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121 Cards in this Set
- Front
- Back
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Hypoxia
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inadequate oxidation of tissues (same definintion as shock)
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Why do we need oxygen
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for ATP (electron acceptor)
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Oxygen saturation
Partial pressure of oxygen |
Amount of oxygen bound to heme
Amount of oxygen dissolved in the plasma (arterial) |
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Three things that carry oxygen in our blood
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Hemoglobin (most important)
Oxygen attached to heme (pulse oximter) - oxygen stauration Partial pressure of oxygen - what is dissolved in the plasma |
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What state does Iron need to be in to carry oxygne
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F2+
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MOST COMMON CAUSE OF TISsue HYPOXIA
Ischemia define: Most common cause of ischemia |
decrease in arterial blood flow (NOT VENOUS)
Thrombis to a muscular artery (myocardial infarction) -produces tissue hypoxia |
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IF partial pressure of oxygen is decreased what will happen to oxygen saturation?
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It has to decrease
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second most common cause of hypoxia
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HYPOXEMIA - causes hypoxia (not same as hypoxia), deals w/ partial pressure of oxygen, when decreased it is called hypoxemia
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Daltons law
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sum of the partial pressueres of gasses must equal 760 (Oxygen, CO2 and Nitrogen)
Note: nitrogen is fixed |
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What happnes to P02 if PCo2 goes up (i.e. respiratory acidosis)
Whenever you have Respiratory acidosis from any cause you have... |
O2 has to go down (have to come out w/ 760)...inverse is true as well
hypoxemia |
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Best examples diseases that are examples of Ventilation defects
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ARDS and hyaline membrane diseases (both involve hyaline around the alveoli)
Perfusion is still fine. |
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What happens when you have a ventilation defect but you still have perfusion?
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Intrapulmonary shunt is created
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Patient w/ hypoxemia, gave 100% oxygen and the PO2 did not increase what does it mean?
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Intrapulmonary SHUNT (massive ventilation defect), if its a kid then hyaline membrane disease if adult ARDS
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What is the most common perfusion defect
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PE
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DEAD space in the lungs is produced by what overall mechanism
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Perfusion defect (E.G. PE), PO2 will go up if you
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Diffusion defects define
give some classic examples of it |
something in the interface, like fibrosis
examples sarcoidosis is the best example, pulmonary edema, fluid from CHF |
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What is the J reflex
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reflex that is innervated by the tenth nerve and causes dyspnea whenever fluid is in the interstium and irritating the J-receptor
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3 things that produce hypoxemia
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Ventilation defect
perfusion defect diffusion defects |
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define anemia
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decrease in hemoglobin
no hypoxemia in a patient w/ anemia (PO2 and and O2 sat are normal, because breathing is normal), but don't carry much oxygen so get tissue hypoxia |
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common symptom of anemia
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exertional dyspnea
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*ON EVERY BOARD*
These are all common situations to see what in? Closed space w/ a room heater automible exahaust house fire Taxie driver |
carbon monoxide poisoning
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People who come out of house fires commonly have two poisonings?
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Cyanide (burning of apolstery) and carbon monoxide (combustible things) posioning
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What is it in the apolstry that produces Cyanide when it is burned?
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Polyurathane
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VHY**
What is decreased in CO posioning How do you treat it |
Oxygen saturation will be decreased
100% oxygen |
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VHY
What is the first symptom of carbon monoxide posioning? Why don't you see cyanosis in these people (there O2 sat is low so you should see it) |
Headache
Cherry red pigment that is produced during CO posioning |
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What is methemoglobin
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Iron in the 3+ state, oxygen can't bind, so oxygne saturation is decreased (PO2 is normal)
Could see chocolate colored blood |
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VHY
Someone comes out of the Rocky Mountatains and he is cyanotic, they give 100% oxygen but cyanosis is not improved, what is the diagonis, primary and scondary treatment |
Methemoglobinemia (assume he was drinking water in the mountains which has lots of nitrates and can cause methemoglobin to form)
IV - methylene blue Secondary - vitamin C (reducing agent) |
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VHY
What drugs can cause methemoglobinemia? What toxicities can these drugs have? |
Dapsone - sulfa drug (used in treating leporasy, used on USMLE), other sulfa drugs (Trimethylprim-sulfamethaxazol, primaquine)
NITRO durgs (nitroglycerin, and nitroprusside) Produce methemoglobin and can produce hemolytic anemia in people w/ G6PD. |
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VHY
HIV patient develops methemaglobinemia from being treated for what and by what drugs, what lab value will be low? |
Trimethylprim-sulfamethaxozole
treated for PCP O2 sat is low |
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When do yo want the oxygen curve to shift to the right?
