PATHOLOGY: BOARDS AND BEYOND Flashcards
1
Q
What is primary intention in wound healing?
A
Is a wound healing process where the wound edges are sutured together, leading to a more straightforward healing progression.
2
Q
What are the initial events that occur in wound healing within the first 24 hours?
A
In the first 24 hours, clot formation occurs, and neutrophils invade the wound site to help prevent infection.
3
Q
What is the role of macrophages in the wound healing process?
A
Macrophages replace neutrophils after about three days, aiding in debris phagocytosis and promoting healing by releasing growth factors.
4
Q
What occurs in the wound during the proliferative phase?
A
During the proliferative phase, granulation tissue fills the wound space, angiogenesis occurs, and fibroblasts infiltrate, initiating collagen synthesis.
5
Q
What is angiogenesis, and when does it occur in wound healing?
A
Angiogenesis is the formation of new blood vessels, occurring during the proliferative phase of wound healing, typically from about three days to one week post-injury.
6
Q
How long does collagen remodeling continue after the initial wound healing?
A
Collagen remodeling can continue for up to six months to one year after the injury.
7
Q
At one week post-surgery, what phase of healing is the girl’s wound in, and what is happening?
A
At one week post-surgery, the wound is in the fibroblast proliferative phase, where angiogenesis and collagen synthesis are actively occurring.
8
Q
What is granulation tissue, and when does it fill the wound space?
A
Granulation tissue is a thick fluid composed of proteins and cells that fills the wound space from about three days to one week post-injury.
9
Q
What key processes occur during the proliferative phase of wound healing?
A
During the proliferative phase, angiogenesis occurs, fibroblasts infiltrate the wound, and collagen synthesis begins.
10
Q
What happens to inflammatory cells and fibroblasts after one month of healing?
A
After one month, inflammatory cells are absent, and only fibroblasts remain in the wound.
11
Q
What changes occur in collagen during the remodeling phase?
A
During remodeling, changes include the cross-linking of collagen fibers to increase the strength and stability of the healed tissue.
12
Q
What factors determine wound strength?
A
Wound strength depends on the amount and quality of collagen deposition.
13
Q
What is the state of collagen in the first few days after an injury?
A
In the first few days after injury, no collagen is present, making wounds prone to failure.
14
Q
What is used to maintain skin approximation in the early days after injury?
A
Sutures, staples, or other devices are used to maintain skin approximation during this period.
15
Q
When does collagen deposition begin after an injury?
A
Collagen deposition begins around days 3 to 5 after the injury.
16
Q
What type of collagen is initially deposited and what does it get replaced with over time?
A
Initially, type III collagen is deposited, which is then replaced with stronger type I collagen over time.
17
Q
When is collagen synthesis considered complete after an injury?
A
Collagen synthesis is complete by several weeks after the injury.
18
Q
What modifications occur to collagen in the later phases of wound healing?
A
In the later phases, modifications such as crosslinking occur, which further increase wound strength.
19
Q
What is the composition of mature scars in terms of collagen?
A
In mature scars, type III collagen and fibronectin are no longer present, and all collagen is type I.
20
Q
What is the role of vascular endothelial growth factor (VEGF) in wound healing?
A
VEGF is critical for angiogenesis, which occurs after about 3 days post-injury, facilitating the growth of new blood vessels that bring fibroblasts to the wound.
21
Q
Why are fibroblasts important in the wound healing process?
A
Fibroblasts secrete collagen, which is essential for wound strength and integrity.
22
Q
What is the critical process that occurs in the first 24 hours of wound healing?
A
Clot formation is critical for achieving hemostasis at the wound site.
23
Q
What are the first cells to appear at the wound site after an incision?
A
The first cells to appear are platelets.
Platelets rapidly develop into clots to help stop bleeding and facilitate wound healing.
24
Q
What type of wound healing occurs when there is no scar formation?
A
This occurs in tissues capable of regeneration, like the skin, if the basement membrane remains intact and basal layer stem cells are not destroyed.
25
Why do superficial skin wounds often heal without a scar?
Superficial skin wounds do not disrupt the basement membrane, allowing the skin to regenerate without scarring.
26
Which other tissues can heal with no scar formation?
Tissues such as the gastrointestinal mucosa after an ulcer and the lungs after pneumonia can also heal with no scar if they have regenerative capacity and the basement membrane and stem cells remain intact.
27
What processes are absent when tissues heal without scarring?
None of the typical scar processes will occur in tissues that heal without scarring.
28
What is delayed wound healing, and when might it be observed?
Delayed wound healing is a common problem in clinical medicine, characterized by minimal granulation tissue and potential dehiscence of the wound several days post-surgery.
29
What are some common causes of delayed wound healing?
Common causes include infection, diabetes, glucocorticoid therapy, and poor nutritional status.
30
In patients with autoimmune diseases, what therapy is likely to contribute to delayed wound healing?
Glucocorticoid therapy
31
How do glucocorticoids affect the wound healing process?
Glucocorticoids have anti-inflammatory effects, including the inhibition of neutrophil migration, which delays the wound healing process.
32
What does the X-ray of a lung abscess typically show?
A lung abscess appears as a black hole surrounded by white in the lung field on an X-ray.
33
What is a classic complication of Klebsiella pneumonia?
A lung abscess
34
What type of organism is Klebsiella pneumoniae?
A gram-negative rod.
35
In which patient population is Klebsiella pneumoniae infection most common?
In patients with impaired host defenses, particularly heavy alcohol users.
36
What type of necrosis is characteristic of tuberculosis infection?
Caseous necrosis
37
What pathological process leads to the formation of a lung abscess in Klebsiella pneumonia?
A lung abscess forms due to localized liquefactive necrosis within the lung tissue.
38
Involves blood vessels and occurs in vasculitis syndromes.
Fibrinoid necrosis
39
Is a subtype of coagulative necrosis seen with ischemia to limbs or the bowel.
Gangrenous necrosis
40
What characterizes coagulative necrosis?
Coagulative necrosis is characterized by the preservation of tissue architecture despite cell death, often seen in ischemic organ damage, such as myocardial infarction.
41
What is a typical finding in the heart during coagulative necrosis?
A typical finding is a firm, white area in the left ventricle consistent with an infarction, where the tissue remains intact.
42
What occurs during liquefactive necrosis?
Liquefactive necrosis occurs when proteolytic enzymes remain functional, leading to the destruction of large amounts of tissue, resulting in a liquid mass.
43
In which conditions is liquefactive necrosis commonly observed?
Liquefactive necrosis is commonly observed in abscesses and in the brain following a stroke.
44
What was the outcome in the second patient who experienced a stroke?
The second patient experienced tissue loss in the cortex due to liquefactive necrosis.
45
Is seen in pancreatitis when fatty acids bind calcium.
Fat saponification
46
What is coagulative necrosis?
Is a type of tissue death where proteolytic enzymes are destroyed, preserving the tissue architecture. It is commonly associated with ischemic organ damage, such as myocardial infarction.
