Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
194 Cards in this Set
- Front
- Back
|
Path:quiz1|IFN-g|secreted by Th1, NK cells
|
acts on Bcells, macros
|
|
|
Path:quiz1|TGF-b| secreted by Th2 cells, endothelial cells, platelets, macros
|
acts on plasma cells, Th1 cells
|
|
|
Path:quiz1|PAF| derived from phospholipids, acts on platelets, endothelial cells
|
stimulates platelets, causes vasoconstriction, increases ICAM expression|UW
|
|
|
Path:quiz1|LTB4|acts on vascular endothelium and neutrophils
|
leukocyte chemoattractant|UW
|
|
|
Path:quiz1|what are the major histopathologic components of alcoholic hepatitis?| scattered foci of hepatocyte swelling/necrosis
|
Mallory bodies, fibrosis (typically around the central vein), neutrophilic rxn in and around the foci of necrosis| UW
|
|
|
Path:quiz1|molecules of leukocyte adhesion| endothelial molecule: ICAM-1
|
Leukocyte receptor: integrins (CD11, CD18, LFA-1)| UW
|
|
|
Path:quiz1|molecules of adhesion: eosinophils, monocytes, lymphocytes| endothelial molecule: VCAM
|
leukocyte receptor: VLA4| UW
|
|
|
Path:quiz1|molecules of lymphocyte homing to high endothelial venules| endothelial molecule: GlyCam-1
|
Leukocyte receptor: L-selectin| UW
|
|
|
Path:quiz1|NLRs|NOD-like receptors
|
found in cytosol, bind: 1)peptidoglycan 2)flagelin 3) DAMPs|UW
|
|
|
Path:quiz1|RLRs|RIG-like receptors
|
found in nucleus, cytoso, bind ssRNA, dsRNA, 5'ppp ssRNA|UW
|
|
|
Path:quiz1|TNF antagonists|useful for Tx of RA, psoriasis, Crohn's
|
Risks: induced SLE (rare), increased reactivation risk for TB. NO BENEFIT FOR SEPSIS|UW
|
|
|
Path:quiz1| coagulation necrosis| preservation of the structural outline of dead cells, usually resulting from loss of blood supply
|
occurs due to denaturation of enzymes and structural proteins by intracellular accumulation of lactate of heavy metals. Inactivation of cellular enzymes prevents autolysis|UW
|
|
|
Path:quiz1| caseous necrosis: most common cause?| TB
|
caseous material is formed by the release of lipid from the cell walls of M tuberculosis and systemic fungi (Histoplasma) after destruction by macros| UW
|
|
|
Path:quiz1| enzymatic fat necrosis: gross and microscopic appearance| chalky yellow-white deposits in peripancreatic and omental adipose tissue
|
pale outlines of fat cells filled with basophilic staining calcified areas| UW
|
|
|
Path:quiz1| enzymatic markers of cell death: AAT| 1) aspartate aminotransferase: marker of diffuse liver cell necrosis (viral hep)
|
is a mitochondrial enzyme preferentially increased in alohol-induced liver disease| UW
|
|
|
Path:quiz1| reversible injury vs irreversible injury: ER| Rev: dilation with detachment of polysomes
|
Irrev: disruption and fragmentation| UW
|
|
|
Path:quiz1| cyanosis + chocolate colored blood| methemoglobinemia
|
skin does not return to normal after O2 administration| UW
|
|
|
Path:quiz1| uncoupling agents| ex. Thermogenin in brown fat
|
allow protons into mitomatrix without passing through ATPsynthase. Energy is released as heat rather than ATP synthesis| UW
|
|
|
Path:quiz1| 85% of pts with follicular Bcell lymphoma have...| 14
|
18 translocation which juxtaposes bcl2 with Ig heavy chain genes, leading to bcl2 overexpression. Resulting inhibition of cell death leads to malignant transformation in long surviving cells.|UW
|
|
|
Path:quiz1| Histamine is made by...| mast cells
|
basophils
