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Symptoms and Signs – Differential Diagnosis of Cottonwool spots
Diabetes (pre-proliferative retinopathy)
Haematological disorders: anaemia, leukaemia, hyperviscosity states
HIV retinopathy
Hypertensive retinopathy
Papilloedema
Retinal vein occlusion
SLE, polyarteritis nodosa, dermatomyositis
Diabetes (pre-proliferative retinopathy)
Haematological disorders: anaemia, leukaemia, hyperviscosity states
HIV retinopathy
Hypertensive retinopathy
Papilloedema
Retinal vein occlusion
SLE, polyarteritis nodosa, dermatomyositis
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Symptoms and Signs – Differential Diagnosis of Raised Cortisol
ACTH, e.g. bronchial carcinoids, ectopic CRH)
Alcoholism
Cushing's syndrome (pituitary adenoma, adrenal adenoma/carcinoma, ectopic
Depression
Exogenous glucocorticoids
Increased Cortisol-binding globulin (CBG): oestrogen, pregnancy
Stress, acute/chronic illness
ACTH, e.g. bronchial carcinoids, ectopic CRH)
Alcoholism
Cushing's syndrome (pituitary adenoma, adrenal adenoma/carcinoma, ectopic
Depression
Exogenous glucocorticoids
Increased Cortisol-binding globulin (CBG): oestrogen, pregnancy
Stress, acute/chronic illness
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Symptoms and Signs – Differential Diagnosis of Cough
ACE inhibitors
Asthma, COPD, pulmonary emboli, infection (pneumonia, TB, fungal),
bronchiectasis, malignancy, interstitial lung disease, sarcoidosis,
Gastro-oesophageal reflux disease
Heart failure
pneumoconiosis
Post-nasal drip
Psychogenic
Upper respiratory tract infection
ACE inhibitors
Asthma, COPD, pulmonary emboli, infection (pneumonia, TB, fungal),
bronchiectasis, malignancy, interstitial lung disease, sarcoidosis,
Gastro-oesophageal reflux disease
Heart failure
pneumoconiosis
Post-nasal drip
Psychogenic
Upper respiratory tract infection
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Symptoms and Signs – Differential Diagnosis of Crackles
Fine crackles
Pulmonary fibrosis (See Lung function tests, for the causes)
Pulmonary oedema
Crackles continued
Coarse crackles
Bronchiectasis
Consolidation (pneumonia)
COPD
Fine crackles
Pulmonary fibrosis (See Lung function tests, for the causes)
Pulmonary oedema
Crackles continued
Coarse crackles
Bronchiectasis
Consolidation (pneumonia)
COPD
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Symptoms and Signs – Differential Diagnosis of Cramp
Drugs: 13-agonists, Angiotensin II receptor blockers, cisplatin, vincristine
Extracellular volume/salt depletion (diuretics, excessive sweating, fluid removal during haemodialysis)
Flat feet, hypermobility syndrome, inappropriate leg positioning, prolonged sitting
Hypokalaemia
Hypomagnesaemia
Hypothyroidism
Idiopathic
Muscle ischaemia, myopathy, motor neurone disease
Drugs: 13-agonists, Angiotensin II receptor blockers, cisplatin, vincristine
Extracellular volume/salt depletion (diuretics, excessive sweating, fluid removal during haemodialysis)
Flat feet, hypermobility syndrome, inappropriate leg positioning, prolonged sitting
Hypokalaemia
Hypomagnesaemia
Hypothyroidism
Idiopathic
Muscle ischaemia, myopathy, motor neurone disease
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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.
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.
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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.
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.
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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).
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).
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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.
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.
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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.
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.