47
What is a key finding in coagulative necrosis of the heart?
A key finding is a firm, white area in the left ventricle, indicative of an infarction, where the tissue remains intact and not liquefied.
48
What is liquefactive necrosis?
Liquefactive necrosis occurs when proteolytic enzymes remain functional, leading to the destruction of large amounts of tissue, resulting in a liquid mass.
49
In which scenarios is liquefactive necrosis commonly observed?
Liquefactive necrosis is commonly seen in abscess formation and in the brain following a stroke.
50
What happened to the brain tissue in the patient who had a stroke?
The patient who had a stroke experienced tissue loss in the cortex due to liquefactive necrosis.
51
Is seen in pancreatitis when fatty acids bind calcium.
Fat saponification
52
What is the most common cause of acute pancreatitis?
The most common cause of acute pancreatitis is gallstones obstructing the pancreatic duct flow, known as gallstone pancreatitis.
53
How do gallstones lead to acute pancreatitis?
Gallstones can enter the common bile duct and block the flow of pancreatic enzymes into the duodenum, causing accumulation of these enzymes within the pancreas.
54
What is the exception among pancreatic enzymes regarding their activation?
Most pancreatic enzymes are secreted as inactive zymogens; however, pancreatic lipase is secreted in its active form.
55
What role does pancreatic lipase play in acute pancreatitis?
Pancreatic lipase breaks down fat, triggers inflammation, and leads to fat necrosis, contributing to the pathology of acute pancreatitis.
56
What are the potential outcomes of acute pancreatitis?
Mild cases may involve acute inflammatory changes and mild fat necrosis, while severe cases can include vascular inflammatory injury and hemorrhage.
57
Where can fat necrosis occur in the context of acute pancreatitis?
Fat necrosis may occur within the pancreas and in the retroperitoneum, including the omentum, bowel mesentery, and subcutaneous fat.
58
What is the major cause of liver damage in acute hepatitis B infection?
The major cause of liver damage in acute hepatitis B is apoptosis of hepatocytes induced by CD8+ T cells.
59
How does the inflammatory infiltrate in acute viral hepatitis differ from that in bacterial infections?
Acute viral hepatitis shows a lymphocyte infiltrate in the liver, whereas bacterial infections typically present with acute inflammatory infiltrates containing neutrophils.
60
What kind of necrosis is observed in acute hepatitis B, and what does it signify?
Acute hepatitis B may exhibit "spotty necrosis," but apoptosis is the primary process damaging liver cells.
61
What are the microscopic findings in a liver biopsy of a patient with acute hepatitis B?
A biopsy may show shrunken hepatocytes with intensely eosinophilic cytoplasm and fragmented nuclei, indicating apoptosis.
62
What type of immune cells are primarily involved in the liver damage seen in acute hepatitis B?
CD8+ T cells are primarily responsible for causing apoptosis of hepatocytes in acute hepatitis B.
63
What is polyarteritis nodosa (PAN)?
PAN is a vasculitis syndrome involving small to medium-sized blood vessels, characterized by systemic inflammation and various organ involvement.
64
What are the key clinical features of polyarteritis nodosa to remember for exams?
Key features include:
- Evidence of systemic inflammation (fever, elevated white blood cells, elevated ESR)
- Skin rash
- Neurologic symptoms (paresthesias, weakness)
- Renal failure
65
What type of skin lesions are commonly associated with polyarteritis nodosa?
Common skin findings in PAN include vesicles, nodules, and purpura.
66
What neurological symptoms are associated with polyarteritis nodosa?
Neurologic findings in PAN include focal (unilateral) neuropathies, such as paresthesias and weakness.
67
What is the underlying mechanism of polyarteritis nodosa?
PAN is an immune-complex-mediated disease, characterized as a type III hypersensitivity reaction, with immune complexes deposited in blood vessels.
68
What viral infection is strongly associated with polyarteritis nodosa?
Polyarteritis nodosa is strongly associated with hepatitis B infection, with about 30% of patients having chronic hepatitis B.
69
What are the histological findings characteristic of polyarteritis nodosa?
Histologic findings may include inflammatory cells in vessel walls, fibrinoid necrosis, and thrombus filling the lumen of small blood vessels.
70
How is polyarteritis nodosa diagnosed?
Diagnosis is made through biopsy of an affected site (such as the kidney, nerve, or GI tract) since there are no specific blood tests for this disorder.
71
What mediates inflammatory pain, such as that occurring after surgery?
Prostaglandin E2 and bradykinin.
72
What is a potential target for pain control drugs related to inflammatory pain?
Blockade of bradykinin could be a target for pain control drugs.
73
What is Icatibant, and for what condition is it used?
Icatibant is a bradykinin receptor antagonist used to treat hereditary angioedema to prevent vasodilation effects mediated by bradykinin.
74
Have bradykinin antagonists been successful in reducing pain?
Bradykinin antagonists have been tried for pain reduction but have not been successful, although research continues in this area.
75
What is the primary role of anti-histamine drugs in inflammation?
Anti-histamine drugs limit vasodilation and edema from inflammation but do not directly alleviate pain.
76
What role does lipoxygenase play in inflammation?
Lipoxygenase synthesizes eicosanoid signaling molecules, specifically leukotrienes.
77
What is the function of the cytokine IL-6 in inflammation?
IL-6 triggers the liver to synthesize acute-phase reactants.
78
How does angiotensin-converting enzyme (ACE) affect bradykinin levels?
ACE breaks down bradykinin; therefore, ACE inhibitors may raise bradykinin levels and can lead to angioedema.
79
Why are ACE inhibitors not as effective for pain control?
Since bradykinin mediates inflammatory pain and ACE inhibitors raise bradykinin levels, they are not as effective as pain control agents.
80
What is the role of the hypothalamus in the body's response to infection?
The hypothalamus regulates body temperature, altering the temperature set point in response to pyrogens during infection.
81
What are the major cytokines involved in acute inflammation?
IL-1, TNF-alpha, and IL-6.
82
What are endogenous pyrogens?
Endogenous pyrogens are substances produced by the body, such as IL-1 and TNF-alpha, that lead to fever and other systemic responses during infection.
83
What mnemonic can help remember the major cytokines of acute inflammation?
The mnemonic "one-alpha-six" corresponds to IL-1, TNF-alpha, and IL-6.
84
How does fever develop in response to infection?
Cytokines like IL-1 and TNF-alpha circulate and increase production of prostaglandin E2 (PGE2) in the hypothalamus, which alters the temperature set point and causes fever.
85
What systemic responses can occur alongside fever during an infection?
Systemic responses include muscle wasting (cachexia), elevated white blood cell count, and hypotension.
86
What cytokines are primarily involved in chronic inflammation?
The primary cytokines involved in chronic inflammation are IFN-gamma and IL-12.
87
What mnemonic can help remember the cytokines of chronic inflammation?