|
|
|
Path:quiz1|IL-1|secreted mainly by macrophages
|
acts on endothelium
|
|
|
Path:quiz1|IL-1ra| IL-1 antagonist
|
so anti-inflammatory|UW
|
|
|
Path:quiz1|IL-2|secreted by Tcells
|
acts on Tcells
|
|
|
Path:quiz1|IL-4|secreted by Th2 cells
|
acts on Bcells
|
|
|
Path:quiz1|IL-5|secreted by th2 cells
|
acts on eosinophils
|
|
|
Path:quiz1|IL-6|secreted by activated macros
|
acts on lymphocytes
|
|
|
Path:quiz1|IL-10|secreted by Tregs
|
is anti-inflammatory cytokine
|
|
|
Path:quiz1|IL-12|secreted by DCs
|
macros
|
|
|
Path:quiz1|G-CSF|secreted by lymphos and stromal cells
|
acts on progenitor cells
|
|
|
Path:quiz1|GM-CSF|secreted by NK cells
|
acts on eosinophils
|
|
|
Path:quiz1|TNF|secreted by macros
|
mediates septic shock
|
|
|
Path:quiz1|IFN-g|secreted by Th1
|
NK cells; acts on Bcells
|
|
|
Path:quiz1|IFN-a and IFN-b|A type 1 interferon secreted by virus infected cells
|
acts on NK cells to increase cytotoxicity and causes increased Ag presentation|UW
|
|
|
Path:quiz1|TGF-b| secreted by Th2 cells
|
endothelial cells
|
|
|
Path:quiz1|MCP-1| monocyte chemoattractant protein
|
attracts monos
|
|
|
Path:quiz1|PAF| derived from phospholipids
|
acts on platelets
|
|
|
Path:quiz1|PGI2|vasodilator
|
inhibitor of platelet aggregation|UW
|
|
|
Path:quiz1|thromboxaneA|vasoconstrictor
|
signals platelet aggregation|UW
|
|
|
Path:quiz1|morphological types of necrosis and most common cases| coagulative(heart
|
liver
|
|
|
Path:quiz1|CF: clinical picture| bronchiectasis
|
nasal polyps
|
|
|
Path:quiz1|CF: pathophysiology| Cl channel. In sweat ducts
|
lets Cl IN
|
|
|
Path:quiz1| familial hypercholesterolemia: clinical picture| hypercholesterolemia
|
soft tissue xanthomas
|
|
|
Path:quiz1|familial hypercholesterolemia: pathophysiology| LDLR issue
|
so liver cannot see systemic cholesterol
|
|
|
Path:quiz1|regulatory effects of cholesterol| neg feedback: HMG CoA Reductase and LDL Receptors
|
pos feedback: ACAT (cholesterol -> cholesterol esters)|UW
|
|
|
Path:quiz1|dystrophic calcification| calcium loves to bind the phospholipids products of necrosis and become crystalline CaPO4
|
also atheromas in advanced atherosclerosis (that's why vessels get crunchy). |UW
|
|
|
Path:quiz1|metastatic calcification| occurs in normal tissues secondary to hypercalcemia: 1)increased PTH secretion 2)destruction of bone tissue (tumors)
|
3)VitD disorders 4)renal failure (retention of phosphate leads to secondary hyperparathyroidism)|UW
|
|
|
Path:quiz1| What are three common proteins which aggregate as amyloids?| AL protein (Ig light chain
|
limited proteolysis)
|
|
|
Path:quiz1|Describe amyloid deposits in AD| central amyloid core
|
surrounded by astrocytes
|
|
|
Path:quiz1| name a few human forms of TESs| kuru
|
CJD
|
|
|
Path:quiz1| steatosis| intracellular adipose buildup: abnormal retention of lipids within liver cells. Risk factors: diabetes
|
alcohol (cell toxins)| UW
|
|
|
Path:quiz1|what is the main means of EtOH metabolism?| Alcohol Dehydrogenase (metabolizes to acetaldehyde
|
uses NAD+ -> NADH)| UW
|
|
|
Path:quiz1|How is acetaldehyde broken down?| in mitochondria
|
by aldehyde hydrogenase ALDH to acetic acid. | UW
|
|
|
Path:quiz1|what is the major cause of fat accumulation in liver cells of an alcoholic?| NAD+ is required for fatty acid oxidation
|
so if you use it up to metabolize EtOH
|
|
|
