click below
click below
Normal Size Small Size show me how
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) |