The mnemonic "gamma-twelve" corresponds to IFN-gamma and IL-12.
88
What is C-reactive protein (CRP)?
CRP is an acute phase reactant that can activate the complement system but does not play a major role in generating fever.
89
How does CRP function in the context of inflammation?
CRP activates the complement system, aiding in the immune response during inflammation.
90
What characterizes a transudative pleural effusion?
A transudative pleural effusion has lower concentrations of total protein and LDH in the pleural fluid compared to serum.
91
How can Light’s criteria help differentiate between transudative and exudative effusions?
Light’s criteria indicate a transudative effusion if pleural fluid protein and LDH levels are significantly lower than serum levels.
92
What could be the underlying cause of transudative pleural effusions in an elderly patient?
In elderly patients, transudative pleural effusions are often due to diastolic heart failure or conditions like heart failure, which can complicate infections.
93
What is the mechanism by which left heart failure leads to transudative pleural effusion?
In left heart failure, pulmonary capillary hydrostatic pressure rises, driving fluid into the pleural space without changing vascular permeability.
94
What is the significance of performing a thoracentesis in patients with suspected pleural effusions?
Thoracentesis helps determine the nature of the pleural effusion (transudative vs. exudative) and identify potential causes, such as infection or heart failure.
95
What are the characteristics of an exudative pleural effusion caused by bacterial infection?
In an exudative pleural effusion, hydrostatic pressure is normal or low, and vascular permeability is increased, allowing protein and LDH levels in the pleural fluid to be elevated compared to serum.
96
What is pyelonephritis?
Pyelonephritis is a bacterial infection of the kidney that often begins as a urinary tract infection. It can cause symptoms such as dysuria, fever, chills, and elevated white blood cell count.
97
How does pyelonephritis typically develop?
Pyelonephritis typically develops when bacteria ascend from the urinary tract into the kidneys, leading to a systemic response to the infection.
98
What is a leukemoid reaction?
A leukemoid reaction is a physiologic response to infection characterized by a very high white blood cell count (WBC) with immature neutrophils (band forms) in the blood, often resembling leukemia.
99
What are common laboratory findings in pyelonephritis?
Common findings in pyelonephritis include elevated white blood cell count, particularly with immature neutrophils, and signs of infection such as dysuria and fever.
100
What distinguishes leukemia from pyelonephritis in terms of symptoms?
Leukemia often leads to markedly elevated white blood cell counts and may cause "B symptoms" (fever, chills) without focal infectious symptoms like dysuria, which are present in pyelonephritis.
101
What are the peripheral blood smear findings in acute leukemia?
Acute leukemia typically shows blasts in the peripheral smear.
102
What characterizes chronic myelogenous leukemia (CML) on a blood smear?
CML may show neutrophils and band forms, along with other myeloid cells such as eosinophils, basophils, myeloblasts, promyelocytes, or myelocytes.
103
How can the presence of bacteria in urine help differentiate between pyelonephritis and leukemia?
The presence of bacteria in the urine strongly supports the diagnosis of an infection (like pyelonephritis), making it more likely than a hematologic malignancy like leukemia.
104
What are the main myeloproliferative disorders?
Chronic Myelogenous Leukemia (CML)
Polycythemia Vera
Essential Thrombocytosis
Myelofibrosis
105
Which myeloproliferative disorder is characterized by increased white blood cell counts and the presence of band forms?
Chronic Myelogenous Leukemia (CML) is characterized by increased white blood cell counts and the presence of band forms.
106
Do polycythemia vera, essential thrombocytosis, or myelofibrosis typically present with increased white blood cell counts and band forms?
No, polycythemia vera, essential thrombocytosis, and myelofibrosis do not typically present with increased white blood cell counts and band forms as seen in CML.
107
Lymphoma is a malignancy of lymphocytes. Lymphoma generally presents as
A mass (“-oma” indicates mass), often of lymph nodes.
108
What is acute diverticulitis?
Acute diverticulitis is an inflammatory process occurring in a diverticulum of the colon.
109
Name some acute-phase reactants whose levels increase during inflammation.
Ferritin
Fibrinogen
Serum amyloid A
C-reactive protein (CRP)
Hepcidin
110
What is a negative acute-phase reactant, and how does it respond to inflammation?
Albumin is a negative acute-phase reactant; its level decreases in response to acute inflammation.
111
What is the purpose of a positron emission tomography (PET) scan?
A PET scan detects radiation emissions from radiolabeled glucose to identify areas of possible malignancy in the body.
112
What is 18-fluoro-2-deoxyglucose (FDG)?
FDG is a radiolabeled form of glucose commonly used in PET scans to track glucose metabolism in tissues.
113
How do malignant cells, like those in squamous cell carcinoma, metabolize glucose?
Malignant cells metabolize glucose via aerobic glycolysis, preferentially converting it into lactate rather than pyruvate for the TCA cycle, even in the presence of oxygen.
114
What is the Warburg effect?
The Warburg effect describes the phenomenon where cancer cells preferentially use glycolysis to metabolize glucose to lactate, resulting in less ATP production per glucose molecule and excess lactic acid production.
115
Why do cancer cells require more glucose than normal cells?
Cancer cells require more glucose to meet their higher ATP needs due to their reliance on glycolysis, which is less efficient than oxidative phosphorylation.
116
What adaptations do cancer cells have to increase glucose uptake?
Cancer cells have more glucose transporters on their surface and increased levels of hexokinase to trap glucose inside the cell.
117
How can PET scans help distinguish between benign and malignant lung lesions?
Benign lesions typically do not take up excess glucose, while malignant lesions do, allowing PET scans to identify potential malignancies.
118
What is the function of telomerase in cells?
Telomerase stabilizes the ends of chromosomes, allowing replicating cells to divide indefinitely and become immortal.
119
In what percentage of breast carcinomas is telomerase found?
Telomerase is found in over 90% of breast carcinomas.
120
Where is telomerase normally active?
Telomerase is typically active in fetal cells and germ cells, with little to no activity in somatic cells, such as breast tissue.
121
Why is the presence of telomerase significant in cancer biology?
The presence of telomerase in cancer cells allows them to bypass normal cellular aging processes, leading to uncontrolled cell division and tumor growth
122
What percentage of invasive breast carcinomas express hormone receptors such as the progesterone receptor or the estrogen receptor?
About 75 to 80% of invasive breast carcinomas are positive for either the progesterone receptor or the estrogen receptor.
123
Why is the expression of hormone receptors significant in breast cancer?
The expression of hormone receptors (progesterone and estrogen) can influence treatment options, as hormone receptor-positive cancers may respond to hormonal therapies.
124
What are the two primary hormone receptors commonly expressed in breast cancer?
The two primary hormone receptors are the progesterone receptor (PR) and the estrogen receptor (ER).
125
What is the clinical relevance of testing for hormone receptors in breast cancer patients?
