Midterm Flashcards
Huntingtons diseas
30-35 y/o
Striatal nuclei, loss of motion
Chorea (jerking movements)
Dementia
Toxoplasmosis
Toxoplasma gondi
Ghandi was the shit
Thalidomide
Pfizer drug given to pregnant women
Babies born with 1 eye no extremities
Parameningeal infection
Brain abscess due to improper treatment of pimples
Staphylococcus aureus
Streptococcus pyogenes
Sjogrën’s syndrome
Autoimmune
Females over 35
Total dryness of mucous membranes
Bilateral parotitis: inflamed parotid glands, look like hamsters
Local disease
Confined to one organ/region of the bady
Ex: stomach cancer
Focal damage
Limited to one or more distant sites within a diseased organ
Ex: one tumor in stomach
Diffuse damage
Uniformly distributed damage within a diseased organ
ENTIRE ORGAN IS AFFECTED
Ex: entire stomach is cancerous
Alkaptonuria
Oxidanormally phenylalanine is converted to tyrosine
However if oxidase is not produced, homogentistic acid (an intermediate), aka alkapton, is not converted
Homogentistic acid accumulates and is excreted in The urine causing urine to appear black
Homogentistic acid
Can accumulate in specific tissues causing ONCHRONOSIS
Cartilage is site of accumulation
Leads to osteoarthritis and sever degeneration
Calcifies IVDs
Alkapton deposits in ears
Ears look blue
Accumulation of normal metabolite
Alkaptonuria
Homogentistic acid
Activation of an alternative pathway
Phenylketonuria
Phenylketonuria
50% of phenylalanine is used
50% is converted to tyrosine
Non-production of the enzyme hydroxylase results in a switch to an alternative pathway
—> production of phenylpyruvic acid, phenyllactic acid and phenylacetic acid
Accumulation of metabolic byproducts
Gout
Gout
Metabolic disorder
3 factors:
1) gouty arthritis
2) deposition of uric acid salts in joints/ tissues
3) deposition of salts in kidneys–> renal failure
Impaired purine metabolism
Asymmetrical presentation
Tophus
Deposition in tissue
Tropism
Attraction
Malaria
Plasmodium (protozoa) in RBCs
Echinococcus
Meat with worms egg
Balloon shaped bodies
Hydropic changes
Aka cloudy swelling, hydropic degeneration
Nephron tubule cells
Steatosis
Residual bodies
Intracellular accumulation (inside cell)
Possibly due to damaged organelles
Remains of injury left inside the cell
Liver, kidney, nervous tissues
Hyalinization
Reversible change
protein accumulation
Intra (inside) or Inter cellular (in between)
Looks like hyaline cartilage under microscope but is not,
it is protein
Intracellular deposition
Reabsorption droplets Mallory alcoholic hyaline (mallory bodies) Russell bodies Dutcher bodies Waldenström macroglobulinemia Residual bodies
Reabsorption droplets
Aka minimal change disease
Renal proximal convoluted tubule cells
Abnormal protein loss in urine
Cells try to prevent loss and become filled with protein droplets
When no more protein is excreted in urine protein droplets are released back into urine and cells return to normal
Mallory alcoholic hyaline (bodies)
Found in liver hepatocytes
From drinking, reversible
Russell bodies
Deposition of protein into cytoplasm of cell
Seen in multiple myeloma
Dutcher bodies
Protein deposition into the nuclei of cells
Multiple myeloma
Uncontrolled proliferation and disorder function if plasma cells in bone marrow
Bence jones protein seen in urine
Waldenström macroglobulinemia
Aka: -hyper viscosity syndrome -lymphoplasmocytic lymphoma Type of lymphoma due to MONOCLONAL tumor Cancer of B lymphocytes resulting in overproduction of IgM antibodies Russel and dutcher bodies seen in this Bence jones protein seen in urine
Intercellular / extracellulardeposition
Irreversible structural changes
Lacunar infarct
Obstruction of lumen of small vessels
Ischemia/ infarction leads to tissue necrosis
Increased brittleness of vessels leads to intracerebral hemorrhagic stroke
Amyloid
The generic term for a variety of proteinaceous materials that are abnormally deposited in tissue interstitium in a spectrum of clinical disorders
Irreversible
Amyloidosis
Death within a year or two
Poliomyelitis
Irreversible loss of anterior horn of the spinal cord which provide motor function muscles atrophy without neuronal stimulation only prevented by vaccine
Hashimoto’s thyroiditis
