MOs MRCS B Notes - Pathology Flashcards
(173 cards)
1
Q
Define infective endocarditis (IE).
A
Inflammation of the endocardial surfaces of the heart, including heart valves, caused by certain microorganisms.
2
Q
Describe the two types of infective endocarditis.
A
The two types of infective endocarditis are acute and subacute, where microbes colonize the heart valves and form friable vegetations.
3
Q
Explain the diagnosis method for infective endocarditis.
A
Diagnosis is made via Duke’s criteria.
4
Q
What is non-bacterial thrombotic endocarditis?
A
Also known as marantic endocarditis, it occurs in the setting of cancers, such as adenocarcinomas.
5
Q
Describe Libman-Sacks endocarditis.
A
Libman-Sacks endocarditis occurs in the setting of cancers, particularly adenocarcinoma.
6
Q
How does rheumatic heart disease (RHD) increase susceptibility to infective endocarditis?
A
Patients with rheumatic heart disease or valve replacements have damaged valves, increasing the chance for bacterial colonization on these tissues.
7
Q
Explain the pathophysiology of rheumatic heart disease.
A
Acute rheumatic fever results from immune responses to group A streptococcal antigens that cross-react with host proteins, leading to inflammation and damage to heart tissue.
8
Q
What are the consequences of antibody and T cell-mediated reactions in RHD?
A
These reactions can cause recurrent inflammation, progressive fibrosis, narrowing and stiffening of valve leaflets, and ultimately lead to stenosis.
9
Q
Describe the major forms of vegetative endocarditis.
A
The acute phase of RHD shows small, warty vegetations; infective endocarditis features large, destructive masses; and nonbacterial thrombotic endocarditis presents with small, bland vegetations.
10
Q
How do vegetations differ in infective endocarditis compared to nonbacterial thrombotic endocarditis?
A
Infective endocarditis has large, irregular, destructive masses, while nonbacterial thrombotic endocarditis has small to medium-sized, nondestructive vegetations.
11
Q
Describe the gross findings in the acute phase of rheumatic heart disease.
A
Valvular vegetations (verrucae) along the lines of closure, having little effect on cardiac function.
12
Q
Explain the chronic phase findings in rheumatic heart disease.
A
Commissural fibrosis, valve thickening, calcification, and shortened and fused chordae tendineae, resulting in a fish mouth shape.
13
Q
Define Aschoff bodies in the context of rheumatic heart disease.
A
Aschoff bodies are a form of granulomatous inflammation consisting of a central zone of degenerating ECM infiltrated by lymphocytes, plasma cells, and Anitschkow cells, found in all three layers of the heart.
14
Q
How do Aschoff nodules appear macroscopically?
A
Aschoff nodules appear as nodules associated with fibrinoid necrosis.
15
Q
What investigation is used to identify vegetations in rheumatic heart disease?
A
2D echocardiography (2D echo) is used to identify vegetations.
16
Q
List the key features to look for in a 2D echo for rheumatic heart disease.
A
1) Valvular regurgitation, 2) Leaflet prolapse, coaptation failure, thickening, reduced mobility, nodules, 3) Annular dilation, 4) Chordal elongation/rupture, 5) Increased echogenicity of subvalvular apparatus, 6) Pericardial effusion, 7) Ventricular dilatation and dysfunction.
17
Q
Explain the microscopic appearance of an Aschoff body in acute rheumatic carditis.
A
It shows central necrosis associated with a circumscribed collection of mononuclear inflammatory cells, including activated macrophages with prominent nucleoli and central wavy (caterpillar) chromatin.
18
Q
Describe the findings associated with mitral stenosis in rheumatic heart disease.
A
Diffuse fibrous thickening and distortion of the valve leaflets, commissural fusion, and thickening and shortening of the chordae tendineae, along with marked left atrial dilation.
19
Q
What does neovascularization indicate in the context of rheumatic mitral valve pathology?
A
Neovascularization indicates the presence of new blood vessel formation, which can occur in response to chronic inflammation and tissue remodeling.
20
Q
How does rheumatic aortic stenosis appear in surgically removed specimens?
A
It demonstrates thickening and distortion of the cusps with commissural fusion.
21
Q
Describe the common organisms associated with infective endocarditis (IE).