Testing for hormone receptors helps determine the most effective treatment plan, including the use of hormonal therapies such as tamoxifen or aromatase inhibitors for receptor-positive tumors.
126
Familial cases of breast cancer related to the BRCA1 and BRCA2 proteins are responsible for only about ? of cases of invasive breast carcinoma.
10%
127
What does tumor stage refer to?
Tumor stage refers to the degree of metastasis and spread of malignancy.
127
How is tumor stage determined?
CT scans, MRI, or PET scans.
128
What does tumor grade indicate?
Tumor grade indicates the differentiation of tumor cells and how aggressive the tumor is based on pathologic examination.
129
How is tumor grade determined?
Tumor grade is determined by pathologic examination of biopsy specimens
130
What is the main difference between tumor stage and tumor grade?
Tumor stage assesses the extent of spread and metastasis, while tumor grade assesses the aggressiveness and differentiation of tumor cells.
131
What is flow cytometry used for?
Flow cytometry is used to detect cellular fluorescence and analyze the characteristics of cells.
132
How are cells prepared for flow cytometry?
Cells are exposed to fluorescent antibodies that bind to specific surface markers.
133
What does fluorescence indicate in flow cytometry?
Fluorescence indicates that the cells express the surface antigen of interest.
134
What type of markers can flow cytometry detect?
Proteins associated with specific cell types, activation states, or diseases.
135
What is one application of flow cytometry in clinical practice?
Flow cytometry is commonly used in immunophenotyping for diagnosing hematological malignancies.
136
Is a lab technique used to detect DNA
Southern blotting
137
A frozen section
is a biopsy specimen that is quickly frozen after surgical removal of tissue. These can be rapidly reviewed by a pathologist to make quick decisions during an operation (e.g., whether the margins of a tumor have been entirely excised). In contrast, “permanent sections” are biopsy specimens placed in a fixative (usually formalin) for several hours. These are used when time is less critical.
138
What is a hallmark of malignant neoplasms related to immune evasion?
The ability to evade cell death by the immune system, specifically avoiding destruction by natural killer (NK) cells.
139
How do malignant cells respond to growth inhibitors?
Malignant cells demonstrate a weak response to growth inhibitors.
140
What is essential for the invasion and metastasis of malignant cells?
Malignant cells must invade basement membranes to spread beyond their local tissue beds.
141
What role does the p53 protein play in the cell cycle?
p53 arrests cell growth unless specific conditions are met, acting as the "guardian of the cell cycle."
142
What happens in many malignancies regarding p53 function?
Many malignancies are associated with a lack of p53 function, leading to uncontrolled cell growth.
143
What is Li-Fraumeni syndrome?
A hereditary condition where patients have an abnormal p53 gene in all cells, leading to an increased risk of multiple malignancies.
144
What is a pulmonary hamartoma?
A benign lesion responsible for about 10% of pulmonary nodules; the most common benign tumor of the lung.
145
What types of tissue are typically found in a lung hamartoma?
isorganized but normal tissue including fat, epithelial cells, fibrous tissue, and cartilage.
146
How does calcification assist in identifying pulmonary hamartomas?
Calcification may be present, which helps with identification on x-ray or CT scan.
147
What is the growth rate and prognosis of pulmonary hamartomas?
They grow slowly over years and carry an excellent prognosis, classifying them as benign.
148
Malignant lung tumors may spread throughout the lungs and metastasize to the ? but not hamartomas.
Liver
149
May occur in small cell lung cancer, a malignant lung tumor.
Cushing's syndrome and SIADH
150
How do glucocorticoids induce apoptosis in lymphocytes?
By activating caspase enzymes.
151
What is one therapeutic use of glucocorticoids in relation to malignancies?
They can induce apoptosis in malignant cells, including some leukemias.
152
What effect do glucocorticoids have as anti-inflammatory drugs?
They induce apoptosis in lymphocytes, reducing inflammation.
153
In the context of leukemia, what challenge can arise with glucocorticoid treatment?
Leukemic cells may become resistant to the pro-apoptotic effects of glucocorticoids.
154
Glucocorticoids are lipid-soluble steroid drugs that bind to ? not cell surface receptors.
Intracellular receptors,
155
Is the mechanism of some anti-cancer drugs including alkylating agents, but not glucocorticoids
DNA crosslinking
156
Induces apoptosis via the extrinsic pathway. This is used by CD8 T-cells to kill viral-infected cells.
FAS-FAS ligand binding
157
Is the result of cellular free radical damage.
Membrane lipid peroxidation
158
What type of cells are drawn to sites of cell damage during the first 24 hours after injury in the wound healing process?
Neutrophils.
159
What phase of wound healing involves the recruitment of neutrophils?
The inflammatory phase.
160
How do neutrophils die during the wound healing process?
Via the intrinsic pathway of apoptosis.
161
What mediates the intrinsic pathway of apoptosis?
The balance of pro-apoptotic and anti-apoptotic factors.
162
Which pro-apoptotic protein is mentioned as having increased activity in neutrophils undergoing apoptosis?
BAX protein.
163
What happens to neutrophils approximately 48 hours after injury?
They undergo apoptosis.
164
The BAK protein is also pro-apoptotic. Decreased BAK activity would
Limit apoptosis.
165
Is anti-apoptotic. Excess activity limits apoptosis. This is seen in follicular lymphomas where BCL2 protein overexpression prevents apoptosis among malignant cells.
The BCL2 protein i
166
What is the mode of transmission for acute hepatitis B in this patient?
Intravenous drug use.
167
Which immune cells are responsible for destroying viral-infected hepatocytes in hepatitis B?
CD8+ T cells.
168
Through which pathway do CD8+ T cells induce apoptosis in infected hepatocytes during hepatitis B?
The extrinsic pathway of apoptosis.
169
How do CD8+ T cells recognize infected hepatocytes?
By recognizing viral antigens presented on MHC class I molecules.
170
What is the role of Fas ligand (FasL) in the apoptosis process during hepatitis B infection?
It binds to CD95 (Fas) on hepatocytes to trigger apoptosis.
171
What is activated as a result of Fas-FasL binding that leads to cell death?
Caspase enzymes.
172
What is autoimmune lymphoproliferative syndrome (ALPS)?
A rare disorder characterized by excessive lymphocyte growth and defective apoptosis.
173
What defect is primarily responsible for the symptoms seen in ALPS?
Defective FAS-FAS ligand binding, leading to impaired apoptosis of T-cells.
174
What is the consequence of impaired FAS interactions in T-cells?
Overproduction of T-cells, including many auto-reactive T-cells that escape apoptosis.
175
What are common physical findings in children with ALPS?
Enlargement of lymph nodes, liver, and spleen (hepatosplenomegaly).
176
At what age do symptoms of ALPS typically become apparent?
Often by one year of age.
177
What autoimmune diseases commonly develop in children with ALPS?
Immune-mediated hemolytic anemia and thrombocytopenia.
178
What lab findings are characteristic of antibody-mediated hemolytic anemia in ALPS?
