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MOD Flashcards

0
Q

Anti thrombotic agents in the endothelium

A
  • plasminogen activators
  • prostacyclin
  • nitric oxide
  • thrombomodulin
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1
Q

General Thrombin Inhibitors

A
  • anti-thrombin III
  • α1 antitrypsin
  • α2 macroglobulin
  • protein C
  • protein S
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2
Q

What are the three constituents of Virchow’s Triad?

A
  • abnormalities in blood flow
  • abnormalities in blood constituents
  • abnormalities of the blood vessel wall
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3
Q

What is the appearance of arterial thrombi?

A

Pale, granular, lines of zahn (red-rbc, white-wbc), lower cell count.

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4
Q

What is the appearance of a venous thrombi?

A

Soft, gelatinous, deep red, higher cell count

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5
Q

What are the 5 possible outcomes of thrombosis?

A 
Lysis
Propagation
Organisation
Re-canalisation
Embolism
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6
Q

4 types of hypoxia and what they are?

A
  • hypoxaemic hypoxia- arterial O2 contents is low e.g. Altitude or lung disease
  • anaemic hypoxia- decreased ability of Haemoglobin to carry oxygen e.g. CO poisoning
  • ischaemic hypoxia- interruption to blood supply e.g. Emboli
  • histiocytic hypoxia- inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes e.g. Cyanide poisoning
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7
Q

Three free radicals

A

OH. (Most dangerous)
O2
H2O2

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8
Q

What reaction does superoxide dismutase catalyse ?

A

O2–> H2O2

It’s an antioxidant reaction.

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9
Q

The three cell changes that can be seen under light microscopy, and the reversible and irreversible changes.

A
  • Cytoplasmic changes- reduced pink staining due to accumulations of water (reversible) then increased pink staining due to detachment of free ribosomes from the ER (irreversible).
  • nuclear changes- chromatin clumps (reversible) then pyknosis, shrinkage ; karryohexis, fragmentation; and karryolysis, dissolution of the nucleus (irreversible).
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10
Q

The 4 reversible changes that can be seen under electron microscopy.

A
  • swelling- due to sodium-potassium pump failure
  • cytoplasmic bless- due to cell swelling
  • clumped chromatin- reduced pH
  • ribosome separation from the ER- decreased energy in cells
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11
Q

The 6 irreversible cell changes that can be seen with electron microscopy.

A
  • swelling
  • pyknosis, karryolysis, and karryohexis
  • rupture of lysosomes
  • myelin figures
  • ER damage
  • amorphous densities in mitochondria
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12
Q

Brief description of caseous necrosis

A

Microscopically cheesy appearance
Amorphous debris
Infections e.g. TB

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13
Q

Give some key apoptotic molecules (6)

A
  • p53- guardian of the genome (DNA damage)
  • cytochrome c, APAF 1, caspase 9- form the apoptosome
  • BCL1- prevents cytochrome C release from mitochondria (inhibits apoptosis)
  • death ligands e.g. TRAIL
  • death receptors e.g. TRAIL-R
  • Caspases- effector molecules of apoptosis
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14
Q

What is steatosis?

A

Abnormal accumulation of triglycerides in a cell. Often seen in the liver.

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15
Q

What is Mallory’s Hyaline?

A

Damaged protein accumulation seen in hepatocytes in alcoholic liver disease.

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16
Q

What is α1-antitrypsin deficiency and what are the common symptoms.

A

It is a genetically inherited disorder, the liver produces a version of the protein which is misfolded. It cannot be packaged by the ER and accumulates within it, so can’t be secreted by the liver. The systemic deficiency means that proteases within the lung act unchecked and patients with the condition develop emphysema as lung tissue is broken down.

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17
Q

How is alcohol metabolised?

Steps and enzymes

A

Ethanol—(1)—>acetaldehyde—(2)—>acetate

  1. Alcohol dehydrogenase predominantly, also by cytochrome p450 enzyme CYP2E1 and catalase.
  2. Aldehyde dehydrogenase
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18
Q

In alcohol tolerance, which enzyme has been induced?

A

CYP2E1

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19
Q

What are the three main effects on the liver of excessive alcohol intake?

A
  • Fatty Changes- steatosis, reversible
  • Acute alcoholic hepatitis- metabolites are toxic, usually reversible
  • Cirrosis- irreversible and sometimes fatal
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20
Q

How is paracetamol usually detoxified?

A

Via sulphonation and glucuronidation. Small amounts are metabolised by cytochrome p450 oxidation (CYP2E1) into NAPQI.

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21
Q

What detoxifies NAPQI?

A

Glutathione

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22
Q

What happens to glutathione in a high dose of paracetamol and why is this important?

A

Glutathione is used up and NAPQI accumulates. NAPQI is toxic and binds to sulphydryl groups on liver cell membranes causing hepatocyte necrosis and potentially liver failure.

23
Q

How can an aspirin overdose be fatal?

A

aspirin stimulates the respiratory centre of the brain which results in respiratory alkalosis. The metabolic acidosis is created to compensate but results in an increase in lactate, pyruvate and ketone bodies–> more acidosis.

24
Q

What are the 5 classical clinical signs of inflammation?

A
  • Calor -heat
  • Rubor- redness
  • Tumor- swelling
  • Dolor- pain
  • Loss of function
25
Q

What’s the difference between unipotent, multipoint, pluripotent and totipotent.