A
Common organisms include Viridans Streptococcus, coagulase-negative Staphylococcus, Enterococci, and the HACEK group of microorganisms (Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella species).
22
Q
Explain the Dukes criteria for diagnosing infective endocarditis.
A
The Dukes criteria include selection criteria where a diagnosis can be made with either 2 major criteria and 0 minor criteria, 1 major criterion and 3 minor criteria, or 0 major criteria and 5 minor criteria.
23
Q
Define the major criteria for diagnosing infective endocarditis.
A
Major criteria include positive blood cultures for endocarditis, evidence of endocardial involvement via echocardiogram, and specific findings such as a single positive blood culture for Coxiella burnetii or a high antibody titer.
24
Q
List the minor criteria used in the diagnosis of infective endocarditis.
A
Minor criteria include predisposition (heart condition or IV drug use), fever (≥ 38°C), vascular phenomena (e.g., major arterial emboli), immunologic phenomena (e.g., Osler’s nodes), microbiological evidence, and echocardiographic findings consistent with endocarditis.
25
Identify the causes and risk factors for infective endocarditis.
Causes and risk factors include acquired valvular heart disease, valve replacement, structural congenital heart disease, previous IE, hypertrophic obstructive cardiomyopathy, devices like implantable cardioverter-defibrillators, cyanotic congenital heart defects, colorectal cancer, UTI, IV drug abuse, rheumatic heart disease, HIV, malignancy, diabetes mellitus, alcohol use, and tooth extractions.
26
What are the potential complications of infective endocarditis?
Complications of infective endocarditis can include acute myocardial infarction (AMI), pericarditis, arrhythmia, valvular insufficiency, congestive cardiac failure (CCF), and sinus of Valsalva aneurysm.
27
How does an echocardiogram contribute to the diagnosis of infective endocarditis?
An echocardiogram can provide evidence of endocardial involvement, such as abscesses, new partial dehiscence of prosthetic valves, or new valvular regurgitation, which are critical for meeting major criteria.
28
Explain the significance of blood cultures in the diagnosis of infective endocarditis.
Blood cultures are significant as they can yield positive results for typical microorganisms associated with infective endocarditis, which is a major criterion for diagnosis.
29
Describe the immunologic phenomena associated with infective endocarditis.
Immunologic phenomena associated with infective endocarditis include glomerulonephritis, Osler’s nodes, Roth’s spots, and the presence of rheumatoid factor.
30
What role does a history of previous infective endocarditis play in risk assessment?
A history of previous infective endocarditis is a significant risk factor for developing the condition again, making it an important consideration in patient assessments.
31
Describe Osler nodes.
Osler nodes are painful, raised, red lesions caused by immune complex deposition.
32
Explain Janeway lesions.
Janeway lesions are non-painful, nodular or macular red lesions resulting from septic emboli that deposit bacteria, forming microabscesses.
33
What are splinter hemorrhages?
Splinter hemorrhages are tiny blood clots that appear under the nails.
34
How is infective endocarditis (IE) treated?
IE is treated with IV antibiotics based on culture and sensitivity for 6 weeks, commonly using IV ceftriaxone and vancomycin.
35
Define the restrictions related to antibiotic treatment for valvular infections.
Valves lack specific blood supply, preventing antibiotics from reaching them, and bacteria within vegetations form a biofilm that shields them from antibiotics.
36
What happens if IE occurs in the tricuspid valve in younger individuals?
It can lead to right-sided heart failure.
37
What is the course of action if there is no response to medical treatment for IE?
The options include valve replacement or heart transplantation.
38
How is matching done before heart transplantation?
Matching is done based on HLA antigen.
39
What occurs if HLA antigens are not matched?
If not matched, it can lead to Type 1 graft rejection.
40
How can graft rejections be prevented?
Graft rejections can be prevented with immunosuppressant therapy.
41
List some immunosuppressants used in therapy.
Common immunosuppressants include Tacrolimus, Mycophenolate, and Steroids.
42
What are the side effects of long-term steroid use?
Side effects include opportunistic infections, Cushingoid features, cardiovascular issues, endocrine problems, and musculoskeletal complications.
43
Explain the mechanism of action of immunosuppressants.