What compounds cause this |
At the tissues to release oxygen
2,3BPG, fever, low pH, high altitude |
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VHY
WHat happnes at high altitude to your oxygen saturation curve, why? |
shifts to the right
respiratory alkalosis from breathing fast, increase O2 in blood, more 2,3 BPG is made at high altittdue (this is hor are body gets oxygen at higher altittudes) |
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what left shifts the oxygen saturation curve
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CO, Methemoglobin, Fetal-hemoglobin, Alkalosis, dec. 2,3 BPG
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VHY
CN and CO both inhibit? |
Cytocrome oxidase (last enzyme in the oxidative phosphorylation pathway before transfers the electron to Oxygen)
3 C's all like each other |
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VHY
Left shift in oxygen curve (can't release oxygen), dec. in oxygen saturation (can't bind oxygen) inhibition of the cytocrome oxidase are all caused by? |
Carbone monoxide poisioning
The whole system shuts down |
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VHY
dinitro-phenol (wood preservative), salicylates, alcohol do what to the electron transport chain? What does this do to the other energy producing pathways? What effect does this have on the body? |
uncoupling agents - drain protons off w/o making ATP
increases them to try and get more fuel to make ATP Increase in Rxn causes heat to be produced and you can get hyperthermia |
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VHY
why are alcoholics so suceptible to heat stroke on a hot day? What is a common side effect of aspirin? |
Beceause both are uncoupling agents they can produce hyperthermia
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(know all about these, ***VHY)
Causes of tissue hypoxia |
Ischemia
hypoxemia respiratory acidosis ventilation defects perfusion defects diffusion defect Hemoglobin related things (anemia, CO, methemoglobin) problems w/ cytocrome oxidase uncoupling agents left shifted curve |
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What happens when you decrease ATP, during tissue hypoxia (no oxygen to make ATP)?
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anarobic glycolysis (lactic acid produced from inc. in NADH...need NAD+ to keep using glycolysis so you can at least make 2 ATP)
Have to use this pathway because mitochondria is shut down w/ no O2 around but you still need ATP |
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VHY
What happens when you increases lactic acid? |
outside the cell get lactic acidosis (inc. in anion gap...)
inside the cell lactic acid builds up dec. pH - causes denaturing of proteins and enzymes...cell can degrade itself (Coagulation necrosis) |
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VHY
In a nut shell what type of tissue/cell degeneration can result from tissue hypoxia? |
Coagulation necrosis
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When you look at coagulation necrosis grossly what is it called?
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infarction
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VHY
What else happens to the cell during dec. ATP besides lactic acid build up? |
Shut down ATP pump, this allows Na to build up in the cell...brings water and get swelling (reversible)
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VHY (they like to ask it this way on boards)
what happens to the cells during any scenario that produces hypoxia? How do you treat it |
They swell up, from shuting down the ATP pumps
Give them some oxygen, and it will reverse |
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What happens to calcium during tissue hypoxia
*VHY* What happens w/ Ca2+ reentry into the mitochondria |
calcium enters the cell (becasue pump is shut down to keep it out)
inc. in mitochondrial permeability w/ the release of CYTOCHROME C - ACTIVATES APOPTOSIS |
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What happnes when calcium enters tissue
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IT ACTIVATES ENZYMES:
THESE THINGS ARE ALL IRREVERSIBLE (sign of irreversible damage) 1.phospholipases actived (destroys membrane, worst) 2.enzymes in the nucleus (chew on DNA) destroys nucleus 3.Destroys the mitochondria as well THE CELL |
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What happnes when calcium enters the pancreas
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its going to activate all of its ezymes, get acute pancreatitis
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What happens when the cells die from hypoxia and calcium entrance?
