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Medicine > MoD > Flashcards

MoD Flashcards

1
Q

What is Hypoxia?

A

Oxygen Deprivation

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2
Q

What happens in Reversible Hypoxic injury?

A

Reduced O2 reduces ATP production, this slows the Na+ pump, Cell swelling by osmosis, increase in Glycolytic pathway which increases Lactic acid, decreased pH causes clumping of nuclear chromatin, Ribosomes detach due to lack of energy, build up of fat + denatured proteins

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3
Q

What happens in Irreversible Hypoxic injury?

A

Ca2+ enters through damaged plasma membrane, Ca2+ conc. rises, activates ATPases, Phospholipases, Proteases, Endonucleases, this reduces ATP and damages membrane and DNA

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4
Q

What is the marker for Cell damage in the Liver?

A

Transaminase

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5
Q

How does Cyanide work?

A

Blocks Oxidative Phosphorylation by binding to Mitochondrial cytochrome oxidase

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6
Q

What is the Fenton reaction and why is it important?

A

Fe2+ + H2O2 -> Fe3+ + OH- + OHr, Its important in bleeding as when blood is around iron is availible to make FR’s

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7
Q

Which enzyme is involved in the conversion of Hydroxyl groups to Hydrogen Peroxide?

A

Superoxide Dismutase

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8
Q

Which enzymes are involved in the removal of H2O2?

A

Catalases and Peroxidases

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9
Q

What are the Free Radical Scavangers?

A

Vitamines A, C and E, Glutathione

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10
Q

Which storage proteins sequester Iron and Copper?

A

Transferrin and Ceruloplasmin

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11
Q

What do Heat Shock Proteins do?

A

Recognise any misfolding of proteins and repair them, if they cant they destroy the misfolded protein

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12
Q

What changes can you see of cell injury under a light microscope?

A

Swelling (reduced pink staining due to increase in water), Increased staining due to ribosome detachment. Chromatin clumping, Shrinkage, fragmentation, dissolution of nucleus

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13
Q

What cell changes do you see under an electron microscope in Reversible cell injury?

A

Swelling, Blebbing, Clumping chromatin, Seperation of ribosomes

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14
Q

What cell changes do you see under an electron microscope in irreversible cell injury?

A

Shrinkage, fragmentation, dissolution of Nucleus, Rupture of Lysosomes, Membrane defects, Lysis of ER, swollen Mitochondria

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15
Q

What is Oncosis?

A

Cell death by swelling

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16
Q

What is Necrosis?

A

Morphological changes that occur after cell death

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17
Q

When does Coagulative Necrosis happen?

A

When there is more protein denaturation than active proteases being released, cell proteins uncoil and become less soluble

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18
Q

When does Liquifactive Necrosis take place?

A

When the release of active Proteases is greater than the protein denaturation

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19
Q

When is Caseous Necrosis commonly seen?

A

TB in the Lungs

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20
Q

What is fat Necrosis and when is it commonly seen?

A

Destruction of adipose tissue, commonly seen in acute Pancreatitis as lipases are released in inflamation

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21
Q

What is Gangrene?

A

Necrosis visible to the naked eye

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22
Q

Whats the difference between Red and White infarcts and when do they both occur?

A

There is no Haemorrhaging into white infarcts, these are typically found in solid organs. There is Haemorrhaging into red infarcts and they are found in organs with poor stromal support

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23
Q

What does the severity of an infarct depend on?

A

Alternate blood supply, How quickly ischemia takes place, how venerable the tissue is to hypoxia, O2 content of the blood

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24
Q

Which molecules can be released from injured cells?

A

Potassium, Enzymes, Myoglobin

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25
Q

What is apoptosis?

A

Internally controlled cell death by cell shrinkage

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26
Q

How does intrinsic Apoptosis happen?

A

DNA damage or P53 trigger increased mitochondrial permeability -> Release Cytochrome C -> APAFI and caspase 9 activate further caspases

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27
Q

Whats the difference between intrinsic and extrinsic Apoptosis?

