Test: Quiz On Diseases! MCQ

The correct answer is spherocytes. Spherocytes are small, round red blood cells that lack central pallor. They are commonly seen in conditions such as hereditary spherocytosis, autoimmune hemolytic anemia, and certain drug-induced hemolytic anemias. In this case, the patient's peripheral blood smear shows normochromic normocytic anemia, which is consistent with spherocytes. The negative Direct Coombs' test and increased osmotic fragility of the red cells further support the diagnosis of hereditary spherocytosis, a condition characterized by the presence of spherocytes.

In a Type II hypersensitivity reaction, the immune system mistakenly attacks healthy cells or tissues. In this case, the patient received a mismatched ABO transfusion, leading to the immune system targeting and destroying the transfused red blood cells. The kidney pain and hematuria are likely due to the destruction of red blood cells in the kidneys, causing inflammation and damage. This aligns with a Type II hypersensitivity reaction, making it the most likely explanation for the patient's symptoms.

http://upload.wikimedia.org/wikipedia/commons/thumb/f/fc/Congestive_hepatopathy_high_mag.jpg/640px-Congestive_hepatopathy_high_mag.jpg

In hepatology, congestive hepatopathy, also known as nutmeg liver and chronic passive congestion of the liver, is liver dysfunction due to venous congestion, usually cardiac dysfunction, i.e. right heart failure or (less specifically) congestive heart failure. The gross pathological appearance of a liver affected by chronic passive congestion is "speckled" like a grated nutmeg kernel; the dark spots represent the dilated and congested hepatic venules and small hepatic veins. The paler areas are unaffected surrounding liver tissue. When severe and longstanding, hepatic congestion can lead to fibrosis, which is often called cardiac cirrhosis Increased pressure in the sublobular branches of the hepatic veins causes an engorgement of venous blood, and is most frequently due to chronic cardiac lesions, especially those affecting the right heart, the blood being dammed back in the inferior vena cava and hepatic veins. Central regions of the hepatic lobules are red/brown and stand out against the noncongested, tan-coloured liver. Centrilobular necrosis occurs. Macroscopically, the liver has a pale and spotty appearance in affected areas, as stasis of the blood causes pericentral hepatocytes (liver cells surrounding the periportal venules of the liver) to become deoxygenated compared to the relatively better-oxygenated periportal hepatocytes adjacent to the hepatic arterioles. This retardation of the blood also occurs in pulmonary lesions, such as chronic interstitial pneumonia, pleural effusions, and intrathoracic tumors.

The most likely diagnosis in this case is intravascular hemolysis. The patient's presentation of jaundice, icteric sclerae, elevated total serum bilirubin (with a high percentage of indirect bilirubin), increased urinary hemoglobin, and hemosiderin are consistent with intravascular hemolysis. Intravascular hemolysis refers to the destruction of red blood cells within the bloodstream, leading to the release of hemoglobin and subsequent elevation of bilirubin levels. This can be caused by various conditions such as autoimmune hemolytic anemia, paroxysmal nocturnal hemoglobinuria, or mechanical heart valves.

The most likely mechanism behind the development of viral resistance to maraviroc in this patient is a shift to a CCR5-CXCR4 dual-tropism. This means that the patient's viral strain has evolved to use both the CCR5 and CXCR4 co-receptors to enter host cells, instead of solely relying on the CCR5 co-receptor. Maraviroc specifically targets the CCR5 co-receptor, so a shift to dual-tropism would render the drug less effective. This shift in tropism is a common mechanism of resistance to maraviroc.

The patient's presentation with multiple types of cancer suggests a genetic predisposition to cancer development. LOH (loss of heterozygosity) of the p53 gene is a known mechanism that can lead to the development of various types of cancer. The p53 gene is a tumor suppressor gene that plays a crucial role in regulating cell growth and preventing the formation of tumors. LOH of the p53 gene can result in the loss or inactivation of one copy of the gene, leading to an increased risk of cancer development.

Interpretation:
– Negative result: Total absence
of bands associated with HIV-1
(CDC guidelines); According to
the WHO guidelines, a very weak
p17 band would also qualify as a
negative result
– Positive result: Presence of at
least 2 of the following bands
(CDC guidelines):
• p24
• gp41
• gp120/160

Antibodies against ds-DNA would be most helpful in confirming the diagnosis because the presence of these antibodies is strongly associated with systemic lupus erythematosus (SLE), an autoimmune disease. SLE is characterized by the production of autoantibodies against various components of the cell nucleus, including ds-DNA. Therefore, the presence of antibodies against ds-DNA can support the diagnosis of SLE.

