles) is caused by an RNA

togavirus, which is a single-stranded RNA genome.
The prodrome is tender, generalized lymphadenopathy.
The rash is a tender maculopapular rash that starts on
the face and spreads distally. Children do not usually appear
ill and have only a low-grade fever. Petechiae on the palate,
known as Forschheimer spots, may appear. Rubella and
rubeola both have rashes that start on the face and spread

1
known as Forschheimer spots, may appear. Rubella and
rubeola both have rashes that start on the face and spread
distally. Children with rubeola have a high fever and appear
ill while children with rubella only have a low-grade fever.

high suspicion for the patient being infected with the Ebola virus should
immediately be quarantined to ensure the safety of others. Ebola infection
is generally thought to begin when an individual is in contact with infected
meat or the body fluids of an infected individual. Epidemics in West Africa
have shown the disease can spread rapidly and widely with extensive
movement of infected individuals, especially with humanitarian efforts.
Most cases of Ebola begin with the abrupt onset of fever, chills, and general
malaise. Other common signs and symptoms include fatigue, headache,
vomiting, diarrhea, and loss of appetite.

A diffuse, erythematous, nonpruritic maculopapular rash is often seen by

day 5-7 of illness. It usually involves the face, neck, trunk, and/or arms.
Despite the traditional name of "hemorrhagic fever" major bleeding is not
often seen. Rather, blood in the stool, petechiae, ecchymoses, or oozing
from venipuncture sites are more common, as in this patient. They may also
develop signs/symptoms of meningoencephalitis such as altered level of
consciousness, stiff neck, and/or seizures.

What is of immediate concern in this patient is the development of

disseminated intravascular coagulation (DIC) or consumption
coagulopathy. It is a systemic process that can cause thrombosis and severe
life-threatening hemorrhage. When blood is exposed to one or more
procoagulants, such as tissue factor (which many bacterial and viral
products have), the processes of coagulation and fibrinolysis become
abnormally activated within the vasculature, leading to ongoing coagulation
and fibrinolysis. This formation leads to massive consumption of
endogenous coagulation factors, platelets, and anticoagulant factors like
protein S, protein C, and antithrombin.

This consumption of coagulation factors combined with high concentration

of fibrin degradation products leads to severe bleeding diathesis. Findings
consistent with acute disseminated intravascular coagulation (DIC) include
history of trauma, sepsis, or malignancy, bleeding/oozing from catheter or
drain sites, thrombocytopenia, prolonged prothrombin time (PT) and
activated partial thromboplastin time (aPTT), low plasma fibrinogen,
elevated plasma D-dimer, abnormal coagulation testing, and/or
microangiopathic changes on peripheral blood smear. Patients who
have serious bleeding like oozing, hematemesis, or hematochezia, as in this
patient, and a significantly prolonged PT or aPTT, or a fibrinogen level < 50
mg/dL, should immediately receive coagulation factor replacement
like fresh frozen plasma. Patients with a platelet count < 10,000/µL should
also be given platelet transfusions due to the increased risk of spontaneous
bleeding.

Rapid restoration of perfusion in a patient who is hypotensive and

hemodynamically unstable with intravenous (IV) fluids is an important and
vital resuscitation step; however, this choice is not the best answer.
Treatment with an antiemetic and/or antidiarrheal medication may help
control further fluid loss, and if the patient is able to take in oral fluids, that

2
Treatment with an antiemetic and/or antidiarrheal medication may help
control further fluid loss, and if the patient is able to take in oral fluids, that
may be sufficient to restore and maintain proper fluid levels. If oral fluids
are not possible, fluid replacement via IV would be important, but not the
first step in this case. A suspected Ebola-infected patient should first be
quarantined to prevent transmission of the disease to other individuals.
Additionally, this patient has DIC as indicated by the petechiae and bleeding
from the attempted IV site. The patient should receive treatment of the
coagulopathy using fresh frozen plasma.

Ebola virus disease is caused by a virus in the Filoviridae family and is not
susceptible to antibiotics or any antimicrobial therapy. To date, the only
treatment for Ebola virus disease is supportive. In this case, supportive
therapy includes treating the life-threatening DIC with fresh frozen plasma.

The administration of antifibrinolytic agents such as tranexamic acid,

epsilon-aminocaproic acid, or aprotinin, is generally contraindicated because
blockade of the fibrinolytic system may increase the risk of thrombotic
complications.

Acute bleeding is challenging, especially in the setting of DIC secondary to

Ebola virus disease. Patients who have serious bleeding or a platelet count <
50,000/µL should be considered for a platelet transfusion. Although this
patient may need a platelet transfusion in the future with a platelet count of
45,000/µL, quarantine is the most important first step. Additionally, she
requires replacement of the coagulation factors to reverse the coagulopathy
before any other treatments are offered.

