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369 Cards in this Set
- Front
- Back
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Hep A case with elevated bilirubin. What is the cause?
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defects in cell membrane
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Trauma to the liver is regenerated in a few weeks. What process does this exhibit?
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hyperplasia
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What cellular process occurs in response to HTN?
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hypertrophy
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Patient death from CHF. Heavy heart, left ventricular hypertrophy and minial atherosclerosis. No serum abnormalities. Why does the aortic valve show white, rocky clumps?
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dystrophic calcification
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History of transient ischemic attacks for 3 months. A endarterectomy is performed and crystal forming long, cleft like spaces was found? What is this crystal made of?
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cholesterol
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Severe abdominal pain + hypotension --> death. The mesentery appears to have lost fat?
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acute pancreatitis
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A large cystic area in left parietal lobe. What type of necrosis?
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liquefactive
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Cast --> immobilized leg. What cellular process occurs?
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atrophy
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What cells have the highest telomerase activity?
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germ cells
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What process occurs as the result of heartburn? What is the name of this common case?
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columnar epithelial metaplasia
Barret's esophagus |
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What process occurs RIGHT before the onset of menstrual bleeding?
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apoptosis
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Mutational deactivation of what protein product protects cancer cells against apoptosis?
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p53
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What process allows women to breast-feed?
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lobular hyperplasia
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Congenital anemia treated with multiple transfusions. Liver function tests find reduced serum albumin. What is found in a liver biopsy?
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Hemosiderosis in hepatocytes. The iron can't be cleared.
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What cellular process causes prostate enlargement?
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hyperplasia
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After MI and application of tPA, creatine kinase levels rose. Why?
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reperfusion injury
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Tumors cells undergoing apoptosis have are triggered by the release of what substance into the cytosol?
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cytochrome C
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Calcium deposits in gastric mucosa, renal interstitium, and alveolar walls. What condition would cause this?
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chronic glomerulonephritis
These areas normally help lose acid, so a defect would cause an alkaline environment, good for precipitation of calcium. Chronic renal disease helps reduces phosphate excretion. This is dystrophic calcification. |
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Ischemic organ injury normally results in what type of necrosis?
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Coagulative
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Autopsy: Enlarged, yellow liver , normal cholesterol and triglycerides, but decreased serum albumin and increased prothromin time. Normal body weight. What is the disease and likely patient history?
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alcoholic. Steatosis.
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What is the reaction normally associated with eosinophilic mass?
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apoptosis
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What substance is likely found in an elderly man's chocolate brown heart?
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lipochrome (lipofuscin)
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What likely causes dark hilar lymph nodes in a woman with a history of chronic cough?
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smoking and carbon
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What is deposition of calcium with hypercalcemia?
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metastatic calcification
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Knockout of what gene product induces apoptosis?
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Bcl-2
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Cheese-like circular nodule found with mycobacterium tuberculosis?
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caseous necrosis
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What process occurs to increase uterus size for pregnancy?
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Myometrial smooth muscle hypertrophy
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What binds to denatured proteins so they are targeted for catabolism by cytosolic proteasomes?
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ubiquitin
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Possible ways in which the amniotic sac and fluid can become infected:
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Fever
Prolonged interval between rupture of membranes and Preterm delivery |
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What cause most of the cases of sepsis in neonates?
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Group B Streptococcus and E. coli
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What are cardinal signs of inflammation?
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Rubor, Tumor, Dolor, Calor and Functio Laesa
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Stimuli for the acute inflammatory response
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1- Any infection bacterial, viral, fungal or parasitic
2- Tissue necrosis ischemia, trauma, physical or chemical 3- Foreign bodies 4- Immune reactions |
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What are the four types of responses that lead to increased vascular permeability?
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1. Immediate transient response - due to histamine, bradykinin, leukotrienes acts at venule level, short lived: 15-30 minutes.
2. Immediate sustained response - due to direct endothelial damage. Occurs immediately after injury and persists for hours or days. Burns. Effects venules, capillaries and arterioles. 3. Delayed prolonged response - Sun burn, radiation. Mechanism unclear. Delay of 2-12 hours and can last for days. Involves venules and capillaries. 4. Leukocyte dependent response - ARD, glomerulonephritis. A later response. Due to adhesions of leukocytes to endothelium and their later activation. Resulting in increased permeability in pulmonary venules and glomerular capillaries. |
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What does the kinin system activate?
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clotting, pain, complement
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What is the effect of complement on exudate and lysosomal release?
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increase both
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What are the 3 differences between exudate and transudate?
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specific gravity, protein, appearance
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What is wrong with contaminated heparin?
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It can activate complement system
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What event comes after the exudation of fluid?
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transmigration of neutrophils
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What is diapedesis?
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neutrophil migration into the adjacent tissue through the intercellular junctions
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What slows down neutrophils on endothelial surfaces and what stops them?
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selectins and integrins
(you select neutrophils and then you integrate them) |
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Natalizumab
definition and adverse side effects? |
- a recombinant monoclonal antibody against alpha4 integrins -An attempt to treat Multiple Sclerosis
Out of 3000 patients who participated in the trials, 3 developed Progressive Multifocal Leukoencephalopathy. This is a serious viral inflammation of the brain, secondary to an opportunistic infection by reactivation of clinically latent JC virus. Also melanoma |
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Why do cells move towards the area of inflammation and not in a random fashion?
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They follow a gradient of
Bacterial by-products Components of Complement System Chemokines Products of lipoxygenase arachidonic pathways |
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What is the sequence of events for neutrophil mediated phagocytosis?
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Neutrophils operate anaerobically - > increased glycolysis - increased RNA, protein and membrane synthesis to be used in the formation of a phagosome which will fuse with a lysosome - > degranulation of polys - > respiratory burst - > HMP - shunt is activated with eventual production of H2O2, the most important oxygen derived killing agent in a phagosome. After phagocytosis neutrophils rapidly under go apoptotic cell death and are either ingested by macrophages or are cleared by lymphatics.
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What happens to hydrogen peroxide that escapes the cell?
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converted to H2O by glutathione peroxidase
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Autosomal recessive inheritance. Lysosomes within the polys are very large. H2O2 production is normal, but bacterial killing is inefficient.
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Chediak-Higashi Syndrome
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70% X linked recessive form. Genetic defect gp91phos eliminating NADPH
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CHRONIC GRANULOMATOUS DISEASE
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What are the acute phase reactants?
