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Pathological Processes > Mechanisms > Flashcards

Mechanisms Flashcards

1
Q

Fully discuss 3 factors of irreversible hypoxic injury

A
  1. Cell membrane destruction due to protease activation
  2. Influx of Ca2+ from cytoplasm, ER and mitochondria
  3. Activation of destructive enzymes:
    - ATPase: low ATP
    - Phospholipase: decreased phospholipids
    - Endonuclease: increased nuclear chromatin destruction
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2
Q

Fully discuss 3 factors of reversible hypoxic injury

A
  1. Cell swelling due to reduced Na+ pump so get increased influx of Na+, Ca2+ and H20
  2. Reduced cellular pH due to increased glycolysis as a result of low ATP levels
  3. Destruction of protein synthesis due to detachment of ribosomes, leading to increased lipid deposition
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3
Q

Destruction of mitochondria leads to what type of hypoxia?

Explain

A

Oxidative phosphorylation enzymes get destroyed so you get histiocytic hypoxia as oxygen in cells can no longer be used

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4
Q

What features are seen in reversible hypoxic injury?

split it up into the 3 factors seen

A
  1. (Due to cell swelling): blebs, ER swelling, loss of microvilli
  2. (Due to reduced cell pH): increased chromatin clumping
  3. (Due to reduced protein synthesis): increased lipid deposition
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5
Q

What are the effects of free radicals on a cellular level?

A
  1. Oxidise proteins, DNA and carbohydrates - denature, mutations
  2. Lipid peroxidation - forms more radicals
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6
Q

Describe ischaemia-reperfusion injury

A

Return of blood flow brings

  1. Complement proteins, which activates the complement pathway
  2. Brings neutrophils, which stimulates inflammation
  3. Brings free radicals due to mitochondrial burst
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7
Q

Name 3 heat shock proteins

A

Unfoldases

Stress proteins

Chaperonins

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8
Q

What is dystrophic calcification?

A

When necrotic tissue calcifies

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9
Q

Describe the 2 major types of necrosis

Give examples of each

A
  1. Coagulative, e.g. MI, occurs as denatured proteins coagulate
  2. Liquefactive, e.g. Cerebral infarct, occurs as protein undergo autolysis
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10
Q

What are the 2 types of gangrene and what types of necrosis causes each of them?

A
  1. Dry gangrene (air) is caused by coagulative necrosis DC

2. Wet gangrene (bacteria) is caused by liquefactive necrosis LW

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11
Q

What inflammatory marker is found to be high in cells that have undergone apoptosis?

A

Eosinophils

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12
Q

What are the 4 steps of apoptosis?

A
  1. Initiation
  2. Execution
  3. Degradation and Phagocytosis
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13
Q

What does Cytochrome C activate in apoptosis?

What is the function of the thing activated?

A

Cytochrome C activates caspases, which cleaves DNA in the cytoplasm and cleaves proteins in the cell membrane

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14
Q

The cytoplasm in necrosis forms blebs as a result of oncosis (cell swelling), in apoptosis, what does the cytoplasm form as a result of oncosis?

A

Buds

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15
Q

What is Mallory’s hyaline?

A

The breakdown and accumulation of keratin in hepatocyte cytoplasms as a result of alcohol abuse.

(Keratin gives the cells structural support)

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16
Q

What are histamines effects in the formation of an exudate?

A

Histamine stimulates pain, arteriole vasodilation and leaky venules

1) AV: Initially vasoconstriction (s), then vasodilation (m), more leukocytes enter the area and capillary HP increases
2) LV: Histamines lead to the contraction of the endothelial cells lining the venule so proteins can leak out and enter the extracellular space (high capillary HP also causes this)

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17
Q

Discuss 3 functions of neutrophils in inflammation

A
  1. Chemotaxis: be summoned to an area fo inflammation
  2. Phagocytosis: engulf the MO
  3. Killing of MO: oxygen dependent where free radicals are released into the phagosome then the mitochondria will undergo respiratory burst OR oxygen independent where enzymes, proteases and lysozymes, kill the MO in the phagolysosome
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18
Q

Name 3 complement components involved in phagocytosis and discuss their MOA

A

C3a, C4a and C5a all produce tubes that stab into bacteria and kill them.

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19
Q

List 4 local consequences of acute inflammation

A
  1. Damage to normal tissue (due to phagocytosis)
  2. Obstruction of tubes (due to swelling caused by exudate)
  3. Pain and loss of function (to aid rest)
  4. Loss of fluid
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20
Q

List 4 complications of systemic inflammation

A
  1. Leucocytosis
  2. Fever
  3. Shock
  4. Acute phase response
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21
Q

What is shock in inflammation?

A

Drop in blood pressure due to vasodilation and increase in exudate formation due to the increase in venule permeability

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22
Q

Hereditary angio-oedema is an acute inflammatory disorder.

Describe its pathogenesis

A

Deficiency of C1-esterase inhibitors leading to

  • rapid non itchy cutaneous angio-oedema as you get oedema of the dermis and hypo-dermis
  • abdominal pain due to intestinal oedema
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23
Q

Why do people with alpha 1 anti-trypsin deficiency, another acute inflammatory disorder, get liver cirrhosis?

A

Due to a lot of a1 anti-trypsin that has not been folded properly being unable to be pumped out of the sarcoplasmic reticulum, leading to a build up of this malfunctioned protein in the hepatocyte

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24
Q

What is the pathophysiology of chronic granulomatous disease?

A

Phagocytes cannot make superoxide so phagocytes can engulf the bacteria but the bacteria does not die as the mitochondria cannot undergo respiratory burst

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25
Q

What lowers free copper in the blood?

A

Ceruloplasmin

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26
Q

Describe the calcium and phosphate levels in dystrophic calcification

A

Both normal

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27
Q

What type of hypoxia does CO poisoning cause?

How?

A

Anaemic hypoxia as CO binds to Hb and reduces Hb’s ability to bind to oxygen

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28
Q

What type of hypoxia does cyanide poisoning form and how?

A

Histiocytic hypoxia as cyanide irreversibly inhibits Cytochrome C oxidase leading to reduced oxidative phosphorylation in the mitochondria as oxygen present cannot be used.

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29
Q

What exudates are seen in blisters?

Describe their appearance and what they are made up of

A

Serous exudates are clear and made up of few WCC (as there is no MO infection) and have a high plasma protein content

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30
Q

Describe fibrinous exudates

A

Cloudy as they have high fibrin count (seen where blood vessel damage occurs due to inflammation)

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31
Q

When are purulent exudates typically found and why are they creamy/white?

A

Occur when a bacterial infection is present and they are creamy due to the high neutrophil content

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32
Q

Describe the pathogenesis of fibrosis in chronic inflammation

A

Cytokines stimulate fibroblasts to produce excess collagen

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33
Q

Where are the placement of the nuclei in Langerhan type giant cells?

A

Around the periphery

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34
Q

What 5 cells are present in hypersensitive granulomas

A
  • Epithelioid cells
  • Macrophages
  • Giant cells (typically Langerhan’s)
  • Fibroblasts
  • Lymphocytes

(also see central caseous necrosis)

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35
Q

Chrons’ disease and Ulcerative colitis, which one has granulomas and crypt abcesses?

A

Chrons’ disease

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36