Immunosuppressants work by inhibiting the immune response to prevent rejection of transplanted organs.
44
What are the signs and symptoms of infective endocarditis (IE)?
Signs and symptoms include fever, Roth's spots, Osler's nodes, murmurs, Janeway lesions, anemia, nail hemorrhage, and emboli.
45
Describe a Janeway lesion in a clinical context.
A Janeway lesion may appear on the palm of a 36-year-old male with staphylococcus endocarditis.
46
What are Osler nodes and where might they be found?
Osler nodes are painful lesions that can be found on fingers, such as the index finger.
47
What additional signs might be observed in a patient with endocarditis?
Tiny splinter hemorrhages may also be seen on the fingernails.
48
Describe the action of corticosteroids in the treatment of certain conditions.
Corticosteroids, such as prednisone and methylprednisone, act as anti-inflammatory agents and kill T cells.
49
Define cytotoxic drugs and provide examples.
Cytotoxic drugs, like cyclophosphamide, azathioprine, methotrexate, leflunomide, mycophenolate mofetil, and brequinar sodium, block cell division nonspecifically.
50
Explain the role of immunophilins in immunosuppression.
Immunophilins, such as cyclosporin, block T cell responses.
51
What is the purpose of lymphocyte-depleting therapies?
Lymphocyte-depleting therapies, including antilymphocyte globulin and monoclonal antibodies, kill T cells nonspecifically and target activated T cells.
52
How does warfarin function after valve replacement surgery?
Warfarin is used to prevent thromboembolism following valve replacement.
53
Describe the mechanism of action of warfarin.
Warfarin acts as a vitamin K antagonist, inhibiting clotting factors II, VII, IX, and X.
54
How is warfarin therapy monitored?
Warfarin therapy is monitored using the International Normalized Ratio (INR).
55
What are the reversal agents for warfarin?
Reversal agents for warfarin include vitamin K, fresh frozen plasma (FFP), and prothrombin complex concentrate (PCC).
56
Identify the clinical significance of right-sided vegetations in infective endocarditis.
Right-sided vegetations are associated with tricuspid valve infective endocarditis, often seen in IV drug abusers.
57
Explain the current recommendations for antibiotic prophylaxis against infective endocarditis.
Antibiotic prophylaxis against infective endocarditis is not routinely recommended for dental or certain non-dental procedures.
58
What should not be offered as prophylaxis against infective endocarditis during dental procedures?
Chlorhexidine mouthwash should not be offered as prophylaxis against infective endocarditis for at-risk individuals undergoing dental procedures.
59
Describe the clinical picture of aortic stenosis.
The clinical picture of aortic stenosis includes symptoms related to heart failure and reduced cardiac output.
60
List the causes of aortic stenosis.
Causes of aortic stenosis include post-inflammatory scarring (rheumatic heart disease), senile calcific aortic stenosis, and calcification of congenitally deformed valves.
61
What are potential causes of sudden death in patients with aortic stenosis?
Potential causes of sudden death in aortic stenosis include myocardial infarction (MI) and aortic dissection.
62
Explain how stenosis occurs in the aortic valve.
Stenosis occurs due to lipid accumulation, inflammation, and calcification, leading to valve thickening and narrowing.
63
Describe the appearance of aortic valves affected by dystrophic calcification in aortic stenosis.
Aortic valves affected by dystrophic calcification appear markedly narrowed, with thickened and fibrotic semilunar cusps and irregular masses of calcification behind each cusp.
64
Describe the progression of the aortic valve from sclerosis to stenosis.
As the aortic valve progresses from sclerosis to stenosis, the left ventricle faces chronic resistance to systolic ejection, leading to increased afterload and thickening of the left ventricular wall (hypertrophy).
65
Explain the effects of high left ventricular afterload.
High left ventricular afterload results in decreased myocardial elasticity and coronary blood flow, increased myocardial workload, oxygen consumption, and mortality.
66
How does left ventricular hypertrophy (LVH) affect cardiac function?
Late manifestations of LVH include a smaller left ventricular chamber size, which decreases preload and worsens systolic dysfunction, leading to insufficient stroke volume, cardiac output, and ejection fraction.
67
What complications can arise from increased left ventricular pressure?
