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Ayads Gen Path MT2
Ayad's Gen Path MT2
Question | Answer |
---|---|
What cells normally divide throughout life to replace the continually lost cells? | Labile cells |
Surface epithelial cells, crypt cells of gut mucosa, hematopoietic stem cells? | Labile cells |
Following injury, surviving cells proliferate rapidly to replace lost ones? | Labile cells |
Long-life span, very slow rate of division? | Stable cells |
They remain in intermitotic phase for long periods, retain capacity to enter the mitotic cycle when needed (replacement of damaged cells)? | Stable cells |
What are the two types of stable cells? | Parenchymal cells of solid organs, Mesenchymal cells |
No capacity for mitotic division in post-natal life? | Permanent cells |
Neurons, Myocardial cells, skeletal muscle cells are what type of cells? | Permanent cells |
Injury to tissue w/ permanent cells is always followed by a scar formation (no regeneration is possible, irreversible)? | Permanent cells |
What type of necrosis happens following myocardial infarction? | Coagulative necrosis |
Fibroblasts are stimulated by? | Chemical mediators |
Fibroblasts are stimulated to do what? | Proliferate, and secrete: collagen, elastic/reticular fibers, extracellular matrix, actin/myosin filaments (myofibroblasts) |
What is fibronectin? | Glycoprotein |
What does fibronectin do? | Promotes angiogenesis, and is chemotactic to fibroblasts and promotes organization |
What is a glycoprotein derived from plasma? | Fibronectin |
Initial scar formation is laid down by what type of cells? | Myofibroblasts |
Essential for angiogenesis and chemo tactic (direction)? | Capillaries, fibroblasts |
Early contraction is due to? | Myofibroblast |
Late contraction is due to? | Collagen |
What are the 3 types of skin wounds? | Abrasion, Incision/laceration (1st intention), wounds w/ epidermal defect (2nd intention) |
How long does a scar take to increase tensile strength of a scar to 40%? | 4 weeks |
How long does a scar take to increase tensile strength of a scar to 80%? | 4 months |
Secondary wounds are characterized by? | Extensive necrosis, large wounds, secondary infection, inflammation, foreign body |
Causes of defective wound healing? | Fail of synthesis of collagen fibers, excessive collagen production, local factors, diabetes mellitus, and excessive levels of corticosteroids |
What causes failure of synthesis of collagen fibers? | Deficiency of vitamin C, Ehlers-Danlos syndrome |
What is Ehlers-Danlos syndrome? | Deficiency of enzymes involved in collagen synthesis (rubber man) |
List 2 local factors of defective wound healing? | Foreign body, necrotic tissue, infection, abscess formation, abnormal blood supply |
What is the problem with high levels of corticosteroids? | Interfere w/ phagocytosis, decrease arachidonic acid metabolites, decrease collage formation |
Growth factors involved in wound healing? | Platelet-derived Growth factor, Epithelial growth factor, IL-1 and TNF, Thrombin |
PDGF does what? | Proliferation of fibroblasts, enhances wound healing |
EGF does what? | Proliferation of epithelial cells and fibroblasts |
IL-1 and TNF do what? | Chemotactic for fibroblasts, increased collagen synthesis (fibrogenic cytokines) |
Thrombin does what? | Fibroblast mitosis |
Edema in the pleural cavity is known as what? | Hydrothorax |
Edema in the peritoneal cavity is known as what? | Ascites |
Edema in the pericardial cavity is known as what? | Hydropericardium |
What force takes fluid out? | Hydrostatic pressure |
What force brings it back? | Osmotic pressure |
Increase of blood due to active arterial dilation is known as? | Hyperemia |
What are two types of Hyperemia? | Physiologic (muscles during exercise), Pathologic (inflammation) |
Passive increase of blood due to impaired venous drainage? | Congestion |
Localized congestion is due to? | Venous obstruction |
Generalized congestion is seen in? | Right heart failure |