Number one cause of hypothyroidism in the USA
Antibodies attack TSH receptors on the thyroid bind and block TSH
Discovered in 1913
Results and atrophy of the gland
Graves disease
2 to 1 ratio female to male
hyperthyroidism
Antibodies bind to TSH receptor’s in mimic TSH stimulate thyroid to produce excess amount of thyroid hormone thyroid gland hypertrophy’s characterized by toxic going to her and sometimes exophthalmos
Coagulative necrosis
Heart
Conservation of size shape and strength for several days
Characterized by denaturation of cytoplasmic proteins ,breakdown of cell organelles , cells swelling , infarct
White infarct
Occurs in tissue with a single blood supply example heart because only one vessel supplies at the coronary artery
Red infarct
Occurs in tissues with two or more vessels supplying it example longs or liver
Liquefactive necrosis
Brain
Complete digestion of dead cells resulting in transformation of the tissue into liquid viscous mass IE melting of tissue
Example stroke usually ski make type a.k.a. brain infarct formation of a cavity
Casseous necrosis
Lungs
Cheese like a Morphis granular debris coagulated sales debris enclosed within a distinctive inflammatory border known as granulomatous reaction
Tuberculosis leprosy
Gummatous necrosis
Syphilis : treponema palidum
Zenkers necrosis
Severe waxy or glassing the grossest of skeletal muscles in acute infectious disease is especially in typhoid or Colorado Dragon scale appearance
Fat necrosis
Stanton across this in the grossest of adipose tissue you characterized by formation of calcium soaps one fat is hydrolyzed into glycerol and fatty acid’s example is pancreatonecrosis
Fibrinoid necrosis
Heart
Occurs in the walls of blood vessels when endothelial or smooth muscle cells are injured or dining common with immunopathology’s such as rheumatic myocarditis from rheumatic fever
Formation of ASCHOFFS NODES
Aschoffs nodes
Nodes are seeing in intermuscular connective tissue surrounding inflammatory cells
Gangrene
A.k.a. gangrenous necrosis
A considerable mass of body tissue dies
Dry gangrene
A condition when coagulation is sustained
Caused by ischemia atherosclerosis and diabetes mellitus
Systemic sclerosis a.k.a. scleroderma
A form of dry gangrene is vasospasm and obliteration of small blood vessel’s due to too much production of stuff
Birthed s dis as
A.k.a. thromboangiitis obliterans form of dry gangrene seen in smokers results in development of antibodies that attack endothelial cells
What gangrene
Enzymes of invading phagocytic cells breakdown the necrotic to breed and produce some liquefaction an example would be bedsores or naked bones aka polyarteritie modosa
Anaerobic bacteria Clostridium perfringes and bacillus Fusiformis
Gas gangrene
Bacterial infection that produces gas within tissues
Anaerobic streptococci and Clostridium perfringes
Hernia
Apoptosis
Greek for falling off, pathway for cell death, seen in menstruation
Anthracosis
Deposition and accumulation of carbon in the tissues of lungs
Coal worker pneumoconiosis
Lung disease caused by inhalation of carbon particles
Brown atrophy
Lipofuscin a.k.a. lipochrome where in tear pigment free radical peroxidation of poly unsaturated lipids of sub cellular membranes
Homogentisic acid
Black and abnormal pigment onchronosis, alcaptonuria leads to disc calcification
Hemosiderin
Excessive iron
Hemosiderosis
Deposition of hemosiderin in many organs and tissues in the cases of systemic overload of iron does not affect tissue function
Hemochromatosis bantu siderosis
Bantu siderosis
Primary hemochromatosis is genetic seen in males 7 to 1 increased absorption of iron in the G.I. tract up to 50 mg one normal is 5 to 6 accumulation of iron in the liver leads to cancer
Secondary hemochromatosis is acquired a.k.a. transfusion reaction seen in malaria hemolytic anemia ingestion of alcohol kept an iron barrels this is bantu siderosis
Wilson’s disease
A.k.a. hepatolenticular degenerationrare genetic disease and males copper does not bind to alpha-2 globulin copper ring at periphery of cornea KAISER FLEISCHER RING
Damage of midbrain ganglia resulting in motor dysfunction Parkinson’s like syndrome
D-PENICILLAMINE!!!!