Increased left ventricular pressure can lead to backward transmission to the lungs, causing pulmonary venous hypertension and reactive vasoconstriction of the pulmonary vasculature.
68
Define thrombus.
Thrombus is defined as solid material formed from the constituents of blood in flowing blood.
69
List the surgical options for valve replacement.
Surgical options for valve replacement include mechanical valves, tissue valves, the Ross Procedure, and TAVI/TAVR procedures.
70
What is the purpose of aortic valve balloon valvuloplasty?
Aortic valve balloon valvuloplasty is performed to widen the valve using a balloon.
71
Why should a metallic valve be removed if the patient develops infective endocarditis (IE)?
The metallic valve should be removed because it will become a septic focus and may become dehiscent.
72
Identify the causes of microscopic branching hyphae found on a removed metallic valve.
The causes of microscopic branching hyphae on a removed metallic valve include fungal infections such as Candida, Aspergillus, Microsporum, Trichophyton, and Epidermophyton.
73
Compare mechanical and tissue valves in terms of durability and anticoagulation requirements.
Mechanical valves have excellent durability (95% at 10 years) and require warfarin, while tissue valves have lower durability and do not require warfarin.
74
What are the risks associated with mechanical valves compared to tissue valves?
Mechanical valves have a thromboembolism risk of 1-2% per patient per year and a bleeding risk of 2% per patient per year, while tissue valves have a lower thromboembolism risk (0-1%) and a low bleeding risk (0-1%).
75
Define Giant Cell Arteritis (GCA).
Giant Cell Arteritis (GCA) is an inflammatory disease of blood vessels, particularly affecting the large and medium-sized arteries of the head, mainly the branches of the external carotid artery.
76
Describe the most affected part of the blood vessel in GCA.
The tunica media is the part of the blood vessel that is most affected in Giant Cell Arteritis.
77
Explain the pathological changes observed in the microscopic picture of GCA.
In GCA, involved arterial segments show intimal thickening, granulomatous inflammation centered on the internal elastic lamina, elastic lamina fragmentation, and an infiltrate of T cells and macrophages. Multinucleated giant cells are present in about 75% of biopsied specimens, but granulomas and giant cells can be rare or absent.
78
What is a simple blood test that can indicate GCA?
An elevated Erythrocyte Sedimentation Rate (ESR) is a simple blood test that can indicate Giant Cell Arteritis.
79
Identify the most confirmatory test for diagnosing GCA.
The most confirmatory test for diagnosing Giant Cell Arteritis is a temporal artery biopsy.
80
Explain why blindness can occur in patients with GCA.
Blindness can occur in patients with Giant Cell Arteritis due to involvement of the ophthalmic artery.
81
Describe a typical scenario of a patient with GCA.
A typical scenario includes a 60-year-old female presenting with headache (temporal pain), skull tenderness on mastication, and transient loss of vision, with a biopsy revealing giant cell arteritis.
82
What histological features are seen in a temporal artery biopsy of GCA?
A temporal artery biopsy in GCA shows giant cells near the fragmented internal elastic membrane, along with medial and adventitial inflammation.
83
What does an elastic tissue stain reveal in GCA?
An elastic tissue stain in GCA demonstrates focal destruction of the internal elastic membrane and medial attenuation and scarring.
84
Describe the treatment for osteoporosis in patients with evolving visual loss.
Corticosteroids are used, starting with prednisolone 60mg/d PO or IV methylprednisolone if there is a history of amaurosis fugax.
85
Explain the reason for developing a fracture in a patient on corticosteroids after one year.
The fracture may be due to avascular necrosis (AVN) or osteoporosis caused by steroid therapy and post-menopausal status.
86
Define osteoporosis and its pathogenesis.
Osteoporosis is a metabolic bone disease characterized by low bone mass, microarchitectural deterioration of bone tissue, increased bone fragility, and loss of bone matrix.
87
How does corticosteroid therapy contribute to osteoporosis?
Corticosteroids cause osteoporosis by directly inhibiting osteoblast formation, stimulating bone resorption, inhibiting gastrointestinal calcium absorption, increasing renal calcium losses, and inhibiting sex steroids.
88
List the three main mechanisms leading to osteoporosis.