Path:quiz1|acetomenophen metabolism| 95% via phaseII enzymes (safe) and 5% via p-450 which produce NAPQ (highly hepatotoxic: centrilobular necrosis). Alcoholics have upregulated p-450 systems
|
so when they take acetomenophen
|
|
|
Path:quiz1|what are the 3 forms of alcoholic liver dz?| steatosis (reversible)
|
hepatitis (reversible)
|
|
|
Path:quiz1| frequency of types of alcoholic liver dz?| most chronic alcoholics will develop steatosis. 20-30% of these will develop alcoholic hepatitis and 30-60% of those will develop cirrhosis. With continued drinking
|
40-50% of cirrhotic pts will die in 5 yrs| UW
|
|
|
Path:quiz1|causes of steatosis| 1. Starvation
|
mobilization of fatty acids from peripheral tissues
|
|
|
Path:quiz1|what are the major histopathologic components of alcoholic hepatitis?| scattered foci of hepatocyte swelling/necrosis; Mallory bodies
|
fibrosis (typically around the central vein)
|
|
|
Path:quiz1| grades of alcoholic hepatitis| I
|
II
|
|
|
Path:quiz1|acetaldehyde can induce ..| lipid peroxidation and acetaldehyde-protein adducts
|
thus disrupting membrane and cytoskeletal function| UW
|
|
|
Path:quiz1|Impaired methionine metabolism implies?| diminished glutathione levels
|
increased sensitivity to oxidative damage| UW
|
|
|
Path:quiz1|causes of portal hypertension| 1. Increased resistance in liver to blood flow due to contraction of sm musc and distortion of hepatic architecture 2. Vasodilation in spanchnic circulation
|
mediated by inc NO levels due to bacteria not being removed in liver. |UW
|
|
|
Path:quiz1| effects of portal hypertension| 1) collateral circulation in places where portal and systemic circulation share capillary beds (rectum - hemrrhoids
|
gastroesophageal jcn - esophageal varices
|
|
|
Path:quiz1| hepatic failure secondary to cirrhosis| chronic liver dz is most common pathway to hepatic failure. 3 serious complications: 1)hepatic encephalopathy 2)hepatorenal syndrome 3)hepatopulmonary syndrome (chronic liver dz
|
hypoxemia
|
|
|
Path:quiz1|difference between acute and chronic inflammation: inflammatory cells|typically
|
acute= neutrophils
|
|
|
Path:quiz1|PAMPs vs DAMPs|PAMPs detect expogenous patterns
|
DAMPs detect endogenous patterns|UW
|
|
|
Path:quiz1|inflammation outcomes: effect of tissue architecture|if tissue architecture is preserved
|
you can regain normal fxn. If tissue architecture is destroyed
|
|
|
Path:quiz1|vascular events of inflammation|transient vasoconstriction of arterioles
|
then vasodilation of arterioles (due to histamine release from mast cells)
|
|
|
Path:quiz1|cellular events of inflammation|1)migration: RBCs aggregate into rouleaux in venules
|
with neutrophils pushed to periphery 2) rolling: selectins and addressins guide neutrophil rolling along endothelium 3)adhesion|UW
|
|
|
Path:quiz1|molecules of leukocyte rolling| endothelial cells: P and E selectin
|
E for adhesion to activated endothelium. leukocytes: Sialyl-LewisX| UW
|
|
|
Path:quiz1|molecules of leukocyte adhesion| endothelial molecule: ICAM-1; Leukocyte receptor: integrins (CD11
|
CD18
|
|
|
Path:quiz1|molecules of adhesion: eosinophils
|
monocytes
|
|
|
Path:quiz1|transmigration|neutrophils move through the BM of venules and release typeIV collagenase
|
producing an exudates in the interstitial tissue|UW
|
|
|
Path:quiz1|leukocyte adhesion defect|prevents neutrophil adhesion and transmigration into tissue. See failure of umbilical cord to separate after birth