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Fever
Desire to sleep Decreased appetite Acute phase proteins Sedimentation rate C Reactive Protein Neutrophilia, etc |
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test which measures the rate of settling or sedimentation of RBC’S in a glass tube over a specific period of time. The area of clear plasma is measured. A very nonspecific test but an abnormal value can be found in many acute and chronic illnesses. The basis of the abnormal tests is an alteration of plasma proteins such as fibrinogen and globulins which are altered as acute phase reactants
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Erythrocyte Sedimentation Rate (ESR)
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test based on the release of a protein, another acute phase reactant, and a nonspecific measure of systemic inflammation. Recently a high-sensitivity test has been developed which is used as an indicator of coronary artery damage and, hence, a predictor of Coronary Artery Disease
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C-Reactive Protein (CRP)
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What is the action of most prostaglandins?
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vasodilation
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What is the precursor of TXA2?
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Prostaglandin
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What is the effect of leukotrienes?
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vasoconstriction, bronchospasm, increased permeability
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Autocoids?
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– local short range hormones
formed rapidly exert effects locally either decay spontaneously or are destroyed enzymatically |
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Nitric Oxide effects?
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anti-inflammatory, but antimicrobial
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What is a M2? (Hint: activated by IL-13 and IL-4?)
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macrophage that promotes wound healing and repair
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a syndrome caused by diffuse alveolar capillary damage
1) Tachypnea and cyanosis refractory to oxygen therapy 2) markedly reduced lung compliance 3) diffuse alveolar shadowing on chest x-ray 4) Pulmonary edema, congestion, and hyaline membrane formation |
Adult Respiratory Distress Syndrome
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What causes Adult Respiratory Distress Syndrome?
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40-60% due to sepsis
20-35% due to pneumonias and gastric aspirations |
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What is a stasis ulcer?
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breakdown of the skin (ulcer) caused by fluid build-up in the skin from poor vein function (venous insufficiency)
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What are the causes of chronic inflammation? What are the 2 cells that are more prominent?
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1. organisms with a low pathogenicity but stimulate a prolonged immune response ie TB, Syphilis
2. prolonged exposure to a toxic substance 3. autoimmune diseases macrophages, eosinophils |
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How does an infection move from lymph to septic shock?
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Lymphangiitis – an inflammatory exudate moving through a lymphatic (remember where lymphatics finally end)
Lymphadenitis – an enlarged lymph node (rubor, tumor, etc) as the inflammatory exudate containing the bacteria accumulates within and passes through a lymph node causing reactive enlargement of the node Sepsis – a systemic inflammatory response syndrome plus evidence of infection Severe Sepsis – sepsis plus organ failure Septic Shock – severe sepsis plus refractory hypotension |
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What is a pulmonary absess?
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A localized suppurative process associated with necrosis of lung tissue
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What is Chronic Cholecystitis?
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inflammation of the gallbladder
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GRANULOMATOUS INFLAMMATION
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Characterized by dense cellular infiltration and proliferation rather than a fluid exudate
Composed of macrophages that are transformed into epithelial like cells – epitheloid cells – surrounded by lymphocytes and plasma cells and some fibrous reaction Formation of Giant Cells from the macrophages |
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Taenia solium Cysticercosis
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Man may be both definitive and intermediate host to T. solium. As the latter host, the disease carried by larvae cysts is called cysticercosis. The larvae migrate via the blood stream to the viscera
Ingestion of eggs --> migration of larvae |
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What is Sarcoidosis?
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non caseating granuloma that can heal on its own (65-75%), fibrosis in others. Genetic factors.
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FOREIGN BODY GRANULOMA
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CHRONIC RESPONSE TO INERT MATERIALS
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What phase are stabile cells in?
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G0
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What adult stems cells have the most potential?
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Bone marrow cells
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What is method for growing new cells with embryonic stem cells?
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1 diploid nucleus from patient introduced into an enucleated oocyte.
2 oocyte activated and embryonic stem cells are taken from the blastocyst (ES) |
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How do you grow new cells with adult stem cells? What is the problem?
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1 the reprogramming of fibroblasts from adults and newborns
2 this is based on the discovery of 4 transcription factors making changing these cells to induced pluripotent cells (iPS) Still some problems with this method, ie, activation of an oncogene in the process |
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What are the steps of wound healing?
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1. The wound is filled by a blood clot containing fibrin along with trapped red and white blood cells and the surrounding tissues undergo a phase of acute inflammation.
2. Macrophages, neutrophilic enzymes, and plasmin remove the clot. Infiltrating neutrophils cleanse the wounded area of bacteria and are then extruded with the eschar or phagocytosed by macrophages. Monocytes also infiltrate, and become activated macrophages that release growth factors such as platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) which initiates the formation of granulation tissue. 3. Capillaries grow into the wound from the periphery, at first as proliferating solid cords of endothelial cells. A lumen develops in each of these cords which soon join together to form anastomosing capillary loops through which blood flows. 4. The young capillaries soon differentiate into arterioles and venules. 5. Along with the capillaries, fibroblasts grow into the clot and lay down collagen. Wound contraction involves a complex orchestrated interaction of cells, extracellular matrix and cytokines. During the second week of healing fibroblasts assume a myofibroblast phenotype characterized by large bundles of actin-containing microfilaments disposed along the cytoplasmic face of the plasma membrane of the cells and cell by cell matrix linkages. This corresponds to the commencement of connective tissue compaction and contraction of the wound. 6. Lymphatics also grow into the area. The blood vessels are eventually obliterated by the fibrous scar. 8. The newly formed collagen contracts thereby reducing the size of the wound (cicatrization or contracture). In so doing, however, it may also produce tissue distortion and obstruction of blood flow to the area. |
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What are the growth factors in wound healing?
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TGF –TRANSFORMING GROWTH FACTOR
PDGF –PLATELET DERIVED GROWTH FACTOR VEGF – VASCULAR ENDOTHELIAL DERIVED GROWTH FACTOR MMP – MATRIX METALLOPROTEINASES PA – UROKINASE –TYPE PLASMINOGEN ACTIVATOR |
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Possible sources for revascularization in areas of ischemia such as in myocardial infarction
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platelet derived growth factors
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What is markedly elevated in the vitreous of patients with ischemic retinal disease?
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VEGF
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large bulging scar caused by excessive collagen formation
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keloid
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fibrous bands which may develop as a result of organization of fibrinous exudates in the body cavities. They may contract causing distortion and functional disturbances of vital organs.
