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10 in 2010

Exam 2

Peptic Ulcer Open sores on lining of stomach, small intestine and/or esophagus; can result in internal bleeding and if penetrates organ wall peritonitis; scar tissue.
Pernicious anemia Disruption of formation of RBC in bone marrow due to deficiency in vitamin B12. Can be caused by autoimmune gastritis-antibodies against the H+/K+ATPase->HCl in gastric juice (achlorhydria)and lack of synthesis of intrinsic factor.
Zollinger-Ellison syndrome Gastrin-secreting tumors (aka gastrinomas) of pancrease. Hyperplasia and hypertrophy of fundic region; complications include fulminant (sudden onset) stomach ulceration...
Zollinger-Ellison syndrome Causes Diarrhea (gastrin causes the inhibition of water and electrolyte absorption in intestine), steatorrhea (inability to absorb fat due to inactivation of pancreatic lipase by low pH), and hypokalemia (lower than normal level of K+ in the blood)
Zollinger-Ellison syndrome H+ secretion continues regardless of H+ of stomach since pancreatic gastrin is not regulated by negative feedback.
Peptic ulcers Burning pain from breastbone to naval; worse when stomach is empty; improves with food that buffers stomach contents Majority due to bacterial infection (H pylori...)or medication (NSAIDS); 1/5 of people under 30 infected; 1/2 over age of 60
Peptic ulcers stress, smoking, and spicy foods can aggrevate but DO NOT cause. Treatment includes appropriate antibiotics or antifungals; proton-pump inhibitors; antacids
Gastric Reflux Due to extensive gastroesophageal reflux-symptoms include heartburn, indigestion, or gas; burning sensation below and behind the breastbone (sternum); treatment - antacids and acid blocking drugs.
Gastric reflux Barett's esophagus due to a change in epithelium of esophagus (Stratified Squ -> simple columnar)-this change is not accompanied by new symptoms. Patients are at high risk for esophageal adenocarcinomas (risk is 30-125X higher); usually found late
Gluten enteropathy Results from destructive effects of certain glutens (esp rye and wheat) on intestinal villi. Reduces surface area available for absorption. Treated by eliminating wheat and rye from diet
Inflammatory Bowel Disease includes; ulcerative colitis and Crohn's diesease. Clinically characterized by diarhhea, pain and periodic relapses.
Inflammatory Bowel Disease Ulcerative collitis can affect mucosa of large intestine. Crohn's disease affects any segment of the intestinal tract (small or large)
Crohn's Disease Chronic inflammatory process with immune system cells (lymphocytes, neutrophils, and macrophages)producing cytokines damaging intestinal mucosa, progressing into submucosa and musclaris externa; presence of granulomas (lymphocyte aggregates) typical feat.
Crohn's Disease Complications include: occlusion of intestinal lumen by fibrosis, formation of fistulas and intestinal performation
Hirschsprung's Disease (congenital megacolon) Caused by mutation in 1-4 genes preventing migration and differentiation of neural crest cells into neurons of enteric nervous system. It is also called aganglionosis
Hirschsprung's Disease Aganglionic segment is permanently contracted and therefore does not allow entry of contents resulting in abnormal form of constipation. Usually seen shortly after birth. Infants abdomen becomes distended and little meconium is eliminated.
Hirschsprung's Disease Biopsy of mucousa and submucousa confirms diagnosis-thick and irregular nerve bundles and lack of ganglion cells. Treatment is surgical removal of affected region of colon.
Colorectal carcinoma Second highest cause of cancer death in the US (3rd most frequent in men; 2nd most frequent in women);140,000 cases diagnosed in US yearly; usually 55 and older affected
Colorectal carcinoma Usually arises from adenomatous polps; may be asymptomatic for years; rectal bleeding frequently present. Probably diet-related (high-fat, refined carbs and low in fiber)
Diverticulosis Herniation of muscle wall of colon; mucosa and or submucosal layers protrude thru weak sites in muscle wall.