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Release there enzymes and protiens that why you see things like CK, CKMB (MI), transaminases-AST, ALT(Hepatitis), amylase in pancreatitis
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VHY
Lipofuscin (need a history to tell what it is, can't tell just by looking at it) |
Wear and tear molecule; from free radical damage, atrophy,(consits of the things that are not digestible; lipids)
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VHY
What is the damage of the tissue in reperfusion injury caused by? (e.g. when using a thrombolytic to dissolve a clot and blood enters the tissue again) |
Oxygen free radicals and cytoosolic Ca2+
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VHY
Kids w/ respiratory distress syndrome can get what two types of injury from being given to much oxygen |
Retinopathy of prematurity
bronchopulmonary dysplasia |
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Most common cancer of radiation therapy
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leukemia
raidiation (ionization of water forming hydroxyl free radicals)...can induce muttions |
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What do iron free radicals produce in the liver and heart cause
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liver - cirrhosis
Heart - restrictive cardiomyopathy Also get diabetes and malabsorption |
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VHY
What is the number one cause of fluminant hepatits caused by a drug, what is the MOA |
Acetaminophen (tylenol) produces free radicals, this happens when the CYP 450 changes it upon metabolism
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VHY**
Where in the liver does acetaminophen toxicity occur |
Central vein
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VHY
What is the treatment of Acetaminophen toxicity and its mechanism? |
N-Acetyl-cystine
provides substrate for the formation of glutathione (this neutralizes peroxide free radicals). It replenishes it since it gets used up getting rid of the free radicals produced by acetaminophen |
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superoxide free radical is neutralized by
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Superoxide dismutase
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How do acetaminophen and aspirin do to your
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free radicals destroy the renal medulla (destroying renal tubules)
Aspirin - blocks vasodilator PGE2 made at the afferent arteriole allowing angiotensin II to control blood flow to the kidney |
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VHY
sluffing of the renal papilla and/or the inability to concentrate urine caused by acetaminophen toxicity is called? Mechanism was already described |
analgesic nephropathy
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what is apoptosis
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programed cell death
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Mullerian inhibitory factor inhibits the formation of?
How does it do it? |
uterus, cervix, upper 1/3 of vagina
Activates caspases tha cause apoptosis of these structures |
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Wolfian duct structures, how are theses structures destroyed in the female
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epididimis, vas deferens,
singal caspsases which tell the cell to undergo apoptosis |
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Abscence of a thymus and tetani is what disease?
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Di-george (apoptosis destroyed the thymus)
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VHY
What happens when the smooth endoplasmic reticulum undergoes hyperplasia? What can cause this |
increase in drug metabolism
THings like: alcohol, barbiturates and phenytoin |
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VHY**
In this disease hydrolytic enzymes are not marked w/ mannose 6-phosphate so they cannot be packeged into... Symptoms of the disease include psycomotor disease and mental retardation |
I-cell disease (inclusion cell), hydorlyitc enzymes are not put into LYSOSOMES (whichi s necessary to degrade complex substrates)...undigested substrates accumulate as large inclusion in the cytosol
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In this lysosomal storage disease glucocerebrosides accumulate in the lysosome?
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Gauchers disease
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VHY:
patient presenst w/ neutropenia, oculocutaneous albinism and is especially susceptible to staph infections, Dx What is the pathophysiology |
Patient has Chediak-Higashi syndrome (CHS)
Leukocyte defect in chemotaxis, degranulation and killing - (inability of the primary lysozome to fuse w/ phagosomes and produce secondary phaogolysosoemes which is how the bacteria are killed) |
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How do the vinka alkaloids and colchicine interfere w/ the cell cycle
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They bind to tubulin in microtubles preventing the assembly into mitotic spindles
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VHY
what is the marker for intermediate filament degredation? |
Ubiquitin
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VHY:
What are mallory bodies |
damaged (ubiquinated) cytoKERATIN intermediate filaments of the hepatocytes seen in alcoholic liver disease
Look like homgenous pink masses in the hepatocytes (look for the globs of fat to tell that you are in the liver) |
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What are LEWY BODIES
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These are damaged neurofilaments seen in idiopathic parkinsons disease
Eosiniphilic cytoplasimic inclusions in the degenerating substantia nigra |
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VHY***
Patient has tremor (shaking) of the hands at rest, rigitidy, bradykinisia or Akinesia (slowness or absncence of movements) and postural instability, DX and underlying problem |
Parkinsons disease
Dopamine is decreased w/ loss of the substantia nigra |
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VHY**
what is the most common cause of fatty change to the liver (cytosolic accumulation of TG's)? What is the mechanism |
Alcohol
Increase NADH in the cell during the metabolism of the alcohol, accelerates the conversion of DHAP to glycerol 3-phosphate which is the substrate for TG formation |
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VHY
what is the mechanism by which people w/ kwashiorkor develop a fatty liver? |
have enough calories but not enough protein...decreased synthesis of apolipoprotien B-100 leads to fats not being able to leave the liver. and decrease relase of VLDL
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An infant deveolps hemolytic anemia from the Rh factor, what are you concerned about?