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adhesions
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What are factors that affect wound healing?
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Apposition of edges of wound
Infection Blood supply Malnutrition (also vitamin C deficiency) Diabetes Mellitus |
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What are primary and secondary intention wound healing?
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Primary intention- edges brought together
Secondary intentions- grows over on its own. |
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What do kidneys secrete in response to hypoxia? What does it do?
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EPO
stimulates marrow production of erythroid stem cells, increasing red cell production. |
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What are the important tests in a CBC?
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RBC - absolute number of red cells/µl
Hgb - hemoglobin concentration/µl MCV - mean corpuscular volume, cell size RDW - red cell distribution width, variation in cell size |
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What establishes anemia and what are the numerical ranges?
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Normal hemoglobin
14 - 17 g/dl adult male 13 - 16 g/dl adult female Anemia 10 - 12 g/dl mild 8 - 10 g/dl moderate <8 g/dl severe |
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What are the 3 ranges of MCV (mean cell volume - red cells) and what are they useful for?
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MCV > 100 = Macrocytic
MCV < 80 = Microcytic MCV 80 - 100 = Normocytic Clues to differential diagnosis of anemia |
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Why is Red Cell Distribution Width important?
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because cells last 100 days, even if you start to accumulate small cells, large cells could persist
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What does the number of reticulocytes indicate?
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Excellent indication of bone marrow ability to respond to anemia
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How do you interpret reticulocyte count?
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Low = red cell production defect
bone marrow failure (factory deficiency) stem cell defect myelophthisis deficiency anemia (raw material deficiency) erythropoietin defect High = red cell survival problem Hemolysis Hemorrhage |
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Agranulocytosis
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virtually absent neutrophils
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Left shift-
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immature neutrophils appearing in the blood.
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What are the 3 pools of granulocytes?
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blood, marrow, endothelial (marginal cells).
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What are the 3 signs of reacting neutrophils?
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Vacuolization
Toxic granulation Dohle bodies |
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Causes of Neutrophilia, a Left Shift and ReactiveChanges
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Infection
Bacterial Early viral Inflammation/necrosis Trauma Myocardial infarction Severe acute physiologic stress Steroid therapy Malignancy |
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Causes of neutropenia
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Infection
Bacterial Viral Drugs Autoimmune disorders Splenomegaly (sequestration) Bone marrow failure |
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Causes of lymphocytosis
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Acute Infection
Viral (EBV, CMV) Pertussis (whooping cough) Chronic Infection TB Lymphoid malignancies |
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What do reticulocytes look like?
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big and blue
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What is pancytopenia?
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RBCs, WBCs, platelets
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What is poikilocyte
anicytosis polychromasia |
poikilocytes-abnormal shape
anicytosis- variable size polychromasia- increased RNA (blue ie. reticulocytes) |
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What is mean cell volume and parameters?
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microcytic ,80 fl
normocytic 80-100 fl macrocytic > 100 fl |
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What is RDW? What condition has higher RDW?
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Red Cell distribution
iron deficiency anemia |
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Where are the 4 places you make blood cells in utero?
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Yolk sac, liver, spleen bone, marrow
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What are the sites of bone marrow used to synthesize blood? What is extramedullary hematopoesis?
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Infants: both appendicular and axial bones
adults: axial skeleton (ilium, ribcage, spine) liver and spleen become sites of blood cell production in pathological conditions |
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What is the cellularity of marrow?
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Percentrage that is blood cell precursors vs fat
50% typically |
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What is EPO released in response to?
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low O2
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What increases and decreases levels of circulating cells?
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Increases 1) overproduction 2) excess/early release
Decreases 1) decreased survival 2) decreased production |
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What are the presentation and causes of aplastic anemia?
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anemia (fatigue, pallor, cold)
leukopenia (increased infection) thrombocytopenia (increased bleeding time) Causes: drugs, chemo, infection, cancer |
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What does the RBC use for energy?
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glycolysis
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What does reticulocyte count help determine for anemia?
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decreased --> EPO defect or acute problem
increased --> non-hematopoetic or chronic problem |
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What are the levels of anemia?
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10-12g/dL = mild
7-10 = moderate <7 = severe |
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How does the body compensate for chronic anemia?
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increased cardiac output
redistribution of blood right shift in Hb-O2 curve to unload oxygen |
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What are the types of hemolysis?
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intrinsic- defect in RBCs
extrinsic= RBCS are destroyed by outside forces |
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What causes lymphocytosis?
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infection,especially viral.
Also cancer |
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What causes neutrophilia?
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MC = bacteria
corticosteroid therapy (release of arginal neutrophils) |
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What are the neutrophil reactive features in an acute infection?
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left shift, toxic granulation, Dohle bodies, and vacuolization
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What cause eosinophilia? Why?
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allergic reaction and parastic infections
dampens hypersensitivity, anti-histamine, and major basic protein kills helminiths |
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What is the most common cause of basophilia and the others?
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MALIGNANCY
hypersensitivities allergies |
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When do macrophages replaces PMNs?
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2-3 days
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What are the vascular events of inflammation?
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1. Vasoconstriction of arterioles
2. Vasodilation of arterioles (histamine) 3. increased permeabilities of venules (histamine) 4. Edema 5. Blood flow decreases |
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What are the differences between exudate and transudate?
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exudate: cloudy, high protein sg >1.02, inflammatory response
transudate- clear, low protein sg 1.012, from edema |
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What are the neutrophil effects?
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Margination
Rolling Adhesion Diapedesis Chemotaxis Phagocytosis Bacterial killing |
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What does natalizumab block? What does it cause?
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integrin used to treat MS
JC virus --> Progressive Multifocal Leukoencephalopathy |
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What do PMNs follow in chemotaxis?
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C5a, IL-8, LTB4
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Bruton's Agammaglobulinemia
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IgG manufacture defect
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Chediak-Higashi syndrome
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can't form phagolysosome b/c of microtubule defect, recurrent staph and strep infections
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What is the purpose of NADPH oxidase?
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Respiratory burst
O2 --> O2- |
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What is the purpose of superoxide dismutase?
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O2- --> H2O2
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What is the purpose of glutathione peroxidase?
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neutralizes peroxide
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What is Chronic Granulomatous Disease of Childhood? What can they still protect against?
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X-linked recessive deficiency in NADPH oxidase resulting in no respiratory burst
Strep, no catalase so they still make H2O2 which the body takes and converts to HOCl |
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What are the 3 types of inflammation?