|
skin infxns|UW
|
|
|
Path:quiz1|O2 dependent myeloperoxidase system|production of superoxide free rads
|
uses NADPH to convert O2 to O2 rad. "respiratory burst"|UW
|
|
|
Path:quiz1|chronic granulomatous dz|xlinked recessive dz
|
deficient NADPH oxidase resulting in absent respiratory burst. Catalase+ organisms that produce H2O2 (and can metabolize it) are injested but not killed. HOCl* cannot be made due to lack of H2O2
|
|
|
Path:quiz1|Myeloperoxidase deficiency|autosomal recessive dz
|
both O2-* and H2O2 are produced
|
|
|
Path:quiz1|granulomatous (chronic) inflammation: infectious vs noninfectious etiology|infectious: TB
|
caseating. Non-infectious: sarcoidosis
|
|
|
Path:quiz1|cardinal signs of inflammation|calor
|
rubor
|
|
|
Path:quiz1|NLRs|NOD-like receptors; found in cytosol
|
bind: 1)peptidoglycan 2)flagelin 3) DAMPs|UW
|
|
|
Path:quiz1|RLRs|RIG-like receptors; found in nucleus
|
cytoso
|
|
|
Path:quiz1|TLRs|Toll-like R's
|
on cell surface and endosomes
|
|
|
Path:quiz1|NFkB|protein complex that controls the transcription of DNA. NF-_B is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress
|
cytokines
|
|
|
Path:quiz1|E Coli pyelonephritis|ascending route of infxn
|
bacterial products are recognized by TLRs and NLRs on epithelium and interstitial cells -> releasae of inflammatory mediators -> recruitment of leukocytes to interstitium and into tubules|UW
|
|
|
Path:quiz1|inflammation: necrosis vs apoptosis|necrosis is proinflammatory (duh)
|
apoptosis is anti-inflammatory|UW
|
|
|
Path:quiz1|TLR activation|TLRs have binding sites on both sides of PM
|
so can be activated by endogenous mediators and by DAMPs/PAMPs|UW
|
|
|
Path:quiz1|burns
|
asbestos
|
|
|
Path:quiz1|Goodpasture's syndrome|anti-glomerular BM disease with associated pulmonary sx (dyspnea
|
hemoptysis)|UW
|
|
|
Path:quiz1|Goodpasture's syndrome etiology|Abs against a3 chain of TypeIV collagen
|
IgG so recognized by FcgRs on monocytes and neutrophils. Neutrophils release inflammatory mediators that destroy capillaries. Trigger for Auto-Ab production unknown|UW
|
|
|
Path:quiz1|Inflammation: vasodilation|mediated by histamine and NO (mast cells and macros
|
respectively)
|
|
|
Path:quiz1|Inflammation: Stasis|results from increased vessel diameter and loss of fluid
|
resulting in congestion and leukocyte margination|UW
|
|
|
Path:quiz1|what are the opsonin receptors?|CR1
|
CR3
|
|
|
Path:quiz1|which cells contain myeloperoxidase?|neutrophils and monocytes
|
but NOT macrophages|UW
|
|
|
Path:quiz1|name 3 groups of cell derived mediators of inflammation|bioactive amines (histamine
|
serotonin)
|
|
|
Path:quiz1|H1 receptors|1) Endothelium: increase vascular permeability 2) CNS: sedation
|
reduced locomotor and cognitive activity|UW
|
|
|
Path:quiz1|H4 receptors|on hematopoietic cells (DCs
|
mast cells
|
|
|
Path:quiz1|serotonin and inflammation|produced mainly by platelets (also neuroendocrine cells in GI) triggered by stimuli which promote platelet aggregation (including PAMPs and DAMPs)
|
actions similar to H1R (vasodilation and inc permeability)|UW
|
|
|
Path:quiz1|inflammation and AA metabolites|act locally
|
short lived. major enzymes involved in AA metabolism: PLA2 (releases AA)
|
|
|
Path:quiz1|opposing controls in PG pathway|endothelial cells make PGI2 (vasodilation
|
inhibits platelet aggregation) from PGH2