A

Extrinsic apoptosis a ligand binds to a death receptor which activates caspases independent of mitochondria

28
Q

What is Steatosis? Where and when is it often seen?

A

Accumulation of triglycerides, seen in the liver due to Alcohol abuse, diabetes + obesity

29
Q

Where and how is excess Cholesterol stored?

A

Membrane bound droplets in smooth muscle cells + macrophages within atheroma plaques, macrophages in skin and tendons form xanthomas

30
Q

What is Malory’s hyaline?

A

A damaged protein seen in hepatocytes in alcoholic liver disease due to altered Keratin filaments

31
Q

What is a1-antitrypsin deficiency and what does it do?

A

Liver produces incorrectly folded a1-antitrypsin which cant be packaged by the ER or secreted from the liver. Proteases are unchecked and patients develop Emphysema.

32
Q

What is Lipofuscin and whats it a sign of?

A

Age pigment, Sign of previous free radical injury and lipid peroxidation

33
Q

What is Haemosiderin? What happens in systemic overload of iron?

A

Its an iron storage molecule, Systemic overload of iron leads to the deposition of Haemosiderin in the skin, liver, pancreas + heart

34
Q

What is Haemochromatosis and what does it cause?

A

Increased intestinal absorption of iron, leads to ‘Bronze diabetes’ due to scaring of liver and pancreas

35
Q

Where does Bilirubin come from and how is it excreted?

A

Comes from breakdown of Heme, Taken to the liver by albumin and conjugated with glucaronic acid for excretion in the bile

36
Q

What causes Dystrophic Calcification? What does it affect?

A

A local change causes the favoring of nucleation of hydroxyapatite crystals, Affects dying tissue, atherosclerotic plaques, damaged heart valves + TB lymph nodes

37
Q

Metastatic Calcification is caused by hypercalceamia and affects the whole body, what causes hypercalceamia? What are the causes due to?

A

Increased PTH secretion causes bone resorption, due to: Parathyroid hyperplasia or tumor, Renal failure (increased retention of phosphate), secretion by malignant tumors. Destruction of bone, due to: Tumors in bone marrow, Paget’s disease (increased bone turnover), Immobilisation

38
Q

What enzyme is in stem cells and some cancer cells that allows them to divide indefinitely?

A

Telomerase

39
Q

What are the 3 main effects chronic excessive alcohol intake has on the liver?

A

Fatty change (steatosis), Acute alcoholic Hepatitis, Liver Cirrhosis

40
Q

What are the clinical signs of acute inflammation?

A

Redness, Heat, Swelling, Pain + Loss of function due to the others

41
Q

How is exudate formed?

A

Vasodilation of arteries increases capillary pressure which increases fluid + Leucocyte delivery to area. Endothelial cells swell and retract to allow leakage. This increases Haematocrit which slows flow and increases exudate formation

42
Q

What is Starlings law dependent on?

A

Hydrostatic pressure and Osmotic pressure of both the blood and interstitial fluid

43
Q

What are the defensive proteins found in exudate and what do they do?

A

Opsonins - Coat foreign materials ready for phygocytosis, Complement proteins - assemble to produce bacteria perforating structure, Antibodies - act as Opsonins

44
Q

What is Transudate?

A

Same as exudate just with a lower protein count

45
Q

What are the steps of Neutrophils destroying their target in acute inflammation?

A

Chemotaxis (Directional movement towards chemical attractant), Activation (Chemotaxin binds, Ca2+ + Na+ enter, cell gives out Pseadopia), Margination (Leucocytes bind to selectins+ roll, bind tightly to integrins), Diapedesis (Leucocytes produce collagenase to digest the basement membrane, then pull themselves along collagen fibers towards target), Recognition (Opsonins make it easier for phagocytes to recognise targets), Phagocytosis (Particle absorbed and forms Phagosome, Degranulation occurs), Killing (either Oxygen Burst or Enzymes)

46
Q

What are the local complications of acute inflammation?