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Suppurative/purulent
serous fibrinous |
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What are the 4 ways acute inflammation transitions to chronic?
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abscess, ulcer, fistula, granuloa
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What cells are present in chronic inflammation?
What cell is not? |
macrophages, lymphocytes, plasma cells, eosinophils
PMNs |
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What are the 3 types of granulomas and examples?
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caseating- TB
non-caseating- sarcoidosis foreign body- silica |
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What growth factor is associated with macular degeneration?
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VEGF, neovascularization --> too many vessels
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What are the steps in primary wound healing?
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1. scab
2. neutrophils clean 3. epithelial cover 4. Macrophages replace neutrophils and releases GFs 5. Fibroblasts lay down collagen 6. Type III collagen --> I |
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What are the differences between primary and secondary intetion?
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greater inflammation and cell debris
base and sides of wound filed with granulation tissue Scar is fibrous and ugly |
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what are the 3 complications of wound healing?
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keloid- large bulging scar fromexcessive collagen formation
desmoids- excessive CT at wound contracture- excessive contraction of myofibroblasts --> deformed wound --> immobilization |
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What are the 3 types of cells?
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labile, stabile, permanent
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What factors control cell regeneration?
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time, growth factors, age (Hayflick number), and basement membrane maintenance
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What is the normal treatment of low urine output in acute tubular necrosis?
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nothing, just leave it alone.
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What are the causes of hypertrophy?
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increased functional demand, hormonal stimulation, increased nutrition, and mechanical factors
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What are the causes of atrophy?
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ichemia, hormonal effects, loss of innervation, disuse, pressure atrophy, and decreased nutrition or aging
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What is the difference between denervation or disues atrophy of muscles?
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localized versus uniform
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What are the 2 examples of pressure atrophy
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tummor on adjacent brain cells, urine retention pressing on bladder cells
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What are the 2 mechanism of atrophy?
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ubiquitin and autophagy
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What is brown atrophy?
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organ with enough lipofuscin to be seen grossly
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What are the 3 examples of hyperplasia?
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BPH, endometirum during menstrual cycle, alveoli of lactating breast from prolactin
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Wghat are the 2 example of metaplasia given?
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bronchal squamous metaplasia in smoker
esophagal columnar metaplasia in Barret's Esophagus |
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What are the 4 clear accumulations?
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triglycerides, glycogen, cholesterol, and hydropic change
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What are the causes of steatosis?
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ethanol, Non-alcoholic steato-hepatitis (overnutrition), malnutrition, and diabetes
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What cells are lipochrome normally seen in?
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liver heart brain
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What cells are hemosiderin found in?
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liver, spleen, sites of hemorrhage
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What disease is associate with accumulation of hemosiderin?
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hemochromatosis
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Where is carbon normally found?
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lungs, lymph nodes
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What are the causes of dystrophic calcification?
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enzymatic fat necrosis, breat cancer, heart valves, and atheroscletosis
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What are cause of metastatic calcification?
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hyperparathyroidism, destruction of bone tissue, and vit D disorders
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What are possible causes for hypoxemia? What causes atp depletion?
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respiratory acidosis, ventiiation defects, perfusion defects, diffusion defects, anemia
failure or poisoning of cytochrom oxidase system by CO or CN |
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What ares are most susceptible to hypoxia?
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watershed (splenic flexure and CNS between ACA and MCA), subendocardial tissue, and kidney regiosn using most ATP (straight proximal tubule and NKCC in TAL)
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What is the MCC of free radical injury? Others?
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reperfusion injury
APAP metabolism, carbon tetrachloride, and retinopathy in premature babies |
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What are the 3 nuclear changes of necrosis?
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pyknosis- clumping and shrinking of chromatin
karyorrhexis fragmentation of chromatin karyolysis- fading of chromatin material |
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Where do you see pale coagulation necrosis and where do you see hemorrhagic type?
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dense tissue (heart, kidney, spleen) versus loose tissue (lungs, small intestine)
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Where do you see liquifactive necrosis?
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CNS and abcess
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What is responsible for the caseous appearance caseous necrosis?
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release of lipis from mycobacteria
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What is the MCC of enzymatic fat necrosis?
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acute pancreatitis and traumatic fat necrosis
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What does Ca activate in apoptosis?
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pohopholipase, protease, endonuclease, and realease of mitochondrial cytochome C
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What are examples of fibrinoid necrosis?
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immune mediate bvasculitis and malignant HTN
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What genes prevent release of cytochrome C? What gene inactivates that genes?
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BCL2
BAX |
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What gene arrests cell in G1 phase if there is DNA damage and activates BAX if there is too much damage?
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TP53
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What are the different pathways of apoptosis?
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Extrinsic: binding of TNF and FAS-L
intrinsic: mitochondiral leakage of cytochrome C |
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What is the ultimate activation in the apoptotic pathways?
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cas[aces
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What does decreased caloric intake activate in relation to aging?
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Sir-2 gene
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Where do macrophages replace PMNS?
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2-3 days
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What are the 2 major actions of eosinophils?
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inhibitionso f histamien and parasite killing with major basic protein
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The mediates fever?
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IL-1, TNF, PGE2
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What mediates tissue necrosis?
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neutrophils, and free radicals
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What controls chemotaxis?
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LTB4, IL-8, and C5a
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What are the cardinal signs of inflammation?
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rubor, calork, tumor, dolor, and functio laesa
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What are the events of vascular inflammation?
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intial vasoconstriction --> vasodilation, increased venule permeabilit, edema, and loss of blood flow
|
|
|
What are the qualities of exudate?
|
inflammatory resposne, cloud, sg > 1.02 and associate with infection, pneumonia, cnacer, and pulmonary embolus
|
|
|
What are the qualities of transudate?
|
cleat, sg < 1.012 , associated w/ CHF, cirrhosis, and pulmonary embolus
|
|
|
What are the events of neutrophils in inflammation?
|
margination, rolling (selectins) adhesion (integrins), diapedeis, chemotaxis, phagocytosis, and bacterial killing (MPO)
|
|
|
What is natalizumab?
|
antibody to integrin, blocks cellular infiltration of T cells, used to treat multiple sclerosis
|
|
|
What generates oxygen radicals? What generates hydrogen peroxide? What generates bleach?
|
NADPH oxidase, superoxide dismutase, myeloperoxidase
|
|
|
Why does leukocyte adhesion deficiency result in delayed umbilical cord separation?