Diverticulitis inflammation at site of diverticulosis, affects 10% of US > 40 yr; by 60 ~50%.
Diverticulosis/itis abdominal pain and tenderness in left lower side of abdomen; cramping, nausea, vomiting, fever, chills, change in bowel habits; complications include bleeding, infections, perforations, blockage of colon Theory of cause: consumption of low-fiber diet.
Diverticulosis/itis Treatment--Eat more fiber!
Appendicitis Inflammation of appendix due to blockage or previous infection. Symptoms: abdominal pain that originates in navel and shifts to lower right abdomen; pain increases over 12-18 hours becoming severe.
Appendicitis complications-rupture of appendix leading to abscess and/or peritonitis. Treatment-surgical removal
Salivary gland tumors 80% of tumors are benign, most orginate in parotid; most are pleomorphic containing ducts, CT elements (ground substance and collagen), and myoepithelial cells; most common treatment is surgical removal.
Sjogren syndrome major symptoms are xerostommia and dry, gritty eyes; component of systemic disease, second most common autoimmune disease, female dominant
Acute pancreatitis an inflammatory condition of exocrine pancreas that results from injury to acinar cells. Acinar cell injury and duct obstruction are the major initiators.
Acute pancreatitis Some causes: (1) secretion against obstruction (gallstone); (2) inappropriate activation of proenzymes; (3) AIDS; (4) ethanol. Most common causes are alcohol abuse and bile duct obstruction.
Cystic fibrosis (CF) 80% of CF patients have visible secretory abnormalities of the pancreas; CF causes mucous inspissation (′inspi′sāshən) in ducts and secondary atrophy of exocrine glands, atrophy of glands due to blocking lumens.
Centrilobular Necrosis Hepatocytes in Zone 3 undergo ischemic necrosis, in for example, congestive heart failure when they do not receive proper oxygen. No changes of cells in Zones 1 and 2*more added later
Alcoholic hepatitis a) swollen (balloon cells) hepatocytes in centrilobular region, b) Mallory bodies in hepatocytes, c) neutrophils present, d) collagen deposited (fibrosis) around central vein, e) some hepatocytes become fat cells.
Cirrhosis death of hepatocytes leading to scarring or increased production of collagen destroying normal architecture.
Cirrhosis is scarring of the liver and poor liver function as a result of chronic liver disease When symptoms do occur, they can •Abdominal indigestion or pain •Confusion or problems thinking •Impotence, loss of interest in sex, and breast development in men
Cholecystitis gallstone impacted in cystic duct leading to: a) thickened muscular layer due to trying to overcome pressure, b) impaired breakdown of fat, c) high pressure in gall bladder rearranges mucosa.
Role of hepatic stellate cells in portal hypertension •hepatic stellate change function/type to lay down matrix and affect sinusoids
α-1 Anti-trypsin (AAT) deficiency AAT is produced in the liver and one of its functions is to protect the lung from neutrophil elastase activity;50% of patients will develop liver cirrhosis. The ATT accumulates in the liver in PAS positive globules.
α-1 Anti-trypsin (AAT) deficiency Treatment for AAT deficiency is pooled AAT given intravenously and liver and lung transplantation.
X-linked Myotubular Myopathy • defect in lipid phosphatase  embryonic muscle tissue 1:50,000 male live births; females are carriers gene Xq28; 80% of affected individuals have mutation in MTM1 gene  encodes myotubularin protein  lipid phosphatase
X-linked Myotubular Myopathy identified in 1966 by muscle biopsy showing centrally located nucleus in skeletal muscle that resembles the fetal stage of muscle development Diagnosed by “floppy” male infant followed by needle biopsy
X-linked Myotubular Myopathy low muscle tone w/ delayed developmental milestones, fatal in first 2 yr; respiratory failure.