|
|
|
Path:quiz1|COX1 vs COX2|COX1 is constitutive and can be induced
|
COX2 is only induced|UW
|
|
|
Path:quiz1|pan-COX inhibitors|asprin (irreversible)
|
NAIDS (irreversible)
|
|
|
Path:quiz1|selective COX-2 inhibitors|designed to target inflammation and not homeostatic fxns
|
side effects are inc MI/stroke
|
|
|
Path:quiz1|LTC4
|
LTD4
|
|
|
Path:quiz1|omega 3 FAs|substrates for production of resolvins - anti inflammatory mediators
|
decrease neutrophil recruitment
|
|
|
Path:quiz1|ROS and inflammation|amplify inflammatory response
|
inactivate anti-proteases (leading to inc destruction of ECM and emphysema in lungs)|UW
|
|
|
Path:quiz1|what are the three NOSynthases?|2 constitutive: endothelial (eNOS) and neuronal (nNOS)
|
and 1 inducible (iNOS). iNOS induced by inflammatory stimuli and cytokines|UW
|
|
|
Path:quiz1|NO effects|vasodilation
|
platelet aggregation
|
|
|
Path:quiz1|TNF antagonists|useful for Tx of RA
|
psoriasis
|
|
|
Path:quiz1|interferons|type 1: many typeII: IFN-g typeIII: IFN-I
|
IL-28|UW
|
|
|
Path:quiz1|typeI IFNs|produced in response to viral infxns
|
promote anti-viral defenses and Th1 immunity. Used as Tx for HCV. Also prominent in some autoimmune Dz (SLE)|UW
|
|
|
Path:quiz1|effects of IL-6|local: activates lymphos
|
suppresses Tregs
|
|
|
Path:quiz1|IL-17|prominent at mucosal surfaces
|
produced by Th17 cells
|
|
|
Path:quiz1|Th17 cells|play a key role in autoimmune dz
|
effector cytokines are IL17 (neutrophil recruitment)
|
|
|
Path:quiz1|Kallikrein|activator of Factor XII
|
creating amplification loop of kinin cascade|UW
|
|
|
Path:quiz1|proteinase activated receptors (PARs)|GPCRs activated by cleavage of their extracellular domain. Expressed on platelets
|
endothelial cells
|
|
|
Path:quiz1|serine proteases of kinin and clotting cascades can do what?|can activate C3 and C5
|
linking complement system to kinin/clotting cascade|UW
|
|
|
Path:quiz1|what does activated protein C do?|inhibits thrombin
|
useful for Tx of sceptic shock.|UW
|
|
|
Path:quiz1|IL12|produced by DCs
|
macros
|
|
|
Path:quiz1|IFN-g|type II interferon
|
activates macrophages (increased Ag presentation
|
|
|
Path:quiz1|type II interferons|IFNa and IFN b
|
stimulate macros and NK cells
|
|
|
Path:quiz1|IFNa|produced by leukocytes
|
involved in innate immunity against viral infxn|UW
|
|
|
Path:quiz1|IFNb|produced in large quantities by fibroblasts
|
antiviral innate immunity mediators|UW
|
|
|
Path:quiz1|intrinsic vs extrinsic clotting pathways|intrinsic: activated by Factor XII extrinsic: DAMPs/PAMPs -> macros
|
endothelium -> tissue factor -> clotting factors (thrombin pathway)|UW
|
|
|
Path:quiz1|transudate|is a result of hydrostatic or osmotic imbalance
|
is an ultrafiltrate and has low protein content|UW
|
|
|
Path:quiz1|exudates|is a result of inflammation
|
had high protein content|UW
|
|
|
Path:quiz1|fibrinous acute inflammation|exudates present
|
serum proteins and activated clotting cascade with fibrin deposition|UW
|
|
|
Path:quiz1|suppurative acute inflammation|marked by pus formation. See it in acute pneumonia
|
bacterial infxn|UW
|
|
|
Path:quiz1|what diseases might produce a granulomatous response?|TB
|
leprosy
|
|
|
Path:quiz1|describe a granuloma|a collection of epithelioid macrophages (which may fuse to become giant cells)
|
surrounded by lymphocytes and fibroblasts/connective tissue|UW
|
|