Dystrophic calcification
Deposition of calcium salts into necrotic or atrophic soft tissues
Ghons focus
Systemic scleroderma aka sclerodactyly
Calcific stenosis of heart valves
Ghon’s focus
Found in lungs
Metastatic calcification
Hypercalcemia deposition of calcium into tissues that are not necrotic are trophic example kidney stone increase the creation of PTH
destruction of bone
vitamin D related disorders
sarcoidosis
Renal failure in secondary hyperparathyroidism
Two components of information
One vascular component to cellular component
Exudate
Protein rich fluid and blood cells and sometimes micro organism specific gravity 1.020
Transudate
Not protein rich specific gravity less than 1.012
Serous inflammation
Large amount of watery exudate
Response to mild injury
Example common cold watery discharge from eyes and nose or second-degree burns blisters
Fibrinous inflammation
Fibrinogen in the exudate
Enzymatic formation of fibrin strands can be dangerous
Example dramatic pericarditis
Suppurative inflammation
PUS
Three types
Abscess: localize accumulation of pus that develops at a focus
Cellulitis: diffuse, widespread suppurative inflammation
Empyema: in 2 cavities
Plueral and subdural
Hemorrhagic inflammation
Accumulation of red blood cells at site of information right blood cells do not participate in inflammatory response
Neutrophils
55 to 60% in circulation first to arrive at the site of inflammation lifespan eight hours to three days 3 to 4 lobes
Eosinophils
Red granules
2 lobes
2-4%
Basophils
Blue granules
2 lobes
.5-1%
Mononuclear cells
Are agranular
Lymphocytes and monocytes
Lymphocytes
20 to 25%
Monocytes a.k.a. macrophages
4 to 8% in circulation largest cells and blood
lifespan is years
second to arrive at the site of inflammation
antigen presenting cells
Oxygen independent
Enzymes
Defensin
Oxygen dependent
Anions
Chronic granulomatous disease of children
Not able to produce free radicals
Chediak-Higashi syndrome
Impairment of cell motility
White blood cells are not able to degranulate
Phagocytic cells
Neutrophils
Monocytes/ macrophages
Eosinophils
Serotonin
Produced by platelets
Substance P
Neuropeptide promotes pain
Nitric oxide
Mediator of sympathetic nervous system inhibitor of cellular components of inflammation
Bronchospasm
Caused by histamine PGD2 and Lucotirenes
Prostacyclin a.k.a. PGI 2
Opposite is thromboxane
Causes vasodilation platelet inhibition
Phospholipases
Are inhibited by steroids
PGD2
Mast cells bronchospasm baldness
PGE2
Hyperalgesia a.k.a. pain fever and induces labor
PGF 2alpha
Corpus luteum luteolysis
Stops production of progesterone induces labor
Lymphangitis
Appears as a red rope
Lymphadenitis
Large and painful if painless it means cancer
Leukocytosis
Increased leukocytes in blood greater than 9000 per cubic millimeter
Neutrophilia
Percentage more than 60 in blood can increase up to 80 to 90% of circulating white blood cells
Eosinophilia
Parasitic infection
Monocytosis
Chronic bacterial infection can increase up to 50% of circulating white blood cells infectious mononucleosis lymphadenopathy of neck and upper thoracic lymph nodes
Chronic inflammation
Duration 6 to 8 weeks does not contain exudate
Arises from viral infection or persistent microbial infection due to prolonged exposure to potentially toxic agents or autoimmune disease is
Aseptic osteonecrosis
Compressed blood vessels leads to infarction dissolution of bone without infection joint and bone loss
Acute inflammation
Duration 7 to 10 days contains exudate
Revascularization
A.k.a. angiogenesis occurs in a loosely jailed protein rich exudate that forms at the David site granulation tissue
Primary healing
Healing of incision or severing wound of the skin
Secondary healing
Wound edges are not closely opposed asymmetrical healing right angles
Contracture
Newly formed college and demonstrates an exaggerated wound contraction response as it matures
Stricture
Narrowing of lumen of Organ and example is hourglass stomach
Adhesions
Joining of serous membrane’s restriction of movement and structures
Dehiscence
Breaking open of a healing wound possibly due to pressure on the wound
Keloids
Result from the overproduction of dermal college in during healing transforming growth factor beta
Proud flesh
Overproduction of granulation tissue you exuberant granulations
Herniation
Displacement of an organ from its normal body cavity