Reduced hematocrit, elevated bilirubin, and positive direct Coombs test.
179
When considering a child with long-standing lymphadenopathy and new hemolytic anemia, what syndrome should be suspected?
Autoimmune lymphoproliferative syndrome (ALPS).
180
What happens to the p53 protein in response to DNA damage from radiation therapy?
It becomes phosphorylated, regulating the cell cycle.
181
What is the role of phosphorylated p53 in the cell cycle?
It leads to cell cycle arrest, allowing for potential DNA repair.
182
If DNA repair is not possible, what does activated p53 trigger?
The pro-apoptosis factors, BAK and BAX.
183
What is the ultimate result of p53 activation in cancer cells?
Apoptosis of cancer cells, reducing cancer cell burden.
184
How does radiation therapy indirectly promote apoptosis in cancer cells?
By activating the p53 pathway following DNA damage.
185
What is the most common inherited red cell enzyme disorder?
Glucose-6-phosphate dehydrogenase (G6PD) deficiency.
186
What is the primary function of G6PD in red blood cells?
It generates nicotinamide adenine dinucleotide phosphate (NADPH) as part of the HMP shunt.
187
How does G6PD deficiency affect red blood cells?
It leads to limited glutathione supply, making red cells vulnerable to free radical damage.
188
What is the consequence of decreased NADPH production in G6PD-deficient patients?
Depletion of glutathione, which is an antioxidant that protects against oxidative damage.
189
What happens when glutathione levels become depleted in red blood cells?
Red cells cannot metabolize hydrogen peroxide (H2O2), leading to oxidative hemolysis.
190
Which foods and substances can trigger oxidative damage in G6PD-deficient individuals?
Fava beans and certain drugs (e.g., some antibiotics)
191
How is G6PD deficiency diagnosed?
By demonstrating decreased production of NADPH among red cells.
192
What is the respiratory burst in phagocytes?
A process where phagocytes generate reactive oxygen species (ROS) to kill pathogens.
193
Which reactive oxygen species are produced during the respiratory burst?
Superoxide (O2.), hydrogen peroxide (H2O2), and hypochlorous acid (HOCl)
194
What enzyme catalyzes the formation of hypochlorous acid in neutrophils?
Myeloperoxidase (MPO)
195
Why is hypochlorous acid important in the respiratory burst?
It amplifies the killing capacity beyond what superoxide and hydrogen peroxide can achieve.
196
What is MPO deficiency?
A rare immunodeficiency syndrome where patients lack myeloperoxidase.
197
What are common infections associated with MPO deficiency?
Recurrent infections, particularly with Candida.
198
How is MPO deficiency diagnosed?
By staining neutrophils to check for MPO activity.
199
What is chronic granulomatous disease (CGD)?
An immunodeficiency caused by a deficiency in NADPH oxidase, leading to infections with catalase-positive pathogens.
200
What is the structural formula of hypohalous acids?
HOX, where X can be chloride, bromide, or another halide.
201
What is the most important takeaway about MPO deficiency?
It demonstrates the role of free radical generation in the immune response.
202
What role do neutrophils play in response to pulmonary infections?
Neutrophils are drawn to the site of infection as part of the acute inflammatory response.
203
What is the major role of neutrophils during an infection?
Phagocytosis of bacteria.
204
How do neutrophils kill bacteria after phagocytosis?
Bacterial killing occurs via the respiratory burst within phagosomes of neutrophils.
205
What is the first step in the respiratory burst?
The first step is catalyzed by NADPH oxidase.
206
What are the main products generated during the respiratory burst?
Superoxide (O2.)
hydrogen peroxide (H2O2)
hypochlorous acid (HOCl)
207
What enzyme is responsible for generating hypochlorous acid in neutrophils?
Myeloperoxidase (MPO)
208
Why is hypochlorous acid significant in bacterial killing?
It amplifies the killing capacity beyond that of superoxide and hydrogen peroxide.
209
What defines chronic granulomatous disease (CGD)?
CGD is caused by a deficiency in NADPH oxidase, leading to susceptibility to catalase-positive pathogens.
210
Is an enzyme that breaks down hydrogen peroxide to protect cells from free radical damage.
Catalase
211
Protects cells against free radical damage by converting hydrogen peroxide into water. It is not a component of bacterial death within neutrophils.
Glutathione peroxidase
212
Which leads show ST-segment elevations during her myocardial infarction? (Inferior wall)
ST-segment elevations in leads II, III, and aVF.
213
What is the consequence of myocardial ischemia?
Myocyte necrosis occurs.
214
What happens to cell membranes during necrosis?
They fragment, releasing biomarkers like creatinine kinase and troponin into the blood.
215
What is the standard treatment for ST-segment myocardial infarction (STEMI)?
Emergent placement of a coronary stent (revascularization)
216
How does restoring blood flow benefit ischemic myocytes?
It relieves symptoms and improves long-term outcomes; many reversibly injured myocytes can recover.
217
What risk is reduced by restoring blood flow to ischemic myocytes?
The long-term risk of ischemic cardiomyopathy and heart failure.
218
What is a downside of reperfusion after an infarction?
It generates free radicals in myocytes, which can cause additional cell death.
219
How does reperfusion injury manifest in terms of cardiac biomarkers?
There is a rise in cardiac biomarkers like creatinine kinase and troponin due to additional cell damage.
220
What is a common complication of reperfusion after successful restoration of blood flow?
Arrhythmias can occur.
221
What is “reperfusion injury”?
A classic example of free-radical cell damage occurring after restoring blood flow.
222
What mechanism of cell damage is associated with reperfusion-related free radicals?
Membrane lipid peroxidation, which causes loss of membrane integrity and cell damage.
223
Can myocardial ischemia lead to apoptosis?
Yes, myocardial ischemia may lead to both apoptosis and necrosis.
224
What distinguishes apoptosis from necrosis in terms of cellular integrity?
Apoptosis maintains cell membrane integrity, while necrosis leads to cell membrane rupture
225
How does chronic ethanol consumption affect the liver's metabolism?
It activates the microsomal ethanol-oxidizing system (MEOS), increasing cytochrome P-450 enzyme metabolism.
226
What is the toxic metabolite of acetaminophen?
NAPQI (N-acetyl-p-benzoquinone imine)
227
Why is NAPQI considered toxic to the liver?
It is a reactive oxygen species that can cause liver damage.
228
How does chronic alcohol use influence acetaminophen toxicity?
Chronic alcohol users produce higher quantities of NAPQI, increasing the risk of toxicity even at standard dosages of acetaminophen.
229
When else is acetaminophen toxicity commonly observed?
Following suicide attempts with massive dosages of Tylenol.
230
What role does cytochrome P-450 play in acetaminophen metabolism?
It is involved in the metabolism of acetaminophen to the toxic metabolite NAPQI.
231
What is the Fenton reaction?