|
Path:quiz1|name two acute phase proteins|(plasma proteins
|
synthesized in the liver) CRP
|
|
|
Path:quiz1|what are the systemic effects of inflammation?|fever
|
acute phase protein synthesis
|
|
|
Path:quiz1|name 4 kinds of excessive inflammatory response|sepsis
|
septic shock
|
|
|
Path:quiz1|difference between moderate and severe sepsis?|moderate sepsis = systemic inflammatory response
|
severe sepsis is distinguished by lactic acidosis
|
|
|
Path:quiz1|shock|arterial blood flow becomes inadequate to meet metabolic needs. Hypotension (<60mmHg)
|
tachycardia
|
|
|
Path:quiz1|sceptic shock mechanism|LPS stimulates TLRs and NLRs
|
NFkB pathway results in TNFa
|
|
|
Path:quiz1|what are the three mechanisms of shock?|distributive shock (systemic vasodilation)
|
cardiogenic shock (diminished myocardial contractility)
|
|
|
Path:quiz1|describe the inhibitors of the coagulation cascade (and their targets)|TFPI (TF)
|
activated prot C (Factor Va and VIIIa)
|
|
|
Path:quiz1|Sepsis increases PAI-1 levels. What does it do?|inhibits plasminogen
|
decreases plasmin activity on fibrin|UW
|
|
|
Path:quiz1|what are the 11 criteria for SLE? SOAP BRAIN MD|Serositis (pleuritis or pericarditis) Oral ulcers Arthritis Photosensitivity Blood/hemotologic disorder
|
Renal disorder
|
|
|
Path:quiz1|how many of 11 criteria for SLE are required for Dx?|4+
|
simultaneously
|
|
|
Path:quiz1|nephritic syndrome|proteinuria (>3.g/day) low blood protein levels
|
high cholesterol levels
|
|
|
Path:quiz1|glomerular crescent
|
defn|2 or more layers of cells in the bowman space. Presence of crescents is a marker of severe injury|UW
|
|
|
Path:quiz1|homogenous antinuclear Ab pattern|anti dsDNA
|
anti Histone|UW
|
|
|
Path:quiz1|speckled antinuclear Ab pattern|anti RNP (anti Smith
|
anti SS-A
|
|
|
Path:quiz1|RA pathogenesis|unknown trigger activates autoreactive Tcells -> activate autoreactive B cells
|
activate macrophages -> immue complexes in joint space -> macros activated by immune complexes
|
|
|
Path:quiz1| hyperplasia: defn and causes?| defn= increase in number of normal cells. Causes: 1)hypersecretion of a trophic hormone 2)chronic irritation 3)chemical imbalance (ex
|
hypocalcemia stimulates parathyroid hyperplasia)| UW
|
|
|
Path:quiz1| hypertrophy defn and causes?| defn= increase in cell size. Causes: 1)increased workload 2) removal of an organ (remove one kidney
|
see hypertrophy of other kidney)| UW
|
|
|
Path:quiz1| atrophy: expect to see...| reduction in tissue mass
|
presence of vacuoles containing lipofuscin| UW
|
|
|
Path:quiz1| lipofuscin| "wear and tear" pigment
|
associated with free radical damage and tissue atrophy. Is an indigestible lipid derived from lipid peroxidation of cell membranes| UW
|
|
|
Path:quiz1| permanent cells (nonreplicating)| highly specialized cells
|
undergo hypertrophy ONLY (ex cardiac
|
|
|
Path:quiz1| metaplasia| replacement of one fully differentiated tissue by another. Involves reprogramming cells in response to signals (hormones/vitamins/chem.irritants)
|
sometimes reversible| UW
|
|
|
Path:quiz1| what are the two types of metaplasia?| squamous (replacement of columnar epithelium w columnar epithelium - happens in mainstem bronchus of smokers)
|
glandular (replacement of squamous epithelium with intestinal cells
|
|
|
Path:quiz1| what are the microscopic features of dysplasia?| 1)increased mitotic activity 2)disorderly proliferation of cells 3)nuclear variation in size