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Kernicterus - fat soluble unconjugated bilirubin deposition in the basal ganglia nuceli causing permenant brain damage
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In diabetes mellitus what endogenous substance can accumulate in the proximal renal tubules?
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Glycogen - the cells are insensitive to glycogen and become overloaded
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What happens to the liver in hemochromatosis?
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excess hemosiderin depostion in the parenchymal cells of the liver leading to free radical damage and organ dysfunction (cirrhosis); inc. in serum ferritin
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This disease causes destruction of the adrenal cortex and results in hypocortisolism...leads to an increase in ACTH and hyperpigmentation
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Addisons - excess synthesis of melanin and diffuse hyperpigmentation
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VHY
Patient presents w/ basophilic stiplings and acid fast inclusions in proximal renal tubular cells, DX? |
Lead poisoning
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What happens to the serum ferritin levels during iron deficiency anemia?
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Decreases - major soluble form of iron and the best way to evaluate iron.
Most abundant site is macrophages of the bone marrow |
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VHY
This product is the ferritin degredation product? |
Hemosiderin - gold brown pigment
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VHY
This type of calcification occurs in necrotic tissue? Two good examples ae atherosclerotic plaques and calcification in the pancreas |
Dystrophic calcification
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VHY
This process results in the deposition of calcium phosphate in normal tissue, due to increased levels of calcium and/or phosphate |
Metastatic calcification - usually occurs in areas where there are pH gradients (kidney, lungs, Duodenum/stomach)
Phosphate drives calcium into the tissue |
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What are two important causes of hypercalcemia
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primary hyperparathyroidism
Malignancy-induced hypercalcemia (medullary carcinoma of thryoid, MEN diseases) |
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What are two important causes of hyprphosphatemia
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renal failure (thats why they need dialysis)
Primary hypothyroidism |
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What is the most common cause of aortic stenosis and what is the mechanism
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bicuspid aortic stenosis
they get damaged because two are doing the work of three and DYSTROPHIC CALCIFICATION OCCURS |
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VHY
How do signals initiate apoptosis? |
activating caspases - group of cysteine proteases
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Involution of the thymus, creating a lumen inside of the GI tract, and loss of mullerian structures in a male fetus are all due to?
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Apoptosis
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Death of tumor cells occurs throught the process of ?
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apoptosis
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Death of a group of cells often accompanied by inflammatory infiltrate is called?
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necrosis
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VHY
In this type of necrosis you have preservation of the structural outline of dead cells, what is the mechanism? |
COAGULATION NECROSIS
Denaturing of enzymes and structural protiens (inactivation of enzymes that cause dissolution (autolysis)) |
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VHY
Buildup of lactic acid (hypoxia), lead (heavy metals and exposure to ionizing radiation all cause what type of tissue necrosis? |
Coagulation
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Microscopic - indistinct outlines of cells w/in dead tissue and abscence of nuclie of cells, what type of necrosis is this?
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coagulation necrosis
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VHY
An infarction is a gross manifestation of what type of tissue necrosis? It will be a pale color (ischemic type) |
Coagulation necrosis - secondary to sudden vessel occlusion
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What organs have pale infarcts, what type of necrosis is that?
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heart, kidney, spleen, liver (they all have good consitency so RBCs don't trickle out as well, most don't have dual blood supply either)
examples of coagulation necrosis |
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testicle, lungs, and bowel produce what type of infarction?
What type of necrosis is this? |
Hemorrhagic
examples of coagulation necrosis loose tissue so RBC can diffuse through necrotic tissue |
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VHY
ALL infarctions produce what type tissue necrosis? VHY: What is the one exception |
Coagulation necrosis - gross manifestation secondary to occlusion of the vessel
an infection will cause the same thing to the brain. Cerebral infarction produces liquifactive necrosis (hardley has any structure)- get a cystic space |
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VHY
What type of tissue necrosis is seen in a Dry gangrene in an individual w/ diabetes mellitus (this is a form o f infarction that results from ischemia? |
Coagulation necrosis
Most likley from atherosclerosis of popliteal artery causing ischemia... Can tell dry from wet gangrene |
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What arrhythmia is most associated w/ Embolisation in the systemic circulation?
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A-FIB (get stasis and fluttering can cause vegetations to break off and embolize)
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VHY
what is the first and second most common cuase of infarction of the bowel |
1.addhesions from previous surgery
2.indirect inguinal hernia sack (will be a small section of bowel trapped) |
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VHY
A wedged shaped hemorrhagic infaction of the lung, goes all the way to the edge of the lung. What is the most likley cause and what are the symptoms associated w/ it? |
-Emboli
knife like pain on inspiration - pleuritic chest pain if you inflame the pleura Note: coagulation necrosis |
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What is liquifactive necrosis?