A reaction that involves metals like copper and iron, leading to the generation of free radicals.
232
What type of damage can the Fenton reaction cause?
Free radical cellular damage.
233
Which conditions are associated with free radical damage from the Fenton reaction?
Hemochromatosis and Wilson's disease.
234
Ischemia can lead to liver damage in settings of hypotension
“shock liver”
235
Metabolism of ethanol produces NADH, and depletes NAD thereby decreasing the ratio of
NAD/NADH.
236
May occur among chronic alcohol users leading to chronic liver disease and cirrhosis.
Fatty acid accumulation
237
What is calciphylaxis?
A rare and dangerous skin complication of chronic renal failure.
238
Why do patients with chronic renal failure develop hyperphosphatemia?
Due to the inability to excrete phosphate in the urine.
239
What happens to serum phosphate levels in chronic renal failure?
Serum phosphate binds to calcium, pulling calcium from circulation and causing hypocalcemia.
240
Where do calcium-phosphate crystals deposit in calciphylaxis?
In the walls of blood vessels in the skin.
241
What is a consequence of calcium-phosphate crystal deposition?
It can lead to ischemic necrosis of the skin.
242
How do renal failure patients manage serum phosphorus levels?
They are prescribed “phosphate binders” to lower serum phosphorus and prevent hyperphosphatemia and calciphylaxis.
243
What is mitral annular calcification (MAC)?
A common incidental finding on echocardiography or other cardiac imaging, particularly in older patients. It is almost always asymptomatic.
244
What causes mitral annular calcification?
It results from endothelial dysfunction and chronic inflammation, leading to dystrophic calcification.
245
How does mitral annular calcification compare to atherosclerosis?
MAC shares many similarities with atherosclerosis, including a higher prevalence with aging.
246
In rare, severe cases of MAC, what complications can arise?
It can impair mitral valve function, leading to mitral regurgitation, mitral stenosis, or heart failure.
247
What imaging technique commonly detects mitral annular calcification?
Echocardiography
248
What is acute appendicitis?
An acute inflammatory process involving the appendix.
249
What are the common pathologic findings in acute appendicitis?
Tissue edema and infiltration by neutrophils
250
What is granulomatous inflammation?
A subtype of chronic inflammation that may be seen in infections like tuberculosis and other disorders.
251
In what conditions might eosinophilic infiltrates be observed?
In hypersensitivity (allergic) reactions.
252
What type of infiltrates occur in chronic inflammatory processes?
Mononuclear cell infiltrates.
253
What is rheumatoid arthritis (RA)?
A chronic, autoimmune inflammatory disorder. Women aged 40 to 60. Small, peripheral joints. No, it rarely involves the axial skeleton (spine). Joint stiffness is classically worse in the morning and improves with movement throughout the day.
254
What cellular infiltrates are found in the synovial fluid of RA patients?
Macrophages, lymphocytes (T cells and B cells), and plasma cells
255
What are "mononuclear cells" and their significance in RA?
Mononuclear cells are hallmarks of chronic inflammation, commonly found in RA.
256
What are the two pathways for macrophage activation during inflammation?
Classically-activated (M1) and alternatively-activated (M2) pathways.
257
What activates classically-activated (M1) macrophages?
Interferon-gamma (IFN-γ).
258
What is the major role of M1 macrophages?
The destruction of pathogens.
259
How do M1 macrophages generate their pathogen-destroying capabilities?
By generating reactive oxygen species (ROS) and lysosomal enzymes.
260
What vasodilator do M1 macrophages release?
Nitric oxide (NO).
261
What is a consequence of M1 macrophage activation during inflammation?
Tissue destruction due to the damage caused by reactive oxygen species and lysosomal enzymes to normal cells.
262
What are the potential negative effects of M1 macrophage activity?
Damage to normal cells and tissues during the inflammatory response.
263
What is the primary role of alternatively-activated (M2) macrophages?
Participation in tissue repair.
264
What activates M2 macrophages?
Cytokines other than interferon-gamma, such as IL-4 and IL-13.
265
When do M1 and M2 macrophages typically participate in the inflammatory response?
M1 macrophages participate early in inflammation, while M2 macrophages are involved later. M2 macrophages are more involved in tissue repair, while M1 macrophages focus on pathogen destruction.
266
Is the precise sequence of activation for M1 and M2 macrophages well understood?
No, the precise sequence of activation remains unclear.
267
What systemic symptoms are associated with IL-1 and IL-6?
Fever, chills, sweats, and production of acute-phase reactants.
268
What is the role of acute-phase reactants in inflammation?
They are proteins produced in response to inflammation that help mediate the body's response to injury or infection.
269
What is the most common cause of community-acquired bacterial pneumonia?
Streptococcus pneumoniae.
270
What do bacteria contain that is recognized as foreign by innate immune cells?
Molecular sequences known as pathogen-associated molecular patterns (PAMPs).
271
What is the role of pathogen-associated molecular patterns (PAMPs)?
They trigger an immune response when recognized by the immune system.
272
Which receptors do bacterial PAMPs bind to on macrophages?
Toll-like receptors (TLRs).
273
What happens after PAMPs bind to toll-like receptors?
Cytokine release occurs, initiating an acute inflammatory response.
274
What is the significance of cytokine release in the immune response?
It helps coordinate the inflammatory response and recruit additional immune cells to the site of infection.
275
The glucocorticoid receptor binds ?and mediates many effects of this hormone.?
Cortisol
276
Alpha receptors and beta receptors are adrenergic receptors activated by ?. They are important components of the sympathetic nervous system which can be activated in the setting of infection, but they do not initiate the inflammatory response.
Epinephrine and norepinephrine.
277
What is the most common cause of urinary tract infections (UTIs)?
Escherichia coli (E. coli).
278
What type of bacteria is E. coli, and what does it produce?
E. coli is a gram-negative bacterium that produces nitrites.
279
What are the early symptoms of a UTI?
Dysuria (painful urination) and urinary frequency.
280
What is the hallmark finding of pyelonephritis in urine?
White blood cell casts.
281
What systemic reaction is indicated by evidence of sepsis?
A severe systemic reaction to infection, including fever and tachycardia.
282
What component of gram-negative bacteria triggers an immune response?
Lipopolysaccharides (LPSs) in the cell wall.
283
How are LPSs related to pathogen-associated molecular patterns (PAMPs)?
LPSs are a prototype example of substances that contain PAMPs, which trigger immune responses.
284
What is the role of toll-like receptors (TLRs) in the immune response?
TLRs bind to PAMPs, triggering macrophages to release cytokines and initiate the inflammatory process.
285
Where else, besides the cell membrane, can toll-like receptors be found?
Within endosomes, which are vesicles formed during endocytosis of extracellular substances.
286
What are toll-like receptors (TLRs)?
Key components of the innate immune response and examples of "pattern recognition receptors."
287
Where are TLRs found?
On the surface of macrophages and other immune cells.
288
What do TLRs recognize?