|
shape
|
|
|
Path:quiz1| necrosis| death of groups of cells
|
often accompanied by an inflammatory infiltrate| UW
|
|
|
Path:quiz1| coagulation necrosis| preservation of the structural outline of dead cells
|
usually resulting from loss of blood supply; occurs due to denaturation of enzymes and structural proteins by intracellular accumulation of lactate of heavy metals. Inactivation of cellular enzymes prevents autolysis|UW
|
|
|
Path:quiz1| Types of infarct| 1) wedge-shaped
|
when dichotomously branching vessels are occluded 2) pale: increased density of tissue prevents RBCs from diffusing through necrotic tissue 3)hemorrhagic: loose-textured tissue allows RBCs to diffuse through necrotic tissue| UW
|
|
|
Path:quiz1| microscopic features of coagulatory necrosis| indistinct outlines of cells within dead tissue
|
absent nuclei or karyolysis (fading of nuclear chromatic)
|
|
|
Path:quiz1| dry vs wet gangrene of the toes of a diabetic patient| dry: coagulation necrosis
|
wet: liquefactive necrosis| UW
|
|
|
Path:quiz1| ex of physiologic hypertrophy: | body building
|
pregnancy
|
|
|
Path:quiz1| caseous necrosis| variant of coagulation necrosis associated with acellular
|
cheese-like material| UW
|
|
|
Path:quiz1|hypertrophic cardiomyopathy| Hypertrophic cardiomyopathy (HCM) is a condition in which the heart muscle becomes thick. The thickening makes it harder for blood to leave the heart
|
forcing the heart to work harder to pump blood. Sudden death in athletes. Autosomal dominant genetic etiology| UW
|
|
|
Path:quiz1| left ventricular cardiomyopathy| LVH itself is not a disease
|
but caused by backflow which can be secondary to aortic stenosis
|
|
|
Path:quiz1| physiologic hypertrophy| due to exercise
|
tissue is well perfused due to corresponding inc in capillary density| UW
|
|
|
Path:quiz1| pathologic hypertrophy| lacks proportional increase in capillary network
|
get damage-> fibrosis|UW
|
|
|
Path:quiz1| signals that initiate apoptosis| 1)binding of TNF to its R'
|
2) injurious agents: viruses
|
|
|
Path:quiz1| half-liver donation: what happens?| both sides (donor and recipient) regrow to full size
|
this is compensatory hypertrophy| UW
|
|
|
Path:quiz1| hormonal pathologic hyperplasia: benign prosthatic hyperplasia| dependent on presence of androgens. Early stages
|
nodules are fibromuscular stromal cells
|
|
|
Path:quiz1| apoptosis: enzymatic cell death| begins with activation of caspases
|
then 1) activation of endonuclease leads to nuclear pyknosis (ink dot appearance) and fragmentation and 2) activation of protease leads to breakdown of cytoskeleton| UW
|
|
|
Path:quiz1| in the adult
|
atrophy is almost always ________| pathologic| UW
|
|
|
Path:quiz1| later events in apoptosis| 1)formation of cytoplasmic buds on cell membrane 2) formation of apoptotic bodies by the breaking off of cytoplasmic buds
|
3) phagocytosis of apoptotic bodies by neighboring cells/macros| UW
|
|
|
Path:quiz1| microscopic appearance of apoptosis| 1)cell detatchment from neighboring cells
|
2) deeply eosinophilic-staining cytoplasm 3)pyknotic
|
|
|
Path:quiz1| metaplasia| thought to be an adaptive response
|
can be reversible if injurious factors are removed
|
|
|
Path:quiz1| enzymatic markers of cell death: amylase and lipase| marker enzymes for acute pancreatitis lipase>amylase (for pancreatitis)