What is the mechanism |
Necrotic tissue that softens and becomes liquified
Lysosomal enzymes of necrotic tissue or neutrophils is released intot he tissue |
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VHY
What is the usual cuase of liquifactive necrosis |
Acute inflammation related to neutrophil infiltration.
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VHY
In wet gangrene (pus formation) of the toes of an individual w/ diabetes mellitus would have what type of tissue necrosis? |
liquifactive - neutrophils are involved
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VHY
Patient had high fever and productive cough and yellow round yellow abscess all over the lung, Dx and type of necrosis? |
Bronchopneumonia - most likley strep pneumonia, abscesses have formed (they don't go to the periphery like you would see w/ hemorrhagic infarction)
Liquifactive necrosis - abscess wall off neutrophils and there enzymes produce liquifactive necrosis |
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VHY
pateint has fever, night sweats and weight loss? Type of necrosis |
TB - most common cause
Caseous necrosis |
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VHY
What types of infections cause caseous necrois Why do they cause this type of necrosis |
systemic fungal infection (histoplasma)
or mycobacterium Formed by the release of lipid from the cell walls- after they have been destroyed by macrophages |
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VHY
Alcholic Pantient has epigastric pain w/ pain radiating to the back, DX On X-ray you see in the area of right upper quandrant little areas of calcification What type of necrosis is this |
Dx, Pancreatititis
Enzymatic fat necrosis (unique to the pancreas), soponification - combination of fatty acids w/ calcium |
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Womnen damages her pendulace breast from running, what type of necrosis?
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Non-enzymatic fat necrosis
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What enzyme is elevted in actue pancreatitis?
What is the underlying cause |
amylase
LIPASE AS WELL, IT IS MORE SPECIFIC, it is activated by alcohol |
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What is fibrinoid necrosis?
What is the cause |
Deposistion of pink-staining proteinaceous material in damaged vessel walls due to damaged basement membranes
Immunological disease (rheumatic hear disease, SLE...when immune complexes form) |
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What type of necrosis is limited to the small muscular arteries, arterioles, venules and glomerular capillaries?
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FIBRINOID NECROSIS
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Patinet presents w/ palpable purpura (e.g. Henoch-Schonlein purpura, would be of the lower extremity), what is the type of hypersensitivity , and type of necrosis?
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That is a small vessel vasculitis, type III hypersensitivity
FIBRINOID NECROSIS |
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VHY
What is the pathogeneisis of how damage results from immune complexes |
It deposits and activtes the compliment system - C5A is produced and attracts nuetrophils...they do the damage
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What are some sinusoid organs
What is characteristic of them |
liver, spleen
HAVE GAPS (as opposed to glomerular basement membrane where it is fenesterated) |
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What is the blood flow to the heart starting at the portal vein and hepatic artery
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They form sinusoids and empty into the central vein...which becomes the hepatic vein...becomes the inferior vena cava...goes to the right side of the heart
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What happens if you block the hepatic vein what happnes?
What happens to the liver if you block the portal vein? |
Bud chiari syndrome - get congested liver
NOTHING |
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What area of the liver is the most sensitive to oxygen deprivation?
This is the same area that is effected in acetaminophen toxicity because it combat oxygen free radicals w/ low levles of oxygen |
CENTRAL VEIN (ZONE 3) you will see fatty change
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YEllow fever affects what zone of the liver
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mid zone necrosis (2)
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VHY*****
Most common casue of fatty change to the liver? What types of metabolic acidosis is seen in an alcoholic? |
Alcohol
Lactic acidosis - inc. the levels of NADH drives pyruvate to become lactate Beta-hydroxybuteric acid (KETONE BODY) - produced because excess acetyl-CoA is around and NADH. Body needs glucose and this is a supplement since gluconeogenesis is not woring well |
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Why do alcoholics have trouble during fasting states (hypoglycemia)
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can't undergo gluconeogenesis because all of pyruvate (which is needed to start gluconeogenesis) is being used up to form lactate (to dec. the NADH levels)
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VHY****
Why do you get fatty change to the liver in alcoholics |
DHAP (from glycolysis) is forced to make glycerol 3-phosphate in because of the high livels of NADH from metabolism of alcohol...this is the backbone to make TG - VLDL and builds up in the liver
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