The three main mechanisms are inadequate peak bone mass, excessive bone resorption, and inadequate formation of new bone during bone turnover.
89
Explain the pathological changes observed in osteoporosis.
In osteoporosis, histologically normal bone is decreased in quantity, with increased osteoclast activity affecting bones with larger surface areas, leading to perforation and thinning of trabecular plates, resulting in micro fractures and vertebral collapse.
90
Identify the primary causes of osteoporosis.
Primary causes include idiopathic, postmenopausal, and senile osteoporosis.
91
What are some secondary causes of osteoporosis related to endocrine disorders?
Secondary causes include Addison disease, type 1 diabetes, hyperparathyroidism, hyperthyroidism, hypothyroidism, pituitary tumors, neoplasia, and carcinomatosis.
92
Describe the gastrointestinal causes of osteoporosis.
Gastrointestinal causes include hepatic insufficiency, malabsorption, malnutrition, and deficiencies in vitamins C and D.
93
What role do drugs play in the development of osteoporosis?
Certain drugs, such as alcohol, anticoagulants, anticonvulsants, chemotherapy agents, and corticosteroids, can contribute to the development of osteoporosis.
94
List miscellaneous factors that can lead to osteoporosis.
Miscellaneous factors include anemia, homocystinuria, immobilization, osteogenesis imperfecta, and pulmonary disease.
95
Describe the causes of pathological fractures.
Pathological fractures can be caused by skeletal metastasis, Paget's disease, multiple myeloma, rickets, osteomalacia, osteogenesis imperfecta, and radiotherapy.
96
Explain multiple myeloma.
Multiple myeloma is a plasma cell neoplasm associated with lytic bone lesions, hypercalcemia, renal failure, and acquired immune abnormalities, producing large amounts of IgG (55%) or IgA (25%). It is the most common primary bone tumor in the elderly.
97
How is multiple myeloma diagnosed?
Diagnosis of multiple myeloma includes identifying punched-out lytic skull lesions on x-ray, an M spike on protein electrophoresis, Ig light chains in urine (Bence Jones proteins), and the CRAB criteria: hypercalcemia, renal insufficiency, anemia, and bone lesions.
98
Define Bence Jones protein.
Bence Jones proteins are monoclonal globulin proteins or immunoglobulin light chains found in urine, produced by neoplastic plasma cells, and are present in 2/3 of multiple myeloma cases.
99
What concerns arise if a patient with multiple myeloma undergoes surgery?
Concerns include the risk of Addisonian crisis due to steroid use.
100
How can the risk of Addisonian crisis be prevented in surgical patients?
To prevent Addisonian crisis, increase the patient's steroid dose prior to surgery and consider converting to IV hydrocortisone.
101
What is a potential cause of sudden death in a patient after total hip arthroplasty (THA)?
A potential cause of sudden death in a patient after THA is fat embolism.
102
Identify the causes of fat embolism.
Causes of fat embolism include long bone fractures (closed), major burns, acute pancreatitis, diabetes mellitus, orthopedic surgery (intramedullary nailing, joint reconstruction), decompression sickness, and cardiopulmonary bypass graft.
103
How is fat embolism managed?
Management of fat embolism is mainly supportive, focusing on preventing complications like acute renal failure (ARF) and acute respiratory distress syndrome (ARDS), including respiratory support, fluid and electrolyte balance, and general care for DVT, sepsis, and nutrition.
104
What are some specific unproven treatments for fat embolism?
Unproven treatments for fat embolism include ethanol, dextran, and heparin.
105
Define gangrene.
Gangrene (or gangrenous necrosis) is a type of necrosis caused by a critically insufficient blood supply.
106
Define necrosis.
Necrosis is an accidental and unregulated form of cell death resulting from damage to cell membranes and loss of ion homeostasis.
107
List the types of cell death.
The types of cell death are necrosis and apoptosis.
108
Describe the cell size in necrosis and apoptosis.
In necrosis, the cell size is enlarged (swelling), while in apoptosis, the cell size is reduced (shrinkage).
109
Explain the changes in the nucleus during necrosis and apoptosis.
In necrosis, the nucleus undergoes karyopyknosis, karyorrhexis, and karyolysis. In apoptosis, the nucleus fragments into nucleosome-sized fragments.