Alveolar macrophages engulf hemosiderin in lung congestion? | Heart failure cells |
Heart failure cells are seen in which organ? | Lungs |
Liver congestion is a result of? | Right side heart failure |
Nutmeg liver is seen in what problem? | Liver congestion, fatty change |
Splenic congestion is due to what? | Liver cirrhosis, portal hypertension |
Secretion of ADP leads to platelet aggregation is known as what reaction? | Platelet release reaction |
ADP is what? | Platelet aggregator |
2 steps in platelet plug? | Adhesion, aggregation |
3 important factors in hemostasis? | Endothelial cell, blood platelet, coagulation factors |
What causes platelet adhesion? | Von Willebrand’s factor |
What causes platelet aggregation? | ADP, Thromboxane |
Injured endothelial cells initiate thrombosis by? | Von willebrand’s factor, Tissue factor (thromboplastin) |
Virchow’s Triad? | Endothelial injury (most important), Alteration of normal blood flow, hyper-coagulability of blood |
What is the most important factor of Virchow’s triad? | Endotherlial injury |
Arterial thrombi, grey Red mass w/ apparent laminations? | Lines of Zahn |
Types of arterial thrombi? | Non-occlusive (mural), Occlusive (most common), Vegetative (occur on cardiac valves) |
What is the most common type of arterial thrombi? | Occlusive |
What are the lines of Zahn? | Red layer of RBC’s |
Lines of Zahn are seen where? | Arterial thrombi |
Venous thrombi commonly occur where? | Lower limbs |
Venous thrombi can result in what type of emboli? | Pulmonary |
Almost always occlusive? | Venous thrombi |
Fragmented or detached thrombi? | Thromboembolism |
Pulmonary embolism is due to? | Venous embolism |
Systemic embolism is due to? | Arteriol embolism |
What causes pulmonary embolism? | Thrombi of systemic veins (usually deep veins of leg) |
Systemic embolisms are derived from what type of thrombi? | Mural thrombi |
What is the most common embolism? | Thromboembolism |
What is the 2nd most common embolism? | Fat embolism |
Fat embolisms are due to? | Fracture, burn, or surgery |
Gas embolism is seen in? | Caisson disease, Decompression sickness |
What gas is involved in gas embolism? | Nitrogen |
What type of necrosis is infarction? | Coagulative necrosis |
What are types of infarcts? | Pale, white anemic and Red, hemorrhagic |
Pale, white anemic infarct is due to what type of obstruction? | Arterial obstruction |
Red, hemorrhagic infarct is due to what type of obstruction? | Venous obstruction |
Hemorrhagic infarcts occur in which organs? | Lung, liver, small intestine, ovary, testis |
White, anemic infarcts occur in which organs? | Spleen, heart, kidney, brain |
Types of shock? | Cardiogenic, hypovolemic, peripheral sequestration of blood volume |
Decreased cardiac output due to heart failure? | Cardiogenic shock |
Decreased cardiac output due to decrease blood volume? | Hypovolemic shock |
3 types of shock due to peripheral sequestration of blood volume? | Septic shock, anaphylactic shock, neurogenic shock |
What type of shock involves endotoxin of gram negative bacteria? | Septic shock |
What type of shock involves chemical mediators of allergy? | Anaphylactic shock |
What type of shock involves anesthesia, spinal cord injury? | Neurogenic shock |
What are 5 causes of shock? | Cardiogenic, neurogenic, hypovolemic, anaphylactic, septic |
Stages of shock? | Compensation, impaired tissue perfusion (decompensation), irreversible stage |
Stage of compensation is associated with? | Mild hypotension |
Stage of impaired tissue perfusion (decompenstion) is associated with? | Lactic acidosis |
Irreversible stage is associated with? | Failure of peripheral vasoconstriction |
Polypoid tumors are usually what? | Benign |
Ulcerated tumors are usually what? | Aggressive |
Carcinomas are from what? | Epithelial cells |
Sarcomas are from what? | Mesenchymal tissue |
Carcinomas are named by what? | Type of epithelium |
Sarcomas are named by what? | Cell component of tumor |