|
amylase inc in salivary gland inflammation (mumps)| UW
|
|
|
Path:quiz1| causes of hypoxemia| 1) respiratory acidosis (CO2 retention)
|
2)ventilation defect (impaired O2 delivery to alveoli) 3)perfusion defect (absence of blood flow to alveoli) 4)diffusion defect (inability of O2 to diffuse through the alveolar-capillary interface (ex interstitial fibrosis))|UW
|
|
|
Path:quiz1| what are fxnal consequences of changes in respiratory epithelim secondary to smoking?| loss of cilia and secretion
|
get lots of infxns| UW
|
|
|
Path:quiz1| reversible injury vs irreversible injury: membrane| Rev: blebbing
|
loss of microvilli. Irrev: disruption| UW
|
|
|
Path:quiz1| kwashiorkor deficiency| virulent form of childhood malnutrition characterized by edema
|
irritability
|
|
|
Path:quiz1| methemoglobinemia| Fe+3 instead of Fe+2
|
oxygen can't bind. So you get reduction in SaO2
|
|
|
Path:quiz1| causes of methemoglobinemia| oxidizing agents ( nitrite or sulfur containing drugs
|
such as nitroglycerin and trimethoprim sulfamethoxazole
|
|
|
Path:quiz1| decreased Na+ pump results in| influx of calcium
|
water
|
|
|
Path:quiz1| effects of switching to anaerobic glycolysis| decreased glycogen reserves
|
increased lactic acid (within and without cell) -> dec pH can cause clumping of nuclear chromatic
|
|
|
Path:quiz1| effect of detergent induced membrane damage| 1) loss of cellular proteins 2) entry of Ca2+ -> activation of multiple cellular enzymes (ATPases
|
endonucleases
|
|
|
Path:quiz1| CO poisoning| CO outcompetes O2 for binding sites at Hb
|
decreases SaO2. Also
|
|
|
Path:quiz1| what factors cause a left shift in the O2 binding curve? | 1) decreased 2
|
3-bisphosphoglycerate 2) CO
|
|
|
Path:quiz1| defective oxphos| CO and CN inhibit cyt oxidase in ETC
|
which normally transfers electrons to O2. CN poisoning is common from combustion of polyurithane (upholstery) and from drugs (nitropruside)| UW
|
|
|
Path:quiz1| Bcl2| inhibits cell death
|
is an oncogene| UW
|
|
|
Path:quiz1| sources of free radicals: Iron| donation or acceptance of free electrons by transition metals (Cu/Fe) produces free radicals
|
ex. Fenton Rxn|UW
|
|
|
Path:quiz1| types of damage associated with free radicals| DNA fragmentation
|
lipid peroxidation
|
|
|
Path:quiz1| 85% of pts with follicular Bcell lymphoma have...| 14;18 translocation which juxtaposes bcl2 with Ig heavy chain genes
|
leading to bcl2 overexpression. Resulting inhibition of cell death leads to malignant transformation in long surviving cells.|UW
|
|
|
Path:quiz1| hypoxia stress response genes| VegfA
|
EPO
|
|
|
Path:quiz1| intrinsic vs extrinsic apoptotic signaling| intrinsic: mitochondrial via bcl-2 effectors (bax
|
bak) leading to caspase 9 then caspase 3. Extrinsic: Fas/FasL signal or TNF receptor -> -> caspase3| UW
|
|
|
Path:quiz1| IGF-1| one of the most potent natural activators of the HYPERLINK "http://en.wikipedia.org/wiki/AKT"AKT HYPERLINK "http://en.wikipedia.org/wiki/Signal_transduction"signaling pathway
|
a stimulator of cell growth and multiplication and a potent inhibitor of HYPERLINK "http://en.wikipedia.org/wiki/Apoptosis"programmed cell death| UW
|
|
|
Path:quiz1| alpha 1-antitrypsin deficiency| mutations in alpha1antitrypsin gene cause misfolding
|
accumulation in ER. Causes dyspnea and emphysema in sever cases| UW
|
|
|
which
|
cell
|