Duchenne’s muscular dystrophy X-linked recessive disorder (Xp21)  mutation in gene that encodes the protein dystrophin  progressive muscular weakness (no longer able to anchor actin to extracellular matrix) Disruption of sarcolemma; Ca+2 enters cell; necrosis occurs
Duchenne's muscular dystrophy Primarily affects males – onset between 3-5 years of age; unable to walk by 12; require respirator to breath by age 20
Duchenne's muscular dystrophy increased serum creatine kinase levels heterogeneous group of congenital muscle diseases characterized by severe muscle weakness, atrophy & destruction of muscle fibers.
Duchenne's mucular dystrophy caused by genetic defects in muscle transmembrane proteins linking dystrophin to laminin; no cure; large calf muscles; usually die of pneumonia or heart complications
Boutulism • Food poisoning caused by Clostridium botulinum toxin (BOTOX)  inhibits ACh release at neuromuscular junctions
Boutulism Light chain of toxin cleaves Snap-25, preventing docking of Ach vesicles on presynaptic terminal membrane; Characterized by muscle paralysis, vomiting, nausea, & visual disorders; Fatal if untreated;
Boutulism treatment – hospitalization, antibiotics, antitoxin (antidote to botulinum toxin) Weaponized (US WWII; Iraq used in 1990)
Myasthenia gravis Autoimmune disease; -ACh receptor antibodies produced Abs bind & block access of ACh to receptor
Myasthenia gravis Characterized by extreme muscle weakness, decrease in number of neuromuscular junctions, ptosis (drooping upper eye lid) & diplopia (single object seen as two)
Myasthenia gravis Treatment: AChase inhibitors, thymectomy, anticholinesterase drugs, immunosuppresive drugs, plasmapheresis (removal of Abs), IV immune globulin
Rhabdosarcoma – cancer arising from striated muscle • Most common type of childhood sarcoma; can occur anywhere in body; in US ~ 350 children diagnosed/year
Rhabdosarcoma – cancer arising from striated muscle • Symptoms include: lump or swelling that continually increases in size, eye bulging, headache, problems urinating or with bowel movements, blood in urine, bleeding in nose, throat, vagina or rectum; histology positive for IF desmin
Rhabdosarcoma – cancer arising from striated muscle • 3 types: Embryonal – most common; occurs most often in head, neck, genital or urinary regions alveolar – common during teens; occurs in arms, legs, chest, abdomen, genital or anal regions anaplastic – rare in children
Rhabdosarcoma - cancer arising from striated muscle • Treatment: surgery, radiation therapy and chemotherapy; new treatments include: high dose chemotherapy with stem cell transplant (blood, bone marrow)
Central Core disease • Autosomal dominant/recessive mutation in ryanodine receptor • Onset – congenital; symptoms – poor muscle tone and weakness in infants; delay in attainment of motor milestones; skeletal deformities (joint dislocations & scoliosis)
Central Core disease Patients susceptible to malignant hyperthermia with some anesthetics H&E appearance – faint central abnormality in myofibers; Myosin ATPase stain reveals central round areas devoid of staining Susceptible to malignant hyperthermia (elevated body temp)
Nemaline Myopathy • Congenital, herediatary disease (1:50,000) due to mutations in nebulin • Characterized by delayed motor development, muscle weakness in arms, legs, trunk, throat, and face muscles (usually non-progressive)
Nemaline Myopathy Trunk muscle weakness leads to respiratory issues without therapy and/or intervention Histology – muscle biopsy reveals thread-like rods called nemaline bodies (positive for actin and -actinin) No cure
Desmin-related Myopathy • Autosomal recessive & dominant forms • Mutation in desmin that prevents its forming intermediate filament rods; instead forms intracytoplasmic desmin aggregates in skeletal & cardiac muscle
Desmin-related Myopathy • Desmin normally found around Z-line; connects Z-lines to cytoskeleton underlying plasma membrane; signaling thru desmosomes
Desmin-related Myopathy • Histology – sarcomers misaligned; loss of Z-lines and normal striated appearance; muscle cells die by apoptosis and necrosis; desmin inclusion bodies in skeletal and cardiac muscles
Desmin-related Myopathy Characterized by weakness and atropy of distal muscles of legs, arms, trunk and neck Respiratory issues due to trunk muscle weakness and loss ~60% of patients also have cardiac involvement; most patients ultimately require wheelchair, walker, etc
Myocardial infarction Irreversible necrosis of cardiac muscle cells due to prolonged ischemia (> than 20 mins) (ischemia= lack of blood supply) Detect lactic dehydrogenase-1 and creatine kinase in serum.