A

Damage to local tissue due to phagocytosis, Obstruction of tubes + compression of structures, Loss of fluid, Pain due to Bradykinin

47
Q

What are the systemic effects of acute inflammation?

A

Fever (due to pyogenic cytokins, increases synthesis of prostoglandin EZ in hypothalemus), Production of colony simulating factors increases production of neutrophils, Liver increases production of fibrinogen, C3, a1-antitripsin, Shock

48
Q

What functions do macrophages have in chronic inflammation?

A

Secretion of substances that effect other cells, Phagocytosis (hard to kill bacteria), Presentation of of antigens, Stimulation of angiogenesis, Inducing Fibrosis + Fever

49
Q

When are T+B Lymphocytes found and what do they do?

A

Presence of antigenic material, Process + Secrete antibodies, Secrete cytokines, Kill cells

50
Q

What are the 3 types of Giant cells and their distinguishing features?

A

Foreign Body (Randomly arranged Nuclei), Langerhans (Peripherally arranged nuclei, seen in TB), Touton (Nuclei arranged in ring towards the center, seen in lesions with high fat content, Fat necrosis + xanthomas)

51
Q

What is Chronic Cholecystitis and what causes it?

A

Chronic inflammation + fibrosis of the gall bladder wall, caused by repeated blockage + acute inflammation

52
Q

How does Healing by Primary Intention happen?

A

Heamostasis -> Neutrophils -> Macrophages scavenge dead cells, secrete cytokines for fibroblasts + endothelial cells -> Wound fills with granulation tissue, collagen is deposited

53
Q

How is a bone fracture healed?

A

Heamotoma -> Fibrin mesh -> Soft Callus -> Hard Callus -> Formation of Laminar bone -> Remodeling to mechanical stress

54
Q

What forms and breaks down blood clots?

A

Platelets adhere to each other + damaged vessel walls to form platelet plug, Prothrombin -> Thrombin which catalyses Fibrinogen -> Fibrin. Breakdown of Fibrin by Plasmin (Plasminogen -> Plasmin)

55
Q

What makes up Virchow’s Triad of things that increase blood clot probability?

A

Abnormalities to; Vessel wall, Blood Flow, Blood components

56
Q

What are the deficiencies present in Type A + B Hemophilia?

A

Type A is deficiency in Clotting factor VIII, Type B is factor IX

57
Q

What is Disseminated Intravascular Coagulation?

A

Pathalogical activation of coagulation mechanisms. Small clots form throughout the body using all clotting factors. Abnormal bleeding from skin is seen. Triggers - Infection, Trauma, Liver Disease

58
Q

How are Atheromas formed?

A

Endothelial injury -> Platelet adhesion, PDGF release -> SMC proliferation + migration -> Uptake of lipid by SMC + Macrophages -> Migration of monocytes to intima -> Foam cells secrete cytokines -> Increased SMC activation + Inflammatory response

59
Q

What is Metaplasia?

A

Reversible replacement of one adult differentiated cell type by another

60
Q

What causes Pus to be white?

A

High number of neutrophils

61
Q

What is Serous exudate and what does it suggest?

A

Contains plasma proteins but few leucocytes suggesting no infection by microorganisms

62
Q

What is Fibrinous Exudate and where is it found? v

A

Significant deposition of fibrin, prevents smooth movement of pericardium and plural sac

63
Q

What is Hereditary Angio-oedema and what does it cause?

A

Deficiency of C1-inhibitor, C1 is a complement protein that cleaves C2 + C4 to form C3, also inhibits Bradykinin, uninhibited it increases permeability of endothelia causing oedema. Experience abdominal pain due to intestinal oedema.

64
Q

What is Chronic Granulomatous Disease?

A

Phagocytes unable to produce free radical superoxide (O2-) so cant produce oxygen burst. Chronic infections form, Granulomas + abscesses form over body.

65
Q

What is Lobar Pneumonia?

A

Basically acute infection in the alveoli of the lungs

Medicine (10 decks)

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