Goljan - cell injury Flashcards

Necrosis
Terms Definitions
Hypoxemia
↓ PaO2
Labile cells
divide continuously
Mitochondrial toxins
alcohol, salicylates
Hemosiderin
ferritin degradation product
Hypertrophy
↑ cell size; ↑workload
Hyperplasia
↑ number of cells
Hypoxia
inadequate oxygenation of tissue
Dysplasia may progress to...
cancer
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
CO and CN
inhibit cytochrome oxidase
CN poisoning Rx
amyl nitrite, thiosulfate
Metaplasia
One cell type replaces another
Coagulation necrosis
preservation of structural outlines
Dystrophic calcification
Calcification of necrotic tissue
Metastatic calcification
Calcification of normal tissue
Most destructive FRs ?
Hydroxyl FRs
common symptom of anemia
exertional dyspnea
Barrett's esophagus
glandular metaplasia, gastric reflux, squamous to glandular
Atrophy
↓ size/weight of tissue or organ
VHY
Patient presents w/ basophilic stiplings and acid fast inclusions in proximal renal tubular cells, DX?
Lead poisoning
VHY
Buildup of lactic acid (hypoxia), lead (heavy metals and exposure to ionizing radiation all cause what type of tissue necrosis?
Coagulation
Ventilation defect
Perfused but NOT ventilated ; intrapulmonary shunt
Where do primary lysosomes derive from?
Golgi apparatus
Ischemia
↓ arterial blood inflow or venous outflow
What do FRs damage?
damage membranes and DNA
Death of tumor cells occurs throught the process of ?
apoptosis
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?
Apoptosis
In this lysosomal storage disease glucocerebrosides accumulate in the lysosome?
Gauchers disease
superoxide free radical is neutralized by
Superoxide dismutase
What is the most common perfusion defect
PE
3 things that produce hypoxemia
Ventilation defect

perfusion defect

diffusion defects
Causes of fatty change in cardiac muscle
anemia, diphtheria
Stable cells
must be stimulated in order to divide
When do you see enzymatic fat necrosis?
acute pancreatitis
MetHb
heme Fe3+ ; Normal Hb and PaO2, ↓SaO2
Anaerobic glycolysis
primary source ATP in hypoxia, causes lactic acidosis
Segment of renal medulla most susceptible to hypoxia?
thick ascending limb
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
Why do we need oxygen
for ATP (electron acceptor)
Death of a group of cells often accompanied by inflammatory infiltrate is called?
necrosis
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
How will pulse oximeter measure metHb and COHb ?
Falsely ↑ SaO2
Perfusion defect
Ventilated but NOT perfused ; ↑ dead space
Cells in liver most susceptible to hypoxia?
Zone III hepatocytes
Type of necrosis in cerebral infarction
liquefactive not coagulative necrosis
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
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
Most common cancer of radiation therapy
leukemia

raidiation (ionization of water forming hydroxyl free radicals)...can induce muttions
*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
Name molecules that neutralized FRs
SOD, GSH, vitamins C and E
Problems with excess iron and copper
hydroxyl FR damage of tissue
Effects of SER hyperplasia
↑ drug metabolism → ↓ drug effectiveness
Name 3 drugs that mitotic spindle defects
Vinca alkaloids, colchicine, paclitaxel
What state does Iron need to be in to carry oxygne
F2+
VHY
What happens when the smooth endoplasmic reticulum undergoes hyperplasia?

What can cause this
increase in drug metabolism

THings like: alcohol, barbiturates and phenytoin
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
What is methemoglobin
Iron in the 3+ state, oxygen can't bind, so oxygne saturation is decreased (PO2 is normal)

Could see chocolate colored blood
Situations in which infarction is less likely?
Dual blood supply, collateral circulation
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
What happnes when calcium enters tissue
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
What happens when you decrease ATP, during tissue hypoxia (no oxygen to make ATP)?
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
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
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
Three things that carry oxygen in our blood
Hemoglobin (most important)

Oxygen attached to heme (pulse oximter) - oxygen stauration

Partial pressure of oxygen - what is dissolved in the plasma
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
YEllow fever affects what zone of the liver
mid zone necrosis (2)
Why do alcoholics have trouble during fasting states (hypoglycemia)
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)
Oxygen saturation

Partial pressure of oxygen
Amount of oxygen bound to heme

Amount of oxygen dissolved in the plasma (arterial)
Best examples diseases that are examples of Ventilation defects
ARDS and hyaline membrane diseases (both involve hyaline around the alveoli)

Perfusion is still fine.
In diabetes mellitus what endogenous substance can accumulate in the proximal renal tubules?
Glycogen - the cells are insensitive to glycogen and become overloaded
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
What happens to the liver in hemochromatosis?
excess hemosiderin depostion in the parenchymal cells of the liver leading to free radical damage and organ dysfunction (cirrhosis); inc. in serum ferritin
Whats going in in a Fatty liver
↑ synthesis TG ; ↓ secretion TG
People who come out of house fires commonly have two poisonings?
Cyanide (burning of apolstery) and carbon monoxide (combustible things) posioning
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
What arrhythmia is most associated w/ Embolisation in the systemic circulation?
A-FIB (get stasis and fluttering can cause vegetations to break off and embolize)
What organs have pale infarcts, what type of necrosis is that?
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
What do iron free radicals produce in the liver and heart cause
liver - cirrhosis

Heart - restrictive cardiomyopathy

Also get diabetes and malabsorption
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)
What happnes when calcium enters the pancreas
its going to activate all of its ezymes, get acute pancreatitis
What is the blood flow to the heart starting at the portal vein and hepatic artery
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
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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