Myocardial infarction Fatal if extensive damage to cardiac muscle Treatment: bypass surgery
Pompe's disease • Loss of acid maltase in muscle  inability to process carbohydrates • Affects storage and breakdown of glycogen in lysosomes (AKA lysosomal storage disease) • In absence of acid maltase, glycogen accumulates & is not converted to glucose
Pompe's disease • Onset in infants – usually fatal by 2; child & adult onset less severe • Characterized by slow progressive weakness in respiratory muscles, hips, upper leg & arms, shoulders; cardiac involvement in childhood forms
Naegeleria Fowleria Infection • N. fowleri (a protist, sometimes called the “brain-eating ameba”) • invade the cental nervous system via the nose, more specifically the olfactory mucosa and cribriform plate of the nasal tissues
Naegeleria Fowleria Infection • The penetration initially results in significant necrosis of and hemorrhaging in the olfactory bulbs. • From there, amoebae climb along nerve fibers through the floor of the cranium via the cribriform plate and into the brain.
Naegeleria Fowleria Infection • The amoebae begin to consume the cells of the brain piecemeal by means of a unique sucker apparatus extended from their cell surface. • It then becomes pathogenic, causing primary amoebic meningoencephalitis (PAM).
Naegeleria Fowleria Infection • PAM is a syndrome affecting the central nervous system, characterized by changes in olfactory perception (taste and smell), followed by vomiting, nausea, fever, headache, and the rapid onset of coma and death in two weeks.
Sinusitis • Maxillary sinus most often involved in adults, ethmoid sinus in children • Blockage of drainage via paralysis of ciliary elevator or viral/bacterial upper respiratory infection or deviated septum.
Sinusitis • Results in fever, nasal congestion, pain over sinus. • Sinuses become congested with mucous and bacterial growth.
CF • Chronic obstructive pulmonary disease of children & young adults • Nasal polyps are associated with it. • Nasal polyps in a child warrant a sweat test to rule it out
CF •What is another name for it? mucoviscidosis •Defective transmembrane pumps for Cl-; decrease Cl- secretion, ^ water & Na+ reabsorption thus mucous is dehydrated & viscous Mucociliary escalator malfunctions & unusually thick mucous builds up
– Respiratory Distress Syndrome in newborns/infants •Decreased synthesis of surfactant resulting in collapse (atelectasis)intrapulmonary shunting •Causes: Prematurity, Maternal diabetes, Cesarean Section-lack of stress-induced ^^ in cortisol from vaginal delivery
– Respiratory Distress Syndrome in newborns/infants •Gross: Purple-Red Lungs, liver-like, ruddy; Microscopic: Alveoli lined by hyaline membranes. •Formerly called hyaline membrane disease. •
– Respiratory Distress Syndrome in newborns/infants Due to an inadequate supply of surfactant at birth which can be related to deficient surfactant production or failure of Type II pneumocytes to develop and mature.