Mixed tumors are composed of what? | Epithelial and Mesenchymal tissue |
Tumor from hepatocytes? | Hepatoma |
Are hepatomas benign or malignant? | Malignant |
Tumors from melanocytes? | Melanoma |
Are melanoma tumors benign or malignant? | Highly malignant |
A mass of mature disorganized tissue? | Hamartoma |
What 2 tumors are non-encapsulated but benign? | Leiomyoma of uterus and Hemangioma |
Why do malignant cells invade? | Physical pressure, secretion of enzymes, low adhesiveness of cells, loss of contact inhibition, vulnerability of adjacent tissue |
How are carcinomas graded? | Numerically |
How are sarcomas graded? | Descriptively |
Why is grading imperfect? | Different parts of the same tumor may display different degrees of differentiation, grade of tumor may change as the tumor grow |
Extent of regional spread of lymph nodes is graded how? | N0- not involved, N1- involved, mobile, N2- involved, fixed |
Presence or absence of distal metastasis is graded how? | M0-absent, M1- present (one organ), M2- present (more than one organ) |
Size of primary lesion is graded how? | T1- less than 2cm, T2- 2-5cm, T3- more than 5cm (movable), T4- infiltrating adjacent structures (any size), not movable |
Second leading cause of death in the USA? | Lung cancer |
Deadliest cancer for males? | Prostate |
Deadliest cancer for females? | Breast |
45 yr. old women, 6 cm diameter non-tender mass in lt. breast, appears fixed to the chest wall, another 2 cm movable non-tender mass is palpable in the lt. axilla. Radiograph reveals multiple .5-2 cm nodules in the lt. lung which of the following classifi | T4, N1, M1 |
45 yr. old women, no chest pain, cough or fever, x-ray shows a 2.5 cm coin lesion in rt. Mid-lung field. Which of the following biologic characteristics best distinguishes this lesion as a malignant neoplasm. Rather than a granuloma? | Uncontrolled (autonomous) growth |
Biopsies were performed on patients who had palpable mass lesion on distal rectal exam of the following microscopic findings, which is most likely? | Invasion |
Type 1 hypersensitivity is known as what? | Immediate (Anaphylactic) reaction |
IgE is seen in what type of hypersensitivity? | Immediate (Anaphylactic) reaction |
Bronchial asthma is seen in what type of hypersensitivity? | Immediate (Anaphylactic) reaction |
IgG and IgM are seen in what type of hypersensitivity? | Type2: Cytotoxic reaction and Type3: Immune complex reaction |
What type of necrosis occurs in blood vessels? | Fibrinoid necrosis |
What type of hypersensitivity is mediated by T cells? | Type 4: Cell mediated hypersensitivity |
What T cell is involved in DTH? | CD4 |
What T cell is involved in T cell mediated cytotoxicity? | CD8 |
Genetic factors of systemic lupus erythematosus? | HLA-DR2 and DR3 |
SLE is hypersensitivity type what? | Type 1 |
ANA react with what? | Nuclei of damaged cells |
Most common cause of SLE death? | Kidney failure |
SLE in the skin is seen as what? | Maculopapular rash |
What are LE cells? | Nuclei of damaged cells |
Heliotrope rash is characteristic of what autoimmune disease? | Polymyositis/Dermatomyositis |
Extracellular accumulation of fibrillar proteins? | Amyloidosis |
Type AL proteins accumulate in the tissue and pass in urine in what disease? | Primary amyloidosis |
AL proteins passed in the urine are known as what? | Bence Jones protein |
Type AA protein accumulation is seen in what disease? | Secondary (reactive) amyloidosis |
Accumulation of B2-microglobulin in joints and synovium? | Hemodialysis-related amyloidosis |
What type of protein is associated with hemodialysis and renal failure? | B2-microglobulin |
Familial Mediterranean Fever is seen in what disease? | Hereditary amyloidosis |
X-linked recessive disorder, absence of B lymphocytes? | Congenital agammaglobulinemia (Bruton’s) |
Normal total lymphocyte count, serum immunoglobulins are markedly decreased, deficient humoral immunity are common in what immune deficiency? | Congenital agammaglobulinemia (Bruton’s) |