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ESA 2 > MOD > Flashcards

MOD Flashcards

0
Q

What are the classes of hypoxia?

A

Hypoxaemic - low arterial O2
Anaemic- decreased ability of haemoglobin to carry O2
Ischemic - interruption to blood supply
Histiocytic - inability to use O2 e.g. Disruption of enzymes/ cyanide

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1
Q

What is the difference between hypoxia and ischemia?

A 
Hypoxia = oxygen deprivation
Ischemia = loss of blood supply
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2
Q

What are the causes of cell injury?

A 
Hypoxia, 
physical agents e.g. Direct trauma, radiation, pressure, electric currents, temperature. 
Chemical agents and drugs
Micro organisms
Immune mechanisms
Dietary deficiencies
Genetic abnormalities.
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3
Q

Describe reversible hypoxia injury

A 
Deficiency of ATP.
Na/K pump stops causing swelling.
Ca accumulates
Increased lactate so lower pH, disrupting enzymes and causing chromatids to clump.
Ribosomes dissociate from ER.
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4
Q

Describe irreversible hypoxic injury

A

Plasmamembrane and ER/mitochondrial membranes are damaged. Ca accumulates further. This activates proteases, endonucleases, phospholipases and ATPases. Lysomsomal membranes are also effected causing more damaging enzymes to be released.
Increased Ca can be detected in the blood.

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5
Q

What is ischemic reproduction injury?

A

Blood flow is restored after ischemia.
Sudden O2 can produce radicles
Neutrophils increase and can trigger inflammation and damage cell.
Complement proteins activate the complement pathway.

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6
Q

What is the role of a heat shock protein?

A

Refolds misfolded/ denatured proteins. Upkeep proteins.

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7
Q

How can the appearance of a tissue with cell damage change under light microscopy

A

Reversible - swelling so light cytoplasm or if irreversible then dark due to accumulations of ribosomes and proteins.
Nuclear changes - chromatin clumping/ shrinkage - pyknosis, karryohexis (fragmentation) or karyolysis.
Intra cellular accumulations.

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8
Q

Cell damage under electron microscope?

A

Cell and organelle swelling.
Myelin figures at membrane (damage that looks like myelin sheath)
Amorphous densities in mitochondria.

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9
Q

What is the difference between oncosis and necrosis?

A

Oncosis: the spectrum of changes that occur within an injured cell before it dies.

Necrosis: the morphological changes that occur following cell death due to degredating proteins.

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10
Q

What is dystrophic calcification? Why does it not happen in every case of necrosis.

A

Necrotic tissues harden/ calcify.

Because normally necrotic tissue is degraded by enzymes and removed via phagocytosis.

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11
Q

What is coagulative necrosis?

A

Produced mostly from ischemia.
Protein denaturation >protein breakdown (active proteases)
Produces a ‘ghost outline’ histologically
Results in inflammation and infiltration by phagocytes.

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12
Q

What is liquifactive necrosis?

A

Protein breakdown by active proteases > protein denaturation
Often caused by infection - neutrophil damage.
E.g. Brain
Causes acute inflammation with lots of luvly pus

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13
Q

What is caseous necrosis?

A

Cheese appearance - granulomatous inflammation

Often caused by TB

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14
Q

What is fat necrosis?

A

Destruction of adipose tissue.
Normal in acute pancreatitis (due to lipases) or from direct trauma to fatty tissues (e.g. Breasts).
FA can react with Ca to form chalky deposits in fatty tissue which can be seen on X-rays or with the naked eye.

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15
Q

What is gangrene?

A

Necrosis that can be seen with the naked eye often caused by limb ischemia.
Can be wet (liquifactive) which can result in septicaemia or dry due to coagulative necrosis.

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16
Q

What is an infarction? How is it different to ischemia? How is infarction different in brain and heart? What do the consequences of infarction depend on?

A

Ischemia is a decreased blood supply to an organ or tissue.
Infarction is a cause of necrosis. It is an area of tissue that has died from an obstruction in blood supply e.g. Twisting of a vessel/ ischemia.
So ischemia causes infarction.
In heart leads to coagulative and brain liquifactive.

Consequences depend on:
Alternate blood supply?
How quickly it has occurred (other perfusion pathways?)
How vulnerable tissue is to hypoxia 
O2 conc in blood.
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17
Q

How is infarction described?

A

White or red.
White occurs in organs with good stromal support after an occlusion of an end artery.
Red occurs in organs with poor stromal support (loose tissue), dual bloody supply, previous congestion or raised Venus pressure.

*think… Will blood (red stuff) build up or not?