A

Unipotent- can only become one type of cell.
multipotent- can produce several types of cell
totipotent- can produce any type of cell including placenta etc.
pluripotent- can become any type of body cell.

26
Q

What are labile cells?

A

cells whose normal state is one of division (they’re in G1-M-G1) e.g. epithelial cells.

27
Q

What is an embolism?

A

The blockage of a blood vessel by a solid, liquid or gas at a site distant from its origin

28
Q

How do you treat a DVT?

A
  • IV heparin

- oral warfarin

29
Q

When are fat emboli commonly found?

A

After a fracture.

31
Q

What’s the definition of atheroma?

A

The deposition of intracellular and extracellular lipid in the intimate and media of large and medium sized arteries.

32
Q

what are the three main features of acute inflammation?

A
  1. vascular and cellular reactions- accumulation of fluid exudate and neutrophils in tissues
  2. controlled by a variety of chemical mediators derived from plasma or cells
  3. protective, but can lead to local complications and systemic effects
33
Q

list some possible causes of acute inflammation

A
  • microbial infections
  • hypersensitivity reactions
  • chemicals
  • tissue nectosis
34
Q

what are the three changes which occur to tissues in acute necrosis?

A
  • changes in blood flow
  • exudation of fluid into tissues
  • infiltration of inflammatory cells
35
Q

what are the changes in blood flow which occur during acute inflammation?

A
  • transient vasoconstriction of arterioles (a few seconds)
  • vasodilation of arterioles and then capillaries to increase blood flow
  • increased permeability of blood vessels- exudation of protein rich fluid into the tissues and slowing circulation
  • concentration of RBCs in small vessels and increased viscosity of blood= STASIS
36
Q

what is the chemical mediator of an early acute inflammatory response?

A

Histamine

37
Q

what is histamine and which cells produce it?

A
  • released from mast cells, basophils and platelets

- in response to many stimuli e.g. physical damage, IL-1, immunological reactions and C3a.

38
Q

what are the effects of histamine?

A
  • vascular dilation
  • transient increase in vascular permeability
  • pain
39
Q

what are the chemical mediator of a late acute inflammatory response?

A
  • many
  • it’s not completely understood
  • leukotrienes and bradykinin
40
Q

describe the factors which lead to exudation of fluid into issues.

A
  • increased hydrostatic pressure–> increased flow of fluid out of vessel
  • increased colloid osmotic pressure of interstitium–> increase of fluid flow out of vessels
41
Q

what features of acute inflammation cause exudate to be formed?

A
  • arteriolar dilation leads to an increase in hydrostatic pressure
  • increased permeability of vessel walls leads to a loss of protein into the interstitium
42
Q

what’s the difference between transudate and exudate?

A

exudate has a high protein content, transudate has low protein.

43
Q

when would tissue fluid be transudate?

A
  • due to a hydrostatic pressure imbalance

- occurs in cardiac failure or venous outflow obstruction

44
Q

what are the main mechanisms of vascualar leakage and what causes them?

A
  • endothelial contraction- caused by histamine and leukotrienes
  • cytoskeleton reorganisation- mediated by cytokines IL-1 and TNF
  • direct injury- toxic burns, chemicals, severe sun burn etc
  • leukocyte dependent injury- toxic oxygen species and enzymes from leukocytes
  • increased transcytosis- VEGF
45
Q

what is the role of exudate during acute inflammation?

A

it delivers proteins to the site of injury e.g. fibrin which localises the injury

46
Q

list the stages or neutrophil infiltration.

A
  • Margination
  • Rolling
  • Adhesion
  • Emigration
47
Q

what is Margination during neutrophil infiltration?

A

stasis causes neutrophils to line up at the edge of blood vessels along the endothelium, which is the opposite of normal laminar flow where the centre is more cellular.

48
Q

what is Margination during neutrophil infiltration?

A

stasis causes neutrophils to line up at the edge of blood vessels along the endothelium, which is the opposite of normal laminar flow where the centre is more cellular.

49
Q

what is Rolling during neutrophil infiltration?

A

neutrophils then roll along the endothelium, sticking to it intermittently. Mediated by selecting on the neutrophil surface membrane.

50
Q

what is Adhesion during neutrophil infiltration?

A

The neutrophils ‘stick’ to the surface, it’s mediated by interns and PECAM.

51
Q

how do neutrophils escape from vessels?

A
  • relaxation of inter-endothelial cell junctions
  • digestion of vascular basement membrane
  • movement (duh)
52
Q

what molecules facilitate phagocytosis?

A

opsonins Fe and C3b

53
Q

what is chemotaxis and what molecules mediate it?

A
  • movement along a concentration gradient of chemical attractants
  • C5a, LTB4, bacterial peptides
54
Q

what are the two broad terms used to describe how phagocytes destroy cells?

A
  • oxygen dependent

- oxygen independent

55
Q

describe the oxygen dependent mechanism of cell apoptosis.

A
  • produces superoxide and hydrogen peroxide
  • H2O2- myeloperoxidase-halide system
  • produces HOCl
56
Q

describe the oxygen dependent mechanism of cell apoptosis.

A
  • produces superoxide and hydrogen peroxide
  • H2O2- myeloperoxidase-halide system
  • produces HOCl
57
Q

describe the oxygen independent mechanism of cell apoptosis.

A
  • occurs in ischaemic tissues
  • lysosome and hydrolases
  • bactericidal permeability increasing protein (BPI)
  • Catatonic protiens ‘defensins’

Things To Remember (17 decks)

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