|
PMNS cannot reach it due a deficiency of integrins or selectins
|
|
|
What is the test for chronic granulomatous disease of childhood?
|
nitroblue tetrazolium test
|
|
|
What are the 3 types of acute inflammation?
|
suppurative/purulent, serous, and fibrinous
|
|
|
What granulomas are caseating?
|
mycobacteria due to the lipids from their walls
|
|
|
How does VEGF cause macular degeneration?
|
nevascularization
|
|
|
What type of collagen is replaced in wound healing?
|
Replacement of type 3 by type 1
|
|
|
keloid
|
large bulging scar caused by excessive collagen formation, black people
|
|
|
desmoid
|
excessive ct formation at wound site
|
|
|
contracture
|
contraction of myofibroblasts deform wound and cause immobilization
|
|
|
How is a wound healed by secondary intention different from a wound healed by primary?
|
greatere inflammation and cell debris
base and sides of wound are filled with granulation tissue, scar is fibrous and covered by epithelium remains red longer large and distorted |
|
|
What factors affect wound healing?
|
infection, blood supply, apposition, nutrition (vit C and zinc)
|
|
|
How is sepsis sundrome different from sepsis? How is septic shock different?
|
signs of organ hypoperfusion, hypotension
|
|
|
What is leuko, neutro, lympho, thrombopenia?
|
too little WBC, neutrophils, lymphocytes, and platelets
|
|
|
What is agranulocytosis?
|
no PMNs
|
|
|
What is granulocytosis, neutrophilia, eosinophilia, basophilia, lymphocytosis, thrombocytosis, and reticulocytosis?
|
increased levels of granulocytes, neutrophils, eosiniophils, basophils,l lymphocytes, platelets, and immature RBCs
|
|
|
In a CBC, what are the following measures? Hb? Hct? RBQ? MCV? RDW? WBC? WBC Differential? Platelet count?
|
hemoglobin, hematocrit, red blood cell count, mean cell volume, red cell distribution width, white blood cell count, subclassification of WBC, number of platelets
|
|
|
Where are blood cells synthesized in utero?
|
yolk sac, liver, spleen, and bone marrow
|
|
|
Where in bone marrow are RBCs synthesized accorded to age? What is extramedullary hematopoesis?
|
infants: all bone
adults: axial skeleton (ilium, ribcage, and spine) liverand spleen beomce sites of blood cell production in pathological conditions |
|
|
What is normal marrow ceullarity? What does aspiration or biopsy of bone marrow normally assess?
|
50% blood cell precursors and 50% fat
cellularity, differential, or morphological abnormalities |
|
|
What is the marker for hematopoetic stem cells?
|
CD34
|
|
|
What causes replication of hematopoietic stem cells? What stimulates granulocyte growwth and granulocytes/macrophage growth, and thrombopoeitin growth?
|
EPO in response to low O2
G-CSF GM-CSF thrombopoeitin |
|
|
What is aplastic anemia? Causes?
|
bone marrow failure with pancytopenia
anemia leukopenia thromocytopenia drugs, chemo, infection, cancer |
|
|
What is a Howell-Jolly Body?
|
left over nucleus normally removed by spleen in RBCs
|
|
|
What do RBCs use for energy? Therefore, what condition results in hemolytic anemia during stressful situations when they lack an enzyme?
|
glycolysis
G6PD |
|
|
When is EPO therapy useful?
|
chronic renal failure because they do not produce sufficient EPO
|
|
|
What are the symptoms of anemia?
|
palpitation, dizziness, pallor, and exercise intolerance
|
|
|
What are compensatory mechanism of anemia?
|
increase cardiac output, redistribution of blood, and right shift in Hb-O2 curve due to increased 2,3-BPG
|
|
|
What is reticulocyte count used for?
|
determining a production problem (low count) or loss problem (high)
|
|
|
What are the different kinds of hemolysis?
|
intrinisc (RBC defect) and extrinsic (infection, drugs, autoimmune)
|
|
|
What will happen to WBC differential in most bacterial infections?
|
neutrophilia
|
|
|
What are the reactive features in neutrophils that indicate an acute reaction?
|
left shift, toxic granulation, Dohle bodies, and vacuolizsation
|
|
|
What does basophilia indicate?
|
malignancy, hypersensitivity, and allergy
|
|
|
What does reactive lymphocytosis indicate?
|
viral (most common, bacterial infection, cancer
|
|
|
What is dysplasia?
|
Abnormal tissue development with loss of uniformity between cells
|
|
|
What is dysplasia?
|
abnormal tissue development with loss of cell uniformity
|
|
|
What is anaplasia?
|
loss of structural differentiation marked by pleomorphism, abnormal nuclear morphology and tumor giant cells
|
|
|
What is pleomorphism?
|
variability in size/shape of cells and their nuclei
|
|
|
What is desmoplasia?
|
hyperplasia of fibroblasts and disproportionate formation of fibrous ct tissue especially in the stroma of a carcinoma
|
|
|
metastasis
|
discontinuous spread of a canceer beyond the primary lesion via lymphatics, blood vessels, seeding into a body space, or mechanically
|
|
|
What words is used to described club shaped amd fomger-like
|
polyp and papilloma
|
|
|
What is a malignant cancer of connective tissue?
|
sarcoma
|
|
|
What is a carcinoid?
|
low grade tumor of neuroendocrine
|
|
|
What is a malignant tumor of plasma cells?
|
multiple myeloma
|
|
|
What is an overgrowth of tisse in its correct anatomical sight and what is normal tissue in an abnormal place?
|
hamartoma and choristoma
|
|
|
What is most common cancer and what is the most deadly cancer?
|
common: prostate and breast
fatal: lung |
|
|
What is tumor grading?
|
microscopic geature of the tumor, use gleason score for prostate cancer
|
|
|
What is tumor staging?
|
tumor- size
nodes- spread metastasis- better predictor of prognosis |
|
|
At what growth of cancer is it normally detected?
|
3/4
|
|
|
What are the 3 stages of neoplasia? what do you call something that combines the first 2 steps together?
|
initiation, promotion, and progression
complete carcinogen |
|
|
What are viruses that cause cancer?
|
HPV, HEP B/C, EBV (Burkitt's lymphona, Hodgkin's Lymphoma, Nasopharyngeal carcinoma), HTLV-1 (T cell leukemia), HHV7 (Kaposi's sarcoma), helicobacter pylori (MALT lymphoma)
|
|
|
What are examples of proto-oncogenes?