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18
Q

How does apoptosis appear under the microscope?

A

Chromatin condensation, pyknosis (degredation of cell nucleus) , nuclear fragmentation.
Cell shrinkage
Very eosinophilic - lots of protein in cytoplasm.

Under electron microscope ‘blebbing’ can be seen of apoptotic cell bodies which are eventually broken down by macrophages

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19
Q

How is apoptosis initiated?

A

Intrinsic - damage to DNA or no growth factors/hormones/p53 can initiate. Mitochondrial membranes become permeable releasing cytochrome c.

Extrinsic- ligands e.g. TRAIL or FAS bind told earth receptors.

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20
Q

What is p53

A

Guardian of genome- can trigger apoptosis if DNA is damaged

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21
Q

What can prevent cytochrome c release from mitochondria?

A

Bcl-2

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22
Q

What is steatosis?

A

Abnormal accumulation of lipids in the liver often caused by alcohol, diabetes mellitus, obesity and toxins. No effect on function.

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23
Q

Where may you find abnormal accumulations of cholesterol within the body?

A

Within smooth muscle and macrophages in atherosclerosis.

In hyperlipideamias, in xanthomas accumulating in tendons.

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24
Q

When might you find abnormal accumulations of protein within the body?

A

Mallory’s hyaline in alcoholic liver disease.

A1 antitripsin genetic defect. It accumulates in liver, and does not degradeproteases in lungs so can cause emphysema.

25
Q

Describe 3 endogenous abnormal accumulations of pigments.

A

Lipofusin - not harmful from radicle damage - aging.
Heamosiderin- from iron e.g. Bruises and haemochromotosis (more iron uptake)
Bilirubin- from poor liver function.

26
Q

Where may you find distrophic pathological calcification?

A

In cell death, atherosclerosis, heart valve aging, tuberculous lymph nodes.

All not from abnormal metabolism.

27
Q

Where may you find metastatic pathological calcification and why?

A

PTH excess or ectopic Ptrh production.
Vit d disorders.
Renal failure
Destruction of bone secondary to tumours.

All errors in metabolism - usually asymptomatic

28
Q

Which cells produce telomerase?

A

Germ and stem cells as they are rapidly dividing.

Some cancers.

29
Q

What are the cofactors for alcohol dehydrogenase?

A

CYP2E1 and p450

30
Q

What occurs in acute alcohol hepatitis?

A

Necrosis of hepatocytes, Mallory’s bodies, fever, tiredness and jaundice.

31
Q

What oxidises paracetamol to napqi and when does this occur?

A 
Cytochrome p450 (cyp2e1)
Normal phase II is saturated (toxic dose)
Occurs in small amounts normally.
32
Q

Why might glutathione reserves be low?

A

Alcohol
HIV/ infection
Malnourishment
Enzyme induced drugs

33
Q

What is the action of asprin?

A

It acetylates platelet cyclooxygenase which stops their ability to make theomboxaine a2 which activates platelet aggregation

34
Q

What are the 3 major consequences of an asprin overdose?

A

Increased respiratory alkalosis - compensatory mechanisms lead to metabolic acidosis.

Effects carbohydrate, protein and lipid metabolism along with oxidative phosphorylation leading to metabolic acidosis.

Inhibits platelet aggregation leading to acute erosive gastritis and GI bleeding.

35
Q

When does blabbing occur?

A

Apoptosis only

36
Q

How is clotting impaired in haemophilia A? What does this mean for the patient?

A 
Defective in factor VIII
X linked recessive
Neonatal bleeding
Haematuria (blood in urine)
Hemarthrosis (bleeding into joint spaces)
Joint deformity
Compartment syndrome
37
Q

What is DIC?

A

Disseminated (wide spread) intravascular coagulation
Widespread clotting, exhausts clotting factors, haemorrhage
Caused by cancer, infections or shock.
Results in large bruises
Bleeding from at least 3 unrelated sites.

38
Q

What is Thrombocytopenia?

A

Reduced platelet count.
Caused by:
Decreased platelet production- metabolic disorders e.g. Hypothyroidism, bone marrow infiltration e.g. Leukaemia
Decreased platelet survival - DIC, antibodies e.g. Drugs/glandular fever
Loss of platelets- enlarged spleen (as this would hold more platelets), massive blood transfusion.

39
Q

What is thrombophilia?

A

Abnormality in blood coagulation that increases the risk of thrombosis.
E.g. Anti thrombin deficiency or abnormalities in factor V

40
Q

Define acute inflammation

A

The body’s response to injury to limit tissue damage.

