​Pathology - Chronic Myelogenous Leukemia 
The symptoms arise as a result of underlying abnormalities in the blood, including infection caused by faulty white blood cell function, and reduced energy due to anemia. Increased proliferation of leukemic cells within the bone marrow can cause bone pain to arise later in the disease. Chronic Myeloid Leukemia (CML) is a result of a genetic rearrangement that occurs between chromosomes 9 and 22, known as the Philadelphia chromosome. The translocation event results in the creation of the BCR-ABL fusion protein, which serves as a target for some chemotherapeutic medications like Imatinib, a type of tyrosine kinase inhibitor. Chronic myeloid leukemia (CML) can be distinguished from other forms of leukemia by the presence of a higher quantity of platelets, a characteristic that is not commonly observed in other types of leukemia.
The leukemoid reaction, which is characterized by an increased white blood cell count in response to infection or stress, can be differentiated from chronic myelogenous leukemia (CML) by observing the rise in leukocyte alkaline phosphatase score in the non-cancerous cells of the leukemoid reaction.

Pathology - Carcinoid Syndrome
The patient is experiencing carcinoid syndrome as a result of a malignant tumor in the small bowel.
The majority of these tumors are located in the appendix. However, tumors detected in the small bowel have the ability to spread to the liver and result in the symptoms mentioned in the vignette. The symptoms arise as a result of the secretion of serotonin by the tumor cells.
Serotonin is transported to the liver by the hepatic portal circulation, where it undergoes metabolism. After being produced, the metabolites, such as 5-hydroxyindoleacetic acid (5-HIAA), are released into the bloodstream and result in vasodilation (flushing), diarrhea, and enhanced production of collagen in the heart valves (murmur). The tricuspid and pulmonic valves are commonly impacted. Octreotide, a somatostatin agonist, can be used to provide symptomatic therapy by reversing vasodilation generated by 5-HIAA. Nevertheless, the administration of chemoembolization to the blood arteries that supply liver metastases may offer extended and sustained relief.

​Pathology - Pancreatic head adenocarcinoma
These patients usually have "painless jaundice" and may have some of the risk factors linked to pancreatitis, such as excessive alcohol use and tobacco use.
Tumors located in the head of the pancreas can exert pressure on the pancreatic part of the common bile duct (CBD), leading to a blockage in the flow of bile and resulting in the enlargement of the CBD and the biliary ducts within the liver. Consequently, there is a higher level of conjugated bilirubin in the bloodstream. It should be emphasized that only conjugated bilirubin may be identified in the urine, and this usually leads to darkening as a result of the urobilin pigment. Jaundice commonly manifests when bilirubin levels exceed 3g/dL. Another consequence of the obstruction is reduced bile flow in the colon, resulting in feces that float because of the higher fat content. The presence of pale "acholic" stools is due to a reduced level of stercobilin, a by-product of bilirubin, which is responsible for the typical brown color of stools. The overall prognosis is typically unfavorable, although, in certain circumstances, it may be possible to perform a surgical removal of the tumor using the Whipple technique (pancreaticoduodenectomy).

​Pathology - Gastrinoma 
Gastrinoma, also known as Zollinger-Ellison Syndrome
The patient is diagnosed with gastrinoma, which is a type of pancreatic tumor that produces and releases gastrin. Gastrin, typically secreted by the G cells in the stomach, activates the parietal cells in the stomach. This leads to an elevation in the proton concentration within the stomach, thereby resulting in an increase in acidity. Gastrin further promotes the growth of parietal cells, leading to an additional rise in the production of acid. The heightened acidity in the gastrointestinal system is not counteracted by the protective mucosal barrier facilitated by prostaglandins, resulting in the formation of ulcers. If the ulcers perforate the vessels, the ulceration might lead to abdominal pain and bleeding. Gastrinomas are predominantly found in the region known as the "gastrinoma triangle," which is defined by the convergence of the hepatic and cystic ducts at the top, the neck of the pancreas, and the intersection of the second and third parts of the duodenum. A gastrinoma can be definitively diagnosed by a secretin stimulation test. Normally, secretin suppresses the production of gastrin. However, in this particular condition, the G cells persist in producing gastrin despite the presence of secretin. Medical therapy involves the use of Proton Pump Inhibitors (PPIs). Excising the gastrinoma cells with surgery, despite its challenging nature, typically leads to a complete cure.

​Pathology - Esophageal Adenocarcinoma 
Esophageal Adenocarcinoma is a type of cancer that affects the esophagus.
The extensive historical record of GERD substantiates this diagnosis. Individuals suffering from GERD commonly have a reduction in the tone of the lower esophageal sphincter, which results in the backflow of stomach contents into the esophagus. Over time, the esophagus undergoes metaplastic changes at the gastroesophageal junction due to exposure to acidic gastric secretions. This results in the transformation of the typical squamous cells of the esophageal tissue into columnar cells, which are characteristic of gastric epithelium, in order to adapt to the gastric acid exposure. This alteration can be observed by endoscopy and is referred to as Barrett's esophagus. It serves as a precursor to the development of esophageal cancer. Administration of drugs such as PPIs and H2 blockers can lead to a reduction in the acidic stimuli, which in turn can result in the reversal of metaplasia. However, persistent reflux is likely to lead to the development of esophageal cancer, which would require surgical intervention for removal. Radiation and chemotherapy may be considered as treatment options, depending on the cancer's stage.