Purine nucleoside phosphorylase deficiency, often called PNP-deficiency, is a rare autosomal recessive metabolic disorder which results in severe combined immunodeficiency.
In addition to the symptoms associated with immunodeficiency, such as depletion of T-cells, decline of lymphocyte activity, and an abrupt proliferation of both benign and opportunistic infections, PNP-deficiency is often characterized by the development of autoimmune disorders. Lupus-erythematosis, autoimmune hemolytic anemia, and idiopathic thrombocytopenic purpura have been reported with PNP-deficiency
PNP-deficiency is extremely rare. Only 33 patients with the disorder in the United States have been documented.
In the United Kingdom only one child has been diagnosed with this disorder.......classic Buxbaum

These young men have Beaver Fever....NO, John, not that kind of beaver.
This is Giardia, which you get from drinking water from a stream in the woods, hence "beaver fever"
THe give away is FOUL SMELLING (malodorous) and gaseous diarrhea.
Tropozites are seen in the stool with Giardiasis.
metronidazole (Flagyl) is the treatment of choice.
remember to warn your patient to avoid alcohol while on flagyl. (aldehyde dehydrogenase reaction)

Physicians clarify what can be realistically expected and distinguish this from what might be wished for, or what is most feared. This is the most appropriate way to deliver the news to the patient because it allows the physician to provide an honest and accurate assessment of the patient's prognosis while also addressing any hopes or fears the patient may have. It ensures that the patient is fully informed and able to make decisions based on realistic expectations.

The most likely diagnosis in this case is squamous cell papilloma. This is supported by the histological examination findings of fibro-capillary stalks covered by proliferating squamous epithelium with preserved polarity and mild cellular atypia. Squamous cell papilloma is a benign tumor that commonly occurs in the larynx and is associated with smoking. It is characterized by the presence of papillomatous growths, which are consistent with the findings on laryngoscopy. The absence of mitotic figures and penetration through the basement membrane further support the benign nature of the lesion.

The most likely diagnosis in this case is uridyl glucuronyl transferase deficiency. This is indicated by the severe jaundice that appeared at birth and has been worsening, along with the high indirect bilirubin and low fecal urobilinogen levels. Uridyl glucuronyl transferase deficiency, also known as Gilbert syndrome, is a genetic disorder that affects the liver's ability to process bilirubin, leading to an accumulation of bilirubin in the blood and resulting in jaundice. The patient's normal CBC and lack of acute distress also support this diagnosis.

The correct answer is "Motile trophozoites from the colon invaded the liver." In this scenario, the man experienced dysentery, which is often caused by an infection with the parasite Entamoeba histolytica. The motile trophozoites of this parasite can invade the liver, leading to the formation of an abscess. The presence of elevated liver enzymes in the blood further supports the diagnosis of liver involvement.

Pyrimidine dimers are the primary cause of melanomas in human beings.
Pyrimidine dimers are molecular lesions formed from thymine or cytosine bases in DNA via photochemical reactions. Ultraviolet light induces the formation of covalent linkages by reactions localized on the C=C double bonds. In dsRNA, uracil dimers may also accumulate as a result of UV radiation. Two common UV products are cyclobutane pyrimidine dimers (CPDs, including thymine dimers) and 6,4 photoproducts. These premutagenic lesions alter the structure of DNA and consequently inhibit polymerases and arrest replication. Dimers may be repaired by photoreactivation or nucleotide excision repair, but unrepaired dimers are mutagenic.

HIV infection and a low CD4+ count are associated with an increased risk of developing certain types of cancers, such as Kaposi sarcoma, uterine cervix carcinoma, and B-cell lymphoma. However, breast carcinoma is less commonly associated with HIV infection and a low CD4+ count compared to the other options. Therefore, breast carcinoma is the least likely tumor to arise in this woman.

Lepirudin may be used as an anticoagulant when heparins (unfractionated or low-molecular-weight) are contraindicated because of heparin-induced thrombocytopenia.
Lepirudin is a recombinant hirudin[1] derived from yeast cells. It is almost identical to hirudin extracted from Hirudo medicinalis. It differs by the substitution of leucine for isoleucine at the N-terminal end of the molecule and the absence of a sulfate group on the tyrosine at position 63.
Baxter Healthcare Corporation has announced that it will cease the production of lepirudin
Brand name: Refludan, Generic: Lepirudin rDNA for injection.

Side effects can be severe and include infection, cardiac damage, hypertension, blurred vision, liver and kidney problems (tacrolimus nephrotoxicity), hyperkalemia, hypomagnesemia, hyperglycemia, diabetes mellitus, itching, lung damage (sirolimus also causes lung damage), and various neuropsychiatric problems such as loss of appetite, insomnia, Posterior reversible encephalopathy syndrome, confusion, weakness, depression, cramps, neuropathy, seizures, tremors, and catatonia.

In addition it may potentially increase the severity of existing fungal or infectious conditions such as herpes zoster or polyoma viral infections.

http://upload.wikimedia.org/wikipedia/commons/c/c3/In_situ_carcinoma.jpgCarcinoma in situ (CIS) is an early form of cancer that is defined by the absence of invasion of tumor cells into the surrounding tissue, usually before penetration through the basement membrane. In other words, the neoplastic cells proliferate in their normal habitat, hence the name "in situ" (Latin for "in its place"). For example, carcinoma in situ of the skin, also called Bowen's disease, is the accumulation of neoplastic epidermal cells within the epidermis only, that has failed to penetrate into the deeper dermis. For this reason, CIS will usually not form a tumor. Rather, the lesion is flat (in the skin, cervix, etc.) or follows the existing architecture of the organ (in the breast, lung, etc.). Some CIS, however, do form tumors, such as in the colon (polyps), in the bladder (pre-invasive papillary cancer), or in the breast (more properly called ductal carcinoma in situ). Many forms of invasive carcinoma (the most common form of cancer) originate after progression of a CIS lesion. Therefore, CIS is considered a precursor or incipient form of cancer that may, if left untreated long enough, transform into a malignant neoplasm.