Bottom Line: Patients undergoing disseminated intravascular coagulopathy

are at risk of severe bleeding due to depletion of coagulation factors and
platelets. Patients should be immediately quarantined to prevent
transmission of the disease to other individuals, and be treated with
coagulation factors.

his patient has symptoms of acute viral hepatitis, most likely caused by the hepatitis A
virus (HAV). HAV is a picornavirus and is the most common type infecting travelers. It is
communicated through the fecal-oral route, often by contact with contaminated food or water
or with an infected person. It has an incubation period of 2 to 6 weeks. Vaccination several weeks
before travel can prevent the illness. Infection is rarely fatal, with worsening symptoms in older
patients. Children often experience a mild form of the disease. Symptoms can include malaise,
nausea, vomiting, abdominal pain, jaundice, clay-colored stool, anorexia, and darkened urine.

Because the patient had gastrointestinal symptoms after travel to Mexico, it is logical to think about

3
Because the patient had gastrointestinal symptoms after travel to Mexico, it is logical to think about
bacterial causes of her symptoms. Enterotoxigenic E. coli is a common cause of traveler's
diarrhea. Because the labs were negative for pathogenic E. coli and the patient did not have
diarrhea along with signs of liver damage, pathogenic strains of E. coli can be logically ruled
out. Salmonella is another infectious organism associated with contaminated food and
water. However, Salmonella is H2S positive and can be ruled out because this patient's stool
sample was negative for H2S bacterium. Therefore, a hepatitis virus is the most likely cause of her
gastrointestinal symptoms and elevated liver enzymes and serum bilirubin levels.

Diagnosis of HAV should be considered in an individual with nausea, fever, malaise, and jaundice/
elevated ALT in an individual at risk for contracting HAV. The diagnosis can be confirmed by
detection of serum anti-HAV antibodies.

Infectious hepatitis may also be due to the hepatitis B, C, D, or E viruses. Both HAV and HEV are
transmitted by the fecal-oral route and HBV, HCV, and HDV are transmitted via body fluids. Other
infectious agents that can be associated with an impact on liver function include Epstein-Barr virus,
cytomegalovirus, yellow fever, Plasmodium (malaria), andTreponema (secondary syphilis).

Treatment of HAV infection is usually supportive care since the disease is normally self limiting with
full clinical recovery in 2 to 3 months. Upon recovery, the individual generally has life-long immunity
to this infection. While rare (< 1% of patients), fulminant hepatic failure is a possibility in individuals
older than 50 years of age and in those with other liver disease. Prevention of HAV disease is via
vaccination. The CDC currently recommends vaccination of all children at 1 year of age and
for individuals who are at risk for infection, such as those traveling to locations where HAV infection
is prevalent.

Answer A: HEV is a nonenveloped single-stranded RNA virus and typically causes asymptomatic or
mildly symptomatic disease. While HEV is also transmitted via fecal-oral contamination, it is more
severe in pregnant women and infants and has a 20% mortality rate in these patients. Given that the
patient described above does not indicate she is pregnant and routine labs are normal, it is less
likely that she is infected with HEV. There is no vaccine for HEV.

Answer B: HAV is an RNA virus. The only hepatitis virus that carries DNA is HBV. Because this
patient is in medical school, she very likely has been vaccinated against HBV and therefore, HBV
can be ruled out.

Answer C: A causative pathogenic, lactose fermenting, gram-negative rod would likely be E.
coli. While E. coli can cause some of her symptoms, it is not typically associated with liver
dysfunction. In addition, E. coli can be ruled out because it was not identified in her stool. There are
other lactose fermenting gram-negative rods such as Klebsiella, but these are not typical pathogens
in an otherwise healthy individual.

Answer D: While HAV can be transmitted sexually, the most common mode of transmission is
fecal-oral. In addition, the patient's boyfriend did not show signs of recent HAV infection. HBV and
HCV can be transmitted sexually, with the most common mode of transmission for HCV being blood
borne.

Bottom Line: Hepatitis A virus is a picornavirus and is the most common hepatitis viral infection in
travelers. Prior vaccination can prevent the infection.

4
 Table 1
Cholera - rice water diarrhea, painful leg cramps (electrolytes imbalance), unsanitary conditions,

- Cholera toxin cause ADP riboysalation of Gsa protein which activates adenylate cyclase —> inc cAMP—
> release of Cl- into gut lumen and dec Na resorption

Corneybacterium - produce toxins that cause ADP riboysalation of enzyme elongation factor , inactivating this enzyme.
diphtheria Inactivation of elongation factor 2 lead to protein synthesis inhibition and cell death

Pseudomonas - produce toxins that cause ADP riboysalation of enzyme elongation factor , inactivating this enzyme.
Aeruginosa Inactivation of elongation factor 2 lead to protein synthesis inhibition and cell death

Bordatella pertussis - whooping cough, releases pertussis toxin that cause ADP riboysaltion of inhibitory Gi protein leading to inc
intracellular cAMP

Clostridium tetani - inhibits gaba and glycine (both inhibit NT)

toxin
- Muscle spasm

- Low jaw
Shigella - toxin that inactivates 60s ribosome—> dec synthesis of host cell

Ecoli