|
HER, ABL, C-MYC, RET, RAS
|
|
|
What are examples of tumor suppressor genes?
|
RB, p53, BRCA1/2, and APC
|
|
|
What are the effects of neoplasms?
|
mass effect, local ulceration, cachexia, paraneoplastic syndrome, hemostasis abnormalities
|
|
|
What is the most successful cancer screening process?
|
cervical cytology (Pap smears)
|
|
|
What cancer screen and screen and treat at the same time?
|
colonscopy
|
|
|
What disease that cancer cancer have vaccines?
|
Hep B and HPV
|
|
|
What type of genetic disorder present early and are severe? When will they recur?
|
chromosomal
balanced translocations |
|
|
Factors Contributing to Gains in Life Expectancy (6)
|
1. Clean water and air
2. Improved sanitation 3. Safer foods, improved nutrition 4. Expanded immunizations 5. Safer environment and workplaces 6. Improved medical care. |
|
|
What are the 4 causes for Down syndrome?
|
maternal non-disjunction, Robertsonian translocation (recurrence), mosaicism, and partial duplication of chromosome 21
|
|
|
What are the disease association of Down's syndrome?
|
hypothyroidism, deafness, duodenal atresia, ALL, early onset lymphoma
|
|
|
What is elevated in quad screen, what is low?
|
hcG and inhibin
AFP and unconjugated estriol |
|
|
What is the presentation of Edward's syndrome?
|
MR, rocker bottom feet, low-set ears, micrognathia, prominent occiput, and VSD
|
|
|
What is the presentation of Patau's?
|
MR, microphthalmia, microcephaly, celft lip/palate, umbilical hernia, polydactyly, VSD, and renal
|
|
|
What are the features of Turner's syndrome? What are the disease associations?
|
short, webbed neck, shield chield, reproductive problems, streak donas, poor breast development, decreased pubic hair
preductal coarctation of the aorta, horseshoe kidney |
|
|
What are the features of klinefelter's?
|
tall, eunuchoid body, long limbs, gynemastia, female hair distribution, small testes, steriliy, learning diabilities, increase risk of breat cancer and autoimmune disorders
|
|
|
XYY
|
taller, lower IQ, increased testosterone, increased acne
|
|
|
X's greater than _____ result in MR?
|
3
|
|
|
What are the causes of true hermaphrodites?
|
XX with Y translocated onto another chromosome or XX/XXY mosaics
|
|
|
What is the main cause of male psuedohermaphrodites and female psuedohermaphrodites?
|
androgen insensitivity
21-hydroxylase deficiency |
|
|
What is anticipation?
|
effects of trinucleotide repeat disorder get worse in succeeding generations
|
|
|
What are the main features of Fragile X?
|
macro-orchidism, large jaw and large everted ears
|
|
|
What are the disease association of Marfan's syndrome?
|
cystic medionecrosis of aorta --> aortic dissection, mitral valve prolaps, and lens dislocation
|
|
|
What are the dissease associations of Ehler's Danlos?
|
berry aneurysms, organ rupture, and aortic dissection
|
|
|
What are the disease associations of familial hypercholesterolemia?
|
early onset MI
|
|
|
What chromosome does neurofibromatosis affect? What is the mechanism. What are the features of type II?
|
17/22, deletion of anti-oncogene, bilateral acoustic neuromas, juvenile cataracts, and neurofibromas
|
|
|
What are the characteristic features of cystic fibrosis?
|
thick broncial mucous, infection, bronchiectasis, pancreatic duct obstruction --> malnutrition, steatorrhea, vitamin deficiency, diabetes, meconium ileus, infertility, positive sweat chloride test
|
|
|
What is deficient in PKU?
|
phenylalanine hydroxylase
|
|
|
What enzymes are mild and severe galactosemia?
|
galactokinase and galactose-1-phosphate uridyl transferase
|
|
|
What is the presentation of galactosemia?
|
jaundice, diarrhea, vomtting --> enlarged liver and spleen, cataracts, brain damage
|
|
|
What is the deficiency in Tay Sach's Disease? what are the characterisitic features?
|
hexosaminidae A with accumulation of GM2
motor deterioration, MR, blindness, death by 3, cherry red spot on macula |
|
|
What is the deficiency of Gaucher's disease? What happens?
|
B-glucocerbrosidease
infants- hepatosplenomegaly plus CNS --> early death anemia and thromocytopenia wrinkled tissue paper cytoplasm |
|
|
What is the deficiency of Niemann-Pick disease? Features?
|
deficiency of sphingomyelinase
neurodegeneration, hepatosplenomegaly, cherry red macula, foam cells type A: infantile, CNS and early death type B: no CNS, splenomegaly |
|
|
What type of glycogen deficiency is in muscle and liver? What about lysosomes?
|
phosphorylase
lysosomal acid maltase --. sever, multiorgan failure. cardiomegaly and death in childhood |
|
|
Where is the defect in Prader0Willi and Angelmann?
|
paternal and maternal
|
|
|
Why are women more likely to pass on cleft lip and pyloric stenosis?
|
women have a higher threshold and therefore have higher deleterious genetic load
|
|
|
what is the deficiency in alkoptonuria? What are the 2 features?
|
homogentisate acid oxidase
black urine and degenerative arthritis |
|
|
What are the steps in microRNAs?
|
bind to risc --> mRNA cleavage --> silence gene translation
|
|
|
What are the examples of deformation, malformation, and disruption?
|
oligohydramnios --> club foot
spina bifida amniotic band |
|
|
What is the potter sequence?
|
malformation of kidneys or ureters --> oligohydramnios --> flat face and less fluid to swallow --> poor lung formation
|
|
|
why do preterm births experience atelectasis? why do they die before week 20?
|
their lungs lack adequate surfactant
no alveoli or type II pneumocyts |
|
|
What is the lecithin to sphinomyelin ratio tell you?
|
lung maturity
|
|
|
What are the major complications of preterm birth?
|
neonatal respiratory ditress syndrome
beronchopulmonary dysplasia brain hemorrhage necrotizing enterocolitis retinopathy of prematurity |
|
|
What are they main perinatal infections?
|
group B strep and herpes simplex virus
|
|
|
Whata are torches?
|
toxoplasmosis (Brain, hydrocephalus, scattered calcification)
other rubella 9deafness, cataracts, and cardiac malformation) cytomegalovirus (cerebral calcification, hepatosplenomegaly, chorioretinis) herpes syphilis |
|
|
why do preterm births experience atelectasis? why do they die before week 20?