110
How does the plasma membrane differ in necrosis and apoptosis?
In necrosis, the plasma membrane is disrupted, while in apoptosis, it remains intact but may have altered structure, especially in the orientation of lipids.
111
What happens to cellular contents during necrosis and apoptosis?
In necrosis, cellular contents undergo enzymatic digestion and may leak out of the cell. In apoptosis, the contents remain intact and may be released in apoptotic bodies.
112
Describe the inflammation associated with necrosis and apoptosis.
Necrosis is frequently associated with inflammation, whereas apoptosis does not typically cause inflammation.
113
Explain the physiological or pathological role of necrosis and apoptosis.
Necrosis is invariably pathologic, resulting from irreversible cell injury, while apoptosis often serves a physiological role in eliminating unwanted cells, though it can be pathologic after certain cell injuries, especially DNA damage.
114
What is the pathogenesis of necrosis?
The pathogenesis of necrosis involves severe or prolonged ischemia, leading to severe swelling of mitochondria, calcium influx into mitochondria and the cell, rupture of lysosomes and plasma membrane, and death by necrosis due to the release of cytochrome C from mitochondria.
115
Describe a scenario involving gangrene.
A scenario involving gangrene could be a worker who is a smoker and experiences toe gangrene.
116
Describe the main differences between dry gangrene and wet gangrene.
Dry gangrene commonly affects limbs and is caused by arterial occlusion, resulting in organs that are dry, shrunken, and black. Wet gangrene is more common in the bowel, caused by venous obstruction, leading to moist, soft, swollen, rotten, and dark parts.
117
Explain the prognosis differences between dry gangrene and wet gangrene.
The prognosis for dry gangrene is generally better due to little septicemia, while wet gangrene has a generally poor prognosis due to profound toxemia.
118
Define atherosclerosis.
Atherosclerosis is a pathological process of the vasculature in which an artery wall thickens due to the accumulation of fatty materials such as cholesterol.
119
List the risk factors associated with atherosclerosis.
Risk factors for atherosclerosis include smoking, hypertension (HTN), diabetes mellitus (DM), family history, and increased LDL levels.
120
What bedside test should be performed for a patient who developed a cough?
Sputum analysis should be performed for a patient who developed a cough.
121
Explain the significance of pleural plaques in relation to asbestos exposure.
Pleural plaques are well-circumscribed plaques of dense collagen that are often calcified and are the most common manifestation of asbestos exposure, indicating an increased risk of malignancy, particularly mesothelioma and lung adenocarcinoma.
122
Describe one classification of lung cancer.
One classification of lung cancer is non-small cell lung cancer, which includes adenocarcinoma, squamous cell carcinoma, and large cell carcinoma, sharing common features of prognosis and management.
123
How does small cell lung carcinoma differ from non-small cell lung carcinoma?
Small cell lung carcinoma is associated with neuroendocrine differentiation, arises in larger airways, disseminates early, and is strongly linked to smoking, while non-small cell lung carcinoma has a slower progression and is less likely to disseminate early.
124
What is the typical behavior of small cell lung carcinoma in terms of treatment response?
Small cell lung carcinoma is usually chemosensitive, but this seldom results in long-lasting remissions.
125
How can one determine the epithelial origin of poorly differentiated metastatic cancer?
Immunohistochemical analysis can be used to determine the epithelial origin of poorly differentiated metastatic cancer.
126
Describe the types of lung cancer.
There are two main types of lung cancer: small cell lung cancer and non-small cell lung cancer.
127
Explain the signs of aggressiveness in lung cancer reports.
Signs of aggressiveness include invading pleura and involvement of lymph nodes.
128
Define the pathogenesis of digital clubbing.
Digital clubbing may be explained by higher plasma growth hormone levels in patients with lung carcinoma and clubbing, as well as the release of platelet-derived growth factor (PDGF) from megakaryocyte clusters in peripheral vasculature.
129
What hormones are associated with Pancoast's paraneoplastic syndrome?
Pancoast's paraneoplastic syndrome is associated with ACTH, which can cause Cushing syndrome.
130
How can one determine the epithelial origin of poorly differentiated metastasis?
The epithelial origin of poorly differentiated metastasis can be determined using immunohistochemistry.