Pathogen-associated molecular patterns (PAMPs), which are small molecular structures found only on pathogens like bacteria.
289
What happens when a PAMP binds to a TLR on a macrophage?
The macrophage becomes activated and releases cytokines to activate the inflammatory response.
290
What are damage-associated molecular patterns (DAMPs)?
Components from normal human cells that can bind to TLRs and initiate the inflammatory response to necrosis
291
What types of DAMPs have been described?
Proteins of the nucleus, heat shock proteins, ATP, uric acid, RNA, and DNA.
292
How do DAMPs contribute to inflammation?
When necrosis occurs, DAMPs bind to TLRs to initiate the inflammatory response.
293
What is the role of TLRs in responding to necrosis?
They help detect DAMPs released from damaged cells, triggering inflammation.
294
Vaccination elicits an immune response by exposing the body to PAMPs without the need for overt infection.
This does not depend on the ability of immune cells to react to normal cellular components.
295
Infections with Candida, Schistosoma, or Staph Aureus also elicit an inflammatory response via PAMPs.
This immune response does not depend on the ability of immune cells to react to normal cellular components
296
What is the inflammasome?
A multi-protein complex that assembles in the cytoplasm of cells in response to cellular damage or infection.
297
What are NOD-like receptors (NLRs)?
Proteins found in the cytoplasm of various cell types, including epithelial cells, that play a role in immune responses.
298
How do NLRs compare to toll-like receptors (TLRs)?
NLRs are similar to TLRs but are located in the cytoplasm rather than on the cell membrane surface.
299
What do NLRs bind to?
Damage-associated molecular patterns (DAMPs) like uric acid, excess ATP, and free DNA, as well as some components of bacteria (PAMPs).
300
How do NLRs initiate the inflammasome formation?
Once activated, many NLRs assemble into a multi-protein complex called the inflammasome.
301
What enzyme is activated by the inflammasome, and what does it generate?
The inflammasome activates caspase-1, which generates interleukin-1 (IL-1).
302
What is the role of IL-1 in the immune response?
IL-1 initiates the inflammatory response.
303
What is the “NLR-inflammasome pathway”?
The pathway by which NLRs and the inflammasome initiate inflammation, potentially playing a role in some autoimmune diseases.
304
Toll-like receptors are found on cell membranes and within endosomes.
NLRs perform a similar function but are intracellular
305
Is secreted by T cells. It has a number of roles including stimulation of eosinophils, class switching to IgA, and B cell growth stimulation.
IL-5
306
Is secreted by T cells and stimulates macrophages
IFN-gamma
307
What is pulmonary histoplasmosis?
A fungal pneumonia caused by Histoplasma capsulatum.
308
Where is histoplasmosis commonly found?
In the Ohio and Mississippi river valleys
309
How are fungal spores of histoplasmosis introduced into the lungs?
They are found in soil contaminated by bird or bat droppings and are inhaled.
310
What happens to histoplasma spores once they are inhaled?
They form yeast in the lungs.
311
What are the typical symptoms of histoplasmosis?
Most cases are asymptomatic, but mild symptoms can include cough and malaise.
312
What is a common chest X-ray finding in pulmonary histoplasmosis?
Hilar lymphadenopathy is common; there are typically no specific diagnostic findings.
313
How does granulomatous inflammation relate to fungal pneumonias?
Fungal pneumonias like histoplasmosis, blastomycosis, and coccidiomycosis lead to granulomatous inflammation.
314
What features do granulomatous fungal pneumonias share with tuberculosis and sarcoidosis?
They share features like hilar lymphadenopathy and granuloma formation.
315
What immune cells are involved in granulomatous inflammation?
CD4 T cells and macrophages.
316
Which cytokines are associated with granulomatous inflammation?
Interferon-gamma and IL-2.
317
What is infliximab?
An antibody drug directed against tumor necrosis factor alpha (TNF-alpha)
318
What cells secrete TNF-alpha?
Activated macrophages and T cells.
319
Why is TNF-alpha referred to as "tumor necrosis factor"?
It was originally shown to have the ability to kill cancer cells.
320
What are some key roles of TNF-alpha in the immune system?
It has multiple effects, including maintenance of granulomas in granulomatous inflammation.
321
How is infliximab used in the context of Crohn’s disease?
It is used to treat Crohn’s disease, which involves granuloma formation, by blunting the effects of TNF-alpha.
322
What type of disease is Crohn’s disease?
A form of inflammatory bowel disease (IBD).
323
How does infliximab improve outcomes for patients with Crohn’s disease?
By reducing the inflammatory effects of TNF-alpha, which helps manage symptoms and complications.
324
What is chronic granulomatous disease (CGD)?
A condition characterized by recurrent infections with catalase-positive organisms due to a deficiency in NADPH oxidase.
325
What types of organisms are patients with CGD particularly susceptible to?
Catalase-positive organisms, including Staphylococcus, Pseudomonas, Aspergillus, and Nocardia.
326
What is the role of NADPH oxidase in phagocytes?
It is part of the respiratory burst, essential for generating superoxide, hydrogen peroxide, and hypochlorous acid for bacterial and fungal killing.
327
What happens in CGD due to the absence of NADPH oxidase?
Patients cannot generate reactive oxygen species, making them vulnerable to infections by catalase-positive organisms.
328
What are the most common sites of infection in CGD?
The lungs (pneumonia) and skin (abscesses).
329
How is CGD diagnosed?
Through neutrophil function testing, specifically using dihydrorhodamine (DHR)
330
What does dihydrorhodamine (DHR) testing measure?
It measures the oxidative burst in phagocytes; poor fluorescence indicates CGD.
331
How is cellular fluorescence detected in DHR testing?
By using flow cytometry to detect the green fluorescence produced when DHR is oxidized.
332
What does poor fluorescence of phagocytes in DHR testing indicate?
It indicates a deficiency in the respiratory burst, consistent with CGD.
333
Leads to underactive B and T cells, which causes severe combined immunodeficiency (SCID). It often presents in the first month after birth with severe, life-threatening infections.
Adenosine deaminase deficiency
334
Glucose-6-phosphate dehydrogenase deficiency leads to recurrent
Hemolysis
335
What type of cellular adaptation do skeletal myocytes like the deltoids undergo in response to strength training?
Hypertrophy, not hyperplasia.
336
Why do skeletal myocytes not undergo hyperplasia?
Myocytes are permanently in the G0 phase of the cell cycle and do not enter the S phase or divide.
337
What is the main mechanism of adaptation for skeletal myocytes during strength training?
Hypertrophy, which increases the size of myocytes.
338
What causes the increase in myocyte size during strength training?
Increased protein synthesis, particularly of actin and myosin.
339
How does endurance training (e.g., long-distance running) affect skeletal muscle cells?
It increases the number of mitochondria per cell (mitochondrial density).
340
What limits muscle adaptation during endurance training?
The ability to produce ATP.
341
How is adaptation to resistance training different from endurance training?