|
their lungs lack adequate surfactant
no alveoli or type II pneumocyts |
|
|
What is the lecithin to sphinomyelin ratio tell you?
|
lung maturity
|
|
|
What are the major complications of preterm birth?
|
neonatal respiratory ditress syndrome
beronchopulmonary dysplasia brain hemorrhage necrotizing enterocolitis retinopathy of prematurity |
|
|
What are they main perinatal infections?
|
group B strep and herpes simplex virus
|
|
|
Whata are torches?
|
toxoplasmosis (Brain, hydrocephalus, scattered calcification)
other rubella 9deafness, cataracts, and cardiac malformation) cytomegalovirus (cerebral calcification, hepatosplenomegaly, chorioretinis) herpes syphilis |
|
|
What can cause fetal hydrops?
|
severe anemia, heart defect, pulmonary defect, chromosomal abnormality, infection (parvovirus 19)
|
|
|
What disease results in kernicterus?
|
hemolytic disease of the newborn
|
|
|
What is the most common benign tumor of childhood? What is the not regressing adult version?
|
strawberry hemangiomas
cherry hemangiomas |
|
|
What is the most common malignant tumor of childhood?
|
ALL
|
|
|
What does ESR measure?
|
degree of inflammation based on RBC rouleuax
|
|
|
What is the clinical presentation of SLE?
|
butterfly rash, glomerulonephritis, raynaud phenomenon, blood issues (anemia), serosal inflammation (fibrous percarditis), Libman-Sach endocarditis, joint symptoms, neurological and psychiatric manifestation
|
|
|
How do you diagnose SLE?
|
ANA, abs for dsDNA and anti-Smith antigen, increased IgG, decreased complement, direct immunofluorescence ( lupus band and glomerulonephritis), false positivie on syphilis test
|
|
|
What are the 2 subtypes of SLE?
|
discoid (skin only), and drug induced
|
|
|
What is diagnostic for drug induced lupus?
|
antihistone antibodies
|
|
|
What is the clinical presentation of Progressive Systemic Sclerosis aka Scleroderma?
|
lung scarrign --> interstitial pulmonary fibrosis
esophagal scarring --> dysphagia kidney arteriole narrowing --> malignant HTN skin --> fixed face and sclerodactyly |
|
|
What is the diagnosis of PSS aka schleroderma?
|
SCL-70 antibody anti-DNA topoisomerase antibody
dermis is 5x thickers onion skin fibrosis of vessels in vascular biopsy |
|
|
What is different about Crest from PSS?
|
no kidney invovlment
|
|
|
What is the mechanism of polymyositis and dermatomyositis?
|
immune cross reactionb etween tumor and muscle
|
|
|
What is the clinical presentation of dermatomyositis? What is the diagnosis?
|
muscle and skin involvement
heliotropic periorbital skin rash Gottron's papules on back of hands cancer anti-Jo-1 antibodies, 50% have ANA CD8 lymphoid inflammation and muscle atrophy |
|
|
What is the clinical presentation of Sjorgen's Syndrome? how do you diagnose? What is the variant?
|
dry eyes, dry mouth, and RA
SS-A and SS-B antibodies Sicca (without RA) |
|
|
Where is the defect in Bruton's?
|
tyrosine kinase gene
|
|
|
Is the CDC normal in Bruton's?
|
yes, lymphocyte count is normal. T cells make up for it.
|
|
|
what is the most common B cell inherited defect? What is the clinical presentation?
|
IgA deficiency
GI, Gu, and respiratory infection anaphylactic reaction during blod transfusion |
|
|
Where is the defect in hyper-IgM syndrome?
|
CD40 on B cells or CD40 ligand on T cells
|
|
|
What is the difference between common variable immunodeficiency and Bruton's?
|
normal level of mature B cells
|
|
|
what causes common variable immunodeficiency? What are the disease associations?
|
T cell signaling defect
autoimmune disorders and lymphoid malignancy |
|
|
What is Wiskott-Aldrich Syndrome? What is the presentation? What is the cancer associated?
|
X-linked recessive defect in IgM response to capsular bacter
low IgM and high IgE/IgA recurrent infection, thrombocytopenic purpura, and eczema nonhodgkin's lymphoma |
|
|
what is the clinical presentationof DiGeorge?
|
chromsome 22 deltion
cardiac defect, abnormal fascies, thymic hpoplasia --> normal ig, cleft palate, hypocalcemia. GVHD |
|
|
What is the importance of IL-12 receptor deficiency?
|
disseminated mycobacterial infection beccause of lack of normal Th1 response and macrophage activation
|
|
|
What is chrominc mucocutaneous candidiasis??
|
T cell dysfunction only against candida
|
|
|
What are the 2 causes fo SCID?
|
Adenosine deaminase deficiceny
cytokine receptor mutation (IL-2) |
|
|
What is the mechanism behind chronnic granulomatous disease?
|
lack of NADPH oxidase
|
|
|
What is the mechanism behind Chediak Higashi?
|
defect in microtbular function --> defect in phagolysosome formation
|
|
|
What is the clinical presentation of LAD?
|
recurrent bacterial infections, absent pus, delayed separationof umbilicus, poor wound healing
|
|
|
What is the disease association with C3 deficiency?
|
increased type III hypersensitivity because C3 opsonizes complexes
|
|
|
what is C5-C9 used for? What is the clinical presentationof its deficiency?
|
MAC neisseria infections
|
|
|
what handles the immediate and late reactions in type I hypersensitivity?
|
proteases, histamine
leukotrienes, prostaglandins |
|
|
What does desensitization therapy up and downregulate?
|
Th1, Th2
|
|
|
what type of hypersensitivity is Graves and myasthenia gravis?
|
II
|
|
|
What do immune complexes activate in Type III?
|
complement
|
|
|
What is the autobody associated with CREST?
|
anticentromere
|
|
|
What is the antibody associated with MCTD?
|
anti-ribonucleoprotein (U1RNP)
|
|
|
How do you detect amyloid?
|
EM, LM, congo red and apple green birefringence, electrophoresis with multiple myeloma only
|
|
|
What are the types of amyloidosis?
|
B-amyloid from alzheimer's (chromosome 21 Down's association)
AL-primary from Ig light chains and multiple myeloma (monoclonal expansino of malignant plasma cells) AA- secondary composed of serum amyloiud associated protein, synthesized by liver chronic inflammatory dieseases |
|
|
Who is at risk of GVHD?