– Respiratory Distress Syndrome in newborns/infants •Signs include cyanosis and labored breathing, caused by inability of pulmonary alveoli to expland or remain open after inspiration. •Require more pressure to inflate
– Respiratory Distress Syndrome in newborns/infants • Diffuse atelectasis occurs initially and progresses. • The lack of oxygen damages endothelial cells and pneumocytes  exudation of a fibrinous matrix from the bloodmatrix accumulates & creates a thick "hyaline membrane" lining the alveoli
RDS •Hyaline membranes are formed within a half hour after birth. •Some healing or regeneration of Type II cells can occur within 36-72 hours. •Type II cells then give rise to type I •Good ratio- Lecithin: Spingomyelin 2:1
α1-Antitrypsin Deficiency leading to Emphysema •Emphysema – Permanent enlargement of alveoli or air spaces, caused by obstructed air flow & destruction of the alveolar wall •Wall of pulmonary vessels thickens
α1-Antitrypsin Deficiency leading to Emphysema •Alpha 1-antitrypsin (produced in liver) inactivates neutrophil elastase •Defect in α-1-AT Elastic fibers are replaced with CT  Emphysema •Elastin proteins are in the alveolar septa •Most common cause is smoking cigarettes
ARDS – Adult Respiratory Distress Syndrome •Smoking  inflammation Neutrophils Secrete elastase (protease) Elastin in wall degraded •hyaline membranes appear
. Atelectasis • loss of lung volume due to inadequate/incomplete expansion of air spaces (collapse of alveoli)
Early Stages of Acute Pneumonia Pneumonia= inflammation of the lungs Alveoli fill with exudates containing wbcs (mainly neutrophils) and rbcs= hepatization
Early Stages of Acute Pneumonia The lung has enlarged, congested capillaries giving it a red color; firm, heavy alveoli are dysfunctional because they are swollen w/ neutrophils, rbcs, and fibrin
Mesothelioma •malignant tumor that originates in the mesothelial lining of the serous membranes (pleura, peritoneum, pericardium). •90% of malignant mesotheliomas are pleural mesotheliomas. •
Mesothelioma Pleural mesothelioma is associated with long time exposure (25 to 40 yrs) to asbestos.
Mesothelioma • can spread to pericardium and diaphragm and invade the subpleural lung tissue and metastasize to any organ. • Imaging of the thorax detects thickening of the pleura and/or asbestos plaques.
Mesothelioma • No etiologic relationship with smoking. • Symptoms include pleural effusion (abnormal liquid in the pleural space), chest pain, dyspnea.
Bronchiectasis •Permanent dilation of the bronchi and bronchioles, due to destruction of cartilage and elastic tissue by an infection; •Causes: CF, TB, obstruction by a carcinoma, primary ciliary dyskinesia;
Bronchiectasis •Most common in lower lobes •Note dilated airways, some filled with pus
Atheroscelerosis •Disease of large & muscular arteries •Accumulation of smooth muscle cells, CT, & lipids in the intima •Macrophages & smooth muscle cells accumulate lipid (mostly LDL)
Atheroscelerosis •Foam cells- macrophages filled w/ lipid •Fatty streaks- first sign of atherosclerosis, lesions in intima containing accumulations of lipid •Fibrofatty plaque- necrotic core w/ cap of foam cells, smooth muscle cells, & lymphocytes
Atheroscelerosis •Can cause ischemic heart disease, MI, stroke, gangrene of limbs •Ischemic heart disease- imbalance b/t supply & demand of heart for oxygenated blood; most common cause is atherosclerosis; coronary arteries narrow due to fibrofatty plaques
Marfan Syndrome •Fibrillin disorder •faulty tunica media = vessels dissect •Mitral valve disorders = prolapse or redundant •Changes in chordae tendinae •Most common cause of death- aortic dissection
Vessel Aneurysms •A localized or diffuse dilation of an artery with a diameter at least 50% greater than the normal size of the artery; •due to weakening of the vessel wall, followed by dilation and a tendency to rupture •
Vessel Aneurysms 2 causes are atherosclerosis and bacterial/fungal infection
Vessel Aneurysms •most common aneurysm in men > 55 is the abdominal aortic aneurysm. •mycotic aneurysm- caused by fungi •syphilitic aneurysm (aorta)- T. pallidum obliterates the vaso vasorum.
Thrombosis •Thrombus- intravascular mass attached to the vessel wall. •composed of varying proportions of coagulation factors, rbcs, and platelets. •Can be caused by endothelial cell injury, especially arterial thrombi.