Resistance training increases actin and myosin content without changing mitochondrial density.
342
For a boy doing both resistance and endurance training, what adaptations will occur in his skeletal muscle?
Increased actin-myosin content and increased mitochondrial density.
343
What is a common consequence of prolonged bed rest and decreased calorie intake?
Muscle atrophy.
344
Why is muscle atrophy particularly significant in elderly or frail patients?
They may experience prolonged weakness, falls, and failure to thrive even after recovering from acute illness.
345
What is a major underlying mechanism of muscle atrophy?
Protein degradation in skeletal myocytes.
346
What process is involved in the degradation of proteins in skeletal muscle?
Ubiquitination.
347
What happens during ubiquitination?
Cellular proteins are combined with ubiquitin, leading to their degradation in proteasomes.
348
Apoptosis is programmed cell death. T-cells trigger apoptosis in virally-infected cells, a process that played a role in this woman’s recovery from influenza.
This is not, however, the mechanism behind her weight loss
349
What is benign prostatic hyperplasia (BPH)?
A condition characterized by the enlargement of the prostate gland, commonly occurring in men over age 40.
350
What are classic symptoms of BPH?
Frequent urination, nocturia, hesitation, slow urinary stream, and possible incontinence.
351
How does BPH affect urinary flow?
Enlarged prostate obstructs urinary flow from the bladder, leading to incomplete bladder emptying.
352
What does hyperplasia mean in the context of BPH?
An increase in the number of cells, specifically glandular prostate cells.
353
How does the increase in cell number due to hyperplasia affect the prostate gland?
It leads to an increase in the total protein and DNA content of the prostate gland.
354
What condition is described in women during perimenopause?
Dysfunctional uterine bleeding
355
What is menopause defined as?
The cessation of ovulation, typically occurring at an average age of 51 years.
356
How do menstrual periods change as women approach menopause?
The time between periods often increases and becomes irregular.
357
What is an “anovulatory cycle”?
A menstrual cycle where no ovum is released from the ovaries.
358
What happens to hormone levels during anovulatory cycles?
The ovary does not produce progesterone, leading to unopposed estrogen exposure.
359
What effect does unopposed estrogen have on the uterus?
It stimulates endometrial hyperplasia, which can result in irregular bleeding.
360
How is menopause ultimately defined in terms of menstruation?
By 12 months of amenorrhea (no menstrual periods).
361
Why is anovulatory bleeding common in younger women, such as those recently starting menstruation?
The hypothalamic-pituitary axis has not yet matured to support regular menstrual cycles.
362
What is the typical cause of irregular bleeding in girls during the first few years after menarche?
Anovulation.
363
May present as abnormal uterine bleeding. The average age of diagnosis is 62 years. Risk factors include excess estrogen exposure from obesity or estrogen therapy.
Endometrial carcinoma
364
What is levothyroxine?
A synthetic form of the thyroid hormone thyroxine (T4).
365
How are serum thyroid hormone levels regulated?
Through the hypothalamic release of thyroid-stimulating hormone (TSH).
366
What happens to TSH levels when a person takes levothyroxine?
TSH release is suppressed, reducing normal stimulation of the thyroid gland.
367
What is the consequence of reduced stimulation of the thyroid gland?
The thyroid gland undergoes atrophy, a common cellular adaptation to the removal of a hormone stimulus.
368
What condition does this woman have that leads to cardiac myocyte hypertrophy?
Hypertension.
369
Why do left ventricular myocytes undergo hypertrophy in response to hypertension?
Increased pressure in the aorta requires the left ventricular myocytes to generate more force to open the aortic valve.
370
What are the structural changes in the heart due to cardiac myocyte hypertrophy?
Hypertrophy of individual myocytes and overall left ventricular hypertrophy.
371
How is left ventricular hypertrophy typically observed in patients with hypertension?
It is commonly found on autopsy.
372
What is a significant health risk associated with left ventricular hypertrophy?
It is an independent risk factor for sudden cardiac death.
373
Is a rare, genetic condition of myocyte hypertrophy. It is far less common than hypertension which affects millions of patients in the US.
Hypertrophic cardiomyopathy
374
What condition is indicated by ischemic chest pain and ST elevations in the anterior wall leads on an ECG?
Anterior ST-elevation myocardial infarction (STEMI).
375
What are creatinine kinase and troponin?
Components of cardiac myocytes that are released into the serum when myocytes undergo necrosis.
376
What happens to serum levels of creatinine kinase and troponin during myocardial necrosis?
They become elevated as cellular contents spill into the plasma.
377
What is one underlying mechanism of necrosis in cardiac myocytes?
Calcium influx into cells.
378
How does calcium influx contribute to myocardial necrosis?
It activates calcium-dependent phospholipases that break down membrane phospholipids.
379
What effect does membrane damage have on cardiac myocytes during necrosis?
It allows cellular contents, including enzymes like creatinine kinase and troponin, to enter the serum.
380
What condition does this man have that involves the femoral head?
Avascular necrosis (osteonecrosis)
381
Which patient population is particularly at risk for avascular necrosis?
Patients with lupus, especially those taking steroids.
382
What is the primary cause of avascular necrosis?
Vascular damage to the bone blood supply leading to necrosis of bone marrow elements.
383
What is the progression of avascular necrosis?
It is progressive, often resulting in joint failure within a few years, necessitating hip replacement surgery.
384
In some cases of osteonecrosis, what is an obvious cause of ischemic damage?
Femoral neck fracture.
385
What is often associated with cases of avascular necrosis aside from obvious causes?
Lupus or glucocorticoid therapy via a poorly understood mechanism.
386
What typical changes of necrosis can be observed on biopsy of the femoral neck?
Karyorrhexis (fragmented nuclei), karyolysis (loss of nuclear basophilia), and pyknosis (nuclear shrinkage).
387
What does karyorrhexis indicate in necrotic cells?
Fragmentation of the nuclei, a sign of cellular damage.
388
What condition does this woman have that involves fatty accumulation in the liver?
Nonalcoholic fatty liver disease (NAFLD).
389
What are common associations with NAFLD?
Obesity, diabetes, and hyperlipidemia.
390
What is the likely pathogenesis of NAFLD?
Insulin resistance.
391
What is a potential progression of NAFLD over time?
It can progress to cirrhosis.
392
Are most patients with NAFLD symptomatic or asymptomatic?
Most patients are asymptomatic, but some may experience fatigue, malaise, or right upper quadrant pain.
393
What treatment has been linked to clinical improvement in NAFLD?
Weight loss is recommended for all patients.
394
How is the fatty change in NAFLD classified in terms of cell injury?
It is an example of reversible cell injury.
395
What happens to the liver with weight loss in NAFLD?
The fatty change can resolve, and the liver can decrease in size and return to normal.
396
What similar condition occurs with heavy alcohol consumption?
Fatty change of the liver, which is also reversible if alcohol consumption is stopped.