Fluid exudation and cellular infiltration

41
Q

List the macroscopic features of acute inflammation

A

Rubor, tumor, calor, dolor, loss of fuction

42
Q

Explain the changes of blood flow that occurs during acute inflammation.

A

Transient vasoconstriction.
Vasodilatation.
Increased endothelium permeability.
Slowing of circulation and exudation of fluid.
Stasis= conc of RBC in small vessels and increased viscosity of blood.

43
Q

Describe how exudation occurs. How is it different to transudate?

A

Increased blood flow and vasodilation increases hydrostatic pressure (starlings forces) and leakage of protein due to increased permeability. Transudate= no protein.

44
Q

Describe the mechanisms for vascular leakage

A

Endothelial contraction - histamine, leukotrienes.
Cytoskeleton remodelling - cytokines IL1 and TNF
Increased endothelial channels- transcytosis- VEGF
Direct trauma
Leukocyte dependent injury- ROS

45
Q

Name and describe some immediate and persistent chemical mediators of acute inflammation

A 
Immediate= histamine! causes pain ect but transient.
Persistent = leukotrienes and bradykinin.
46
Q

Describe cells associated with fibrous repair

A 
Mainly macrophages (phagocytosis, cytokines, complement components, blood clotting factors, proteases) and lymphocytes.
Giant cells- langhans horse shoe in TB. Foreign body groups type and touton clock face in fat necrosis.
Possibly eosinophils with allergy, parasite or tumors, plasma cells or fibroblasts/mayo fibroblasts (recruited by macrophages)
47
Q

Give the possible effects of chronic inflammation and examples of each.

A

Fibrosis e.g. Chronic cholecysitis from repeated acute inflammation/ gall stone blockage. From acute gastritis (alcohol/drugs) or chronic (helicobacter pylori)
Impaired function e.g. Chronic inflammatory bowel disease- cobblestone appearance, idiopathic- dia, rectal bleeding.
Increased function - thyrotoxicosis e.g. Graves’ disease.
Atrophy - gastric mucosa, adrenal gland
Stimulation of immune response - RA
Fibrosis and impaired function e.g. Liver cirrhosis
Fibrosis and impaired function

48
Q

What is a granuloma?

A

Epithelioid histiocytes with associated lymphocytes. Arises with persistant antigenic stimulation e.g. Hypersensitivity, foreign material, TB (caseous leading to arrest, fibrosis and scarring, erosion of lung), or unknown cause e.g. Sarcoid (lymph nodes and lung), crohns, wegners.

49
Q

Difference between ulcerative colitis and Crohn’s disease?

A

Crohns is transmural not superficial.

50
Q

What is the difference between military TB and single organ?

A

Many bugs vs few

51
Q

What is fibrous repair and when does it occur

A

Replacement of functional tissue by scar tissue.

Occurs in permanent cell type tissues or when the collagen framework has been destroyed. - if not then resolution

52
Q

What is the mechanism of fibrous repair

A

1 infiltration of cells, blood clot forms followed by acute and possibly chronic.
2 clot replaced by granulation tissue
3 maturation, less cells, more collagen, less vasculature contraction of myofibroblasts

53
Q

3 key components in making granulation tissue

A

Cell migration - inflammatory cells, myofibroblasts and fibroblasts (produce extracellular matrix) , endothelial cells (angiogenesis)
Angiogenesis.
Production of extracellular matrix to anchor cells, separate tissues, sequester growth factors, cell movement

54
Q

Describe the steps of angiogenesis

A

Chemotactic chemicals released
Proteolysis of basement membrane
Endothelial cell proliferation and migration to form a new tube.
Recruitment of peri-endothelial cells.

55
Q

What factors affect regeneration

A

Growth factors and contact with other cells/basement membrane.

56
Q

Describe healing by primary and secondary intention

A 
Priamry= Apposed edges! epidermis first followed by dermis. Risk of trapping infection. Minimal scad and good strength .
Secondary= large scab/eschar. Dermis upwards, long, scar, lots of granulation tissue. More contraction.
57
Q

What is Alpert syndrome

A

Defective type IV. Renal failure and eye probs

58
Q

Local and general factors affecting wound repair

A

Local- size, radiation, infection, blood supply

General- age, drugs, diet, general Heath

59
Q

What is the difference between strictures and contractures

A

Contractures limit movement

strictures obstruct tubes and channels

60
Q

Describe regeneration of a peripheral nerve

A 
1mm a day, distal proliferation.
Wallerian degeneration (cut or crushed nerve), part not connected to body degenerates

ESA 2 (9 decks)

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