|
Immune compromised (T cell deficiency) and especially bone marrow transplant
|
|
|
What is involved with hyperacute rejection?
|
preformed antibody with fibrinoid necrosis and PMN infilitration
|
|
|
What is involved with acute rejection?
|
Lymphocyte (B and T) response with dense lymphocytic infiltrate
|
|
|
what is involved with chronic rejection?
|
recurrent T and antibody mediated damaged to endothelium with vascular fibrosis, no cellular infiltrates
|
|
|
What is anasarca?
|
generalized edema of all tissue and organs (especially face which is not seen in systemic)
|
|
|
What is non-pitting edema with high triglyceride count? What produces that condition?
|
lymphedema
elephantiasis, lymphoma, removal of lymph nodes |
|
|
increased permeabilit of the endothelium produces what kind of edema?
|
exudate
|
|
|
what is active hyperemia?
|
previously inactive capillaries become open and fill with blood
|
|
|
What is congestion
|
increased volume in venous system due to impaired drainage
|
|
|
What are the compensatory mechanism of inadequate oxygenation?
|
RAAS, sympathetic vessel constriction, heart dilation and hypertrophy
|
|
|
How is left heart failure from right heart failure?
|
pulmonary edema
|
|
|
what are heart failure cells?
|
hemosiderin laden macrophages in lunds
|
|
|
What is nutmeg liver?
|
congestion in liver from RHF
|
|
|
What is cor pulmonale
|
RHF secondary to pulmonary HTN (often caused by LHF)
|
|
|
What is the diagnosis of CHF?
|
ejection fraction <40%
|
|
|
When is the retic count higher in hemorrhage?
|
chronic response
|
|
|
What are petechial hemorrhages?
|
small heorrhages of skin, mucous membranes, and serosal surfaces
|
|
|
Rank ecchymoses, purpura, and petechial hemorrhages in size?
|
ecchymoses > purpura > petechial hemorrhages
|
|
|
What are Virchow's Triad?
|
Endothelial injury, stasis, and hypercoaguble states
|
|
|
What type of thrombi are associated with lines of Zahn?
|
arterial
|
|
|
What are the types of thrombi?
|
mural
vegetation occlusive arterial venous |
|
|
What are the types of emboli?
|
thromboembolism ( pulmonary, saddle, and paradoxical)
systemic (from left atrium.ventricle) fat embolism (bone injury) amniotic fluid embolism (during labor or postpartum; associated with DIC) decompression sickness- nitrogen gas during diving |
|
|
What normally causes the clotting in DIC?
|
amniotic fluid
sepsis malignancies surgery SLE |
|
|
What are the lab findings in DIC?
|
decreased serum fibrinogen, decreased platelet count, prolong prothrombin time, increased fibrin split proudct, and increased D-dimer
|
|
|
What happens to CO, LVEDP, and PVR in hypovolemic shock?
|
decrease, decrease, increase
|
|
|
What happens to CO, LVEDP, and PVR in cardiogenic?
|
decrease, increase, increase
|
|
|
What happens to CO, LVEDP, and PVR in septic shock?
|
increase,same, decrease
|
|
|
Which (depolarizing or nondepolarizng) can be INITIALLY overcome by ACh?
|
nondepolarizing
|
|
|
What are the side effects of curare?
|
histamine release --> vasodilation --> bp drop
block sympathetics --> bp drop |
|
|
When is curare contraindicated?
|
myasthenia gravis
|
|
|
What drug causes initial fasiculation and then flaccid paralysis?
|
succinylcholine
|
|
|
What are the side effects of succinylcholine?
|
muscle pain, hyperkalemia, malignant hyperthermia
|
|
|
What is the MOA of acyclovir?
|
activated by viral TK which inhibits DNA polymerase and terminates viral DNA
|
|
|
What is the main AE of acyclovir?
|
crystal urea if you don't hydrate, hypersensitivty
|
|
|
What is the MOA of cidofovir?
|
nucleotide analog of CMP that inhibits DNA polymerase and chain terminator
|
|
|
What is the AE of cidoFOvir?
|
renal toxicity, give saline and probenecid
|
|
|
What is the MOA of FOscarnet?
|
pyrophosphate analog that inhibits DNA polymerase
|
|
|
What is the MOa of vidarabine? AE?
|
analog that only inhibits DNa polymerase, NOT A CHAIN TERMINATOR
Huge genetic toxicity and quickly metabolized |
|
|
What is the MOa of lamivudine?
|
RT inhibitor and chain terminator
|
|
|
What is the MOA of adefovir? AE?
|
nucleotide RTI
RT inhibitor and chain terminator renal toxicity |
|
|
What is ribavarin used for>?
|
HCV, only with inf-g
|
|
|
What is the AE of ribavarin?
|
anemia
|
|
|
What are the 2 neuramidase blockers?
|
oseltamivir and zanamivir
|
|
|
What is the CD4 count for treatment?
|
>350 or quick drop of more than 100 a year
|
|
|
What are main AEs of NRTIs?
|
lactic acidosis, hepatic steatosis, peripheral neuropathy & pancreatitis in didanosine and stauvidine, lipodystrophy in stauvidine, lamuvidine and emtricitabine are fine, abacavir = hypersensitivity, and tenofovir causes renal impairment. Also, didanosine is degraded by acid.
|
|
|
What are the AE of NNRTIs?
|
rash, hepatotoxicity, efavirenz causes dreams, CI with pregnancy, and don't take with fatty foods
indinavir and atazanavir cause hyperbilirubinemia. Consonant starting ones give you hepatotoxicity. Tipranavir gives you intracranial hemorrhage. Atazanavir gives you prolonged PR. Ritonavir is a CYP3A4 inhibitor. Also endocrine, fat problems. |
|
|
What is the name of FI?
|
enfuviritide
|
|
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What are the numerous AE of amphotericin B?
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Renal toxicity, fever sna drigors, thrombophlebitis, and anemia
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What does flucytosine use to activate itself?
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cytosine deaminase
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What is the MOA of azoles?
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inhibit sterol-14-alpha-demthylase to impair synthesis of ergosterol
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What is the MOA of echinocandins? AE?
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B1,3glucan synthesis inhibitor
HA, hepatotoxic, histamine at site |
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What are the kinetics/AE of griseofulvin?
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Take with fatty foods, increases drug metabolism, HA, hepatotoxic, and hematologic (basophilia with leuk and neutrapenia)
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