Embolism •a detached mass (e.g. clot, fat, gas) carried by the blood to a distant site. •lodge in various places: atrium, microvasculature throughout body, pulmonary system
Hypertension •Aka high blood pressure > 140/90 •Occurs in 25% population •Multiplication of smooth m. occurs and tunica media increases in thickness, smooth m. cells accumulate lipid; •Lumen is reduced
Hypertension •intimal thickness occurs in fat-free diet; •cardiac m. cells increase in size and number (hyperplasia) thus walls are less elastic & require more work to pump blood
Aschoff body •typical lesion of rheumatic myocarditis. •Consists of degenerated collagen surrounded by lymphocytes, plasma cells, and histiocytes. •Amongst these cells the Anitschkow cell is found; this cell is a large histiocyte and may be multinucleated. •
Aschoff body It has a ribbon-like or caterpillar-like nucleus and the nucleus is quite evident, like an owl’s eye
Raynaud's Phenomenon •reversible ischemia of peripheral arterioles usually involving fingers and toes •skin arterioles go into vasospasm •associated with another illness or secondary to another disease and the most common is an autoimmune disease
Lymphedema •a defect in the transport of lymph because of abnormal lymphatic vessel development or damaged lymphatic vessels •accumulation of fluid and proteins in the ECM or interstitial spaces leads to it
Lymphedema •chylothorax ( an accumulation of high fat containing lymph or chyle in the thorax) can be the result of abnormal development of lymphatic vessels or it can be the result of obstruction, trauma.
Lymphedema •How fast can chyle accumulate in the thorax or pleural cavity if the thoracic duct is lacerated by accident or lung surgery? 75-300mL/hr
Giant cell arteritis (GCA) •GCA is also called temporal arteritis, cranial arteritis, and granulomatous arteritis. •GCA is a systemic inflammatory vasculitis of unknown etiology that affects medium- and large-sized arteries.
Giant cell arteritis (GCA) •it is a disease of the over 50 age group and can result in a wide variety of systemic, neurologic, and ophthalmologic complications. •Visual loss is one of the most significant causes of morbidity in GCA.
Giant cell arteritis (GCA) • Permanent visual impairment may occur in as many as 60% of patients. • GCA typically involves inflammation of the aortic arch and its branches, but almost any artery of the body as well as some veins may be affected occasionally.
Giant cell arteritis (GCA) •The inflammation tends to involve the arteries in a segmental or patchy manner, although long portions of arteries may be involved. •
Giant cell arteritis (GCA) The likely determinant of arterial susceptibility to it is the presence and/or quantity of internal elastic lamina within the vessel wall
Giant cell arteritis (GCA) •intracranial cerebral vasculature is not affected in it because these vessels lack an internal elastic lamina.
Giant cell arteries (GCA) The extracranial vertebral arteries, superficial temporal arteries, posterior ciliary arteries, and ophthalmic arteries are the most commonly involved arteries.
Giant cell artreies (GCA) •it reveals inflammatory infiltrate surrounding a fragmented internal elastic lamina within the media of an arterial wall. •The infiltrate consists predominantly of mononuclear cells with giant cell formation.
Portal Hypertension Stellates lose storage function and begin to produce collagen and ECM material; also convert to myofibroblasts and constrict sinusoids. •Matrix increase and constriction leads to portal hypertension
alpha-1 anti-trypsin AAT • 50% of patients will develop liver cirrhosis. • The ATT accumulates in the liver in PAS positive globules. • Treatment for AAT deficiency is pooled AAT given intravenously and liver and lung transplantation
Centrilobular •Hepatocytes in Zone 3 (closest to central vein) undergo ischemic necrosis, in for example, congestive heart failure when they do not receive proper oxygen. •No changes of cells in Zones 1 and 2 •
Centrilobular This disease supports the liver acinus theory of liver lobulation
Created by: vpack87



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