Pathology - ​Gastric adenocarcinoma
 The historical background of peptic ulcer disease suggests a possible infection with H. pylori, a bacterium known to induce gastritis and intestinal metaplasia. If a left supraclavicular node, also known as Virchow's node, is present, it indicates metastasis through lymphatic drainage. Additional observations include of acanthosis nigricans, which is the darkening of the skin, the Leser-Trelat sign, which indicates the presence of a large number of seborrheic keratosis, and the Sister Mary Joseph sign, which suggests metastasis to periumbilical nodes based on the existence of a palpable periumbilical node. It is crucial to emphasize that the diffuse type of gastric adenocarcinoma is not linked to H. pylori infection. This illness has a bleak prognosis, and the treatment may involve a mix of surgical intervention, chemotherapy, and/or radiation therapy. Palliative care is typically initiated soon after diagnosis because this disease is frequently inoperable.

Pathology - Colorectal cancer
The patient exhibits symptoms consistent with anemia, and the test results suggest that the underlying cause is iron deficiency resulting from ongoing blood loss. Lesions affecting the descending colon typically result in obstructive symptoms because to its narrower diameter, but lesions in the ascending colon tend to produce bleeding, which can lead to iron-deficiency anemia. His risk factors consist of his smoking history and a confirmed family history of colon cancer. A well-documented series of genetic mutations takes place in colorectal cancers: APC → K-RAS → DCC → p53. Colon cancer encompasses a range of different kinds, some of which have a hereditary component. Hereditary nonpolyposis colorectal cancer is linked to genetic alterations in mismatch repair. This patient should have additional assessment, specifically a colonoscopy, to gather tissue samples and get a more conclusive diagnosis.

Pathology - Heparin-Induced Thrombocytopenia (HIT)
Heparin-induced thrombocytopenia (HIT) is a problem that can occur as a result of heparin treatment and can lead to the formation of blood clots in veins or, less commonly, arteries. The pathogenesis of this condition is characterized by the production of an immunological complex that is antigenic, leading to the development of a type II hypersensitivity reaction. Heparin molecules attach to the platelet-specific chemokine platelet factor 4 (PF4) and, as a result, trigger the creation of IgG (HIT antibodies). These antibodies then connect to the heparin-PF4 molecule, creating an immunological complex. The FcγIIa receptor found on platelets in the bloodstream attaches to the heparin-PF4-IgG immunological complex. As a result, macrophages in the spleen eliminate the platelets, leading to thrombocytopenia. Nevertheless, since both the PF4 and IgG components of the complex have the ability to attach to platelets, it is possible for a platelet that is carrying this immunological complex to adhere to another platelet while circulating in the bloodstream.
The process of cross-linking platelets through the immune complex results in more platelet aggregation and activation, which leads to the release of more PF4 capable of binding heparin. This, in turn, causes the creation of a paradoxical thrombus despite the presence of the anticoagulant. Arterial emboli resulting from HIT have become trapped in the microvasculature surrounding the first metatarsal in this patient, causing ischemia. The initial measure in the therapy process involves discontinuing the administration of heparin.

​Pathology - Thrombotic Thrombocytopenic Purpura (TTP)
This condition is medically identified by the presence of five specific symptoms: fever, low platelet count, kidney failure, abnormal breakdown of red blood cells with fragmented cells called schistocytes, and abnormalities in the nervous system. The idiopathic form of this thrombotic microangiopathy commonly presents with a deficit of the vWF cleaving protease ADAMTS-13, caused by an autoimmune response. This leads to the presence of excessively large multimers of vWF, which in turn promote excessive platelet aggregation. Thrombocytopenia occurs due to the excessive formation of microvascular thrombi. Petechiae and purpura occur as a consequence of thrombocytopenia. Cerebral microvascular occlusion can result in various neurological symptoms such as headache, seizures, localized neurological impairments, or alterations in mental status. Renal microinfarcts result in the development of acute renal failure, which is characterized by an increase in serum creatinine levels. Erythrocytes undergo shearing when they come into contact with microthrombi, leading to the development of hemolytic anemia. This condition causes the formation of schistocytes and jaundice. Plasma exchange is the preferred treatment and platelet transfusion can actually exacerbate the production of microthrombi.

Pathology - Idiopathic (Immune) Thrombocytopenic Purpura
Idiopathic thrombocytopenic purpura (ITP), sometimes called immunological thrombocytopenic purpura, a type II hypersensitivity reaction. This acute onset of the illness most typically occurs in children following a viral upper respiratory tract infection. The pathogenesis relies around the development of IgG antibodies against platelet membrane glycoproteins, notably GpIIb/IIIa receptors. Coating of platelets by IgG leaves them vulnerable to opsonization and phagocytosis by macrophages in the spleen. The lower platelet counts lead to localized cutaneous hemorrhages known as petechiae, described in the vignette, as well as ecchymoses. Other symptoms may include epistaxis, hematuria, or hematochezia. Splenomegaly and lymphadenopathy could be expected in malignant causes of thrombocytopenia. ITP is normally selflimiting in children; nevertheless, severely low levels of platelets (<10,000/mm3) produces risk for serious hemorrhage, bleeding into vital organs, and cerebral hemorrhage. In adults, the problem is most often chronic and is connected with other autoimmune diseases or large array of medications.