131
Explain the FISH technique in cancer diagnosis.
Fluorescence in situ hybridization (FISH) is a cytogenetic technique that uses fluorescent probes to bind parts of chromosomes, allowing visualization of sequence complementarity through fluorescence microscopy.
132
Identify the chemotherapeutic agent for epidermal growth factor positive tumors.
The chemotherapeutic agent for epidermal growth factor positive tumors is a tyrosine kinase inhibitor, such as imatinib.
133
What could be the reason for back pain in a cancer patient six months later?
Back pain in a cancer patient six months later could be due to bone metastasis.
134
List other tumors that can metastasize to bone.
Other tumors that can metastasize to bone include breast cancer, lung cancer, and prostate cancer.
135
Define adenocarcinoma.
Adenocarcinoma is a type of cancer that forms in mucus-secreting glands throughout the body.
136
Describe emphysema and its effects on breathing.
Emphysema is a lung condition that causes shortness of breath due to damage to the air sacs (alveoli) in the lungs, leading to weakened and ruptured inner walls, creating larger air spaces.
137
What are paraneoplastic syndromes?
Paraneoplastic syndromes are symptom complexes that occur in patients with cancer and cannot be readily explained by local or distant spread of the tumor or by hormones from the tissue of origin.
138
Describe the clinical syndrome associated with small cell carcinoma of the lung.
Small cell carcinoma of the lung is associated with Cushing syndrome due to the secretion of ACTH or ACTH-like substances, and it can also cause the syndrome of inappropriate anti-diuretic hormone secretion (SIADH).
139
Explain the causal mechanisms behind hypercalcemia in malignancies.
Hypercalcemia in malignancies is often caused by parathyroid hormone-related protein (PTHrP) secreted by squamous cell carcinoma of the lung, breast carcinoma, renal carcinoma, and adult T cell leukemia/lymphoma.
140
Define the term 'paraneoplastic syndrome'.
Paraneoplastic syndrome refers to a group of clinical syndromes that are a consequence of cancer in the body, often due to the production of hormones or other substances by the tumor.
141
How does insulin relate to hypoglycemia in certain cancers?
Hypoglycemia can occur in cancers such as fibrosarcoma, other mesenchymal sarcomas, and ovarian carcinoma due to the secretion of insulin or insulin-like substances.
142
What is the relationship between renal carcinoma and polycythemia?
Renal carcinoma can lead to polycythemia through the production of erythropoietin, which stimulates red blood cell production.
143
Explain the immunologic disorders associated with myasthenia.
Myasthenia is associated with bronchogenic carcinoma and thymoma, indicating an immunologic mechanism affecting the neuromuscular junction.
144
Describe the dermatologic disorder acanthosis nigricans and its association with cancer.
Acanthosis nigricans is associated with gastric carcinoma, lung carcinoma, and uterine carcinoma, often linked to the secretion of epidermal growth factor.
145
What is Trousseau's syndrome and its association with cancer?
Trousseau's syndrome is characterized by venous thrombosis and is associated with pancreatic carcinoma, bronchogenic carcinoma, and other cancers due to tumor products that activate clotting.
146
How does advanced cancer relate to nonbacterial thrombotic endocarditis?
Nonbacterial thrombotic endocarditis is associated with advanced cancers, often due to a state of hypercoagulability.
147
Define the term 'hypertrophic osteoarthropathy' and its association with cancer.
Hypertrophic osteoarthropathy is a condition characterized by clubbing of the fingers and is associated with bronchogenic carcinoma.
148
Explain the significance of tumor antigens in nephrotic syndrome.
Nephrotic syndrome can occur in various cancers due to the presence of tumor antigens and immune complexes that affect kidney function.
149
Describe the role of immunologic factors in dermatomyositis related to cancer.
Dermatomyositis is an immunologic condition associated with bronchogenic and breast carcinoma, indicating an autoimmune response triggered by the tumor.
150
What are the major forms of neoplasia associated with paraneoplastic syndromes?
Major forms of neoplasia associated with paraneoplastic syndromes include adenocarcinoma, squamous cell carcinoma, and small (oat) cell carcinoma.
151
How does the syndrome of inappropriate anti-diuretic hormone secretion (SIADH) manifest in cancer patients?
SIADH can manifest in cancer patients, particularly those with small cell carcinoma of the lung and intracranial neoplasms, leading to water retention and hyponatremia.
152
Explain the connection between hypercoagulability and cancer.
Hypercoagulability in cancer patients can lead to complications such as venous thrombosis and is often due to tumor products that activate the clotting cascade.
153
Describe the differential diagnosis for tuberculosis (TB).
Hodgkin’s lymphoma is a differential diagnosis for TB, particularly in the same age group, as it commonly involves cervical lymph nodes.
154
Explain the types of labs to which sputum should be sent for TB testing.
Sputum should be sent to Microbiology and Cytology labs for testing.
155
List the tests used to diagnose tuberculosis (TB).
The tests for TB include sputum examination (culture, Ziehl Neelsen stain), Mantoux test, PCR to differentiate Mycobacterium tuberculosis from other species, QuantiFERON (interferon gamma assays), and FNAC of lymph nodes.
156
How should sputum specimens be labeled for TB testing?
Sputum specimens should be labeled as Category - B UN3373.
157
Where should sputum specimens for TB be placed?
Sputum specimens should be placed in a biohazard bag.
158
Identify the organism responsible for tuberculosis (TB).
The primary organism responsible for TB is Mycobacterium tuberculosis, along with Mycobacterium avium intracellulare (MAC) and Mycobacterium bovis.
159
What are the culture media used for mycobacteria?
Culture media for mycobacteria include solid media such as Lowenstein Jensen media and Middlebrook media, and liquid media like BACTEC/MIGT (mycobacteria growth indicator tube).
160
How long does it typically take to culture mycobacteria?
It typically takes 1 to 8 weeks to culture mycobacteria.
161
Define amyloid in the context of tuberculosis.
Amyloid refers to a type of protein deposition that can occur in various conditions, including tuberculosis.
162
Interpret the FNAC result showing necrotic tissue, histiocytes, and giant cells.
The FNAC result indicates tuberculosis (TB).
163
What are giant cells and their significance in TB?
Giant cells are multinucleated cells formed from macrophages, often found in granulomas, such as Langerhans’ giant cells and Reed-Sternberg cells.
164
What public health concerns should be addressed in cases of tuberculosis?
Public health concerns include notifying the consultant in communicable disease control (CCDC), avoiding work in food factories, using masks during sneezing or coughing, implementing DOTS (Directly Observed Treatment, Short-course) anti-TB therapy, and conducting contact tracing.
165
What advice should be given to contacts of a tuberculosis patient?
Contacts should receive counseling, screening, and treatment if necessary.
166
Define a granuloma in the context of tuberculosis.
A granuloma is an organized collection of macrophages that fuse to form Langerhans’ giant cells, often seen in tuberculosis.
167
Describe the scenario involving a young Indian lady related to tuberculosis.
The scenario involves a young Indian lady who returned from foreign travel with cervical lymphadenopathy (anterior triangle mass), weight loss, and night sweats.
168
Describe the sequence of events in primary pulmonary tuberculosis.
The sequence begins with the inhalation of virulent Mycobacterium tuberculosis organisms, leading to early infection events before T-cell mediated immunity activation, followed by the initiation of T-cell mediated immunity and the development of resistance to the organism.
169
Explain the role of T-cell mediated immunity in tuberculosis.
T-cell mediated immunity is crucial for developing resistance to Mycobacterium tuberculosis, and its activation is marked by the appearance of a positive tuberculin test.
170
List other causes of granuloma formation besides tuberculosis.
Other causes of granuloma formation include leprosy, schistosomiasis, sarcoidosis, Crohn's disease, and rheumatoid arthritis.
171
Define granuloma and its significance in pathology.
A granuloma is a small area of inflammation in tissue, typically formed in response to infection or foreign substances, and is significant as it indicates chronic inflammation and immune response.
172
Do granulomas always indicate an infectious process?
No, granulomas can form due to various non-infectious conditions, such as autoimmune diseases and reactions to foreign materials.
173
How does a positive tuberculin test relate to tuberculosis infection?
A positive tuberculin test indicates that the individual has developed cell-mediated immunity to Mycobacterium tuberculosis, suggesting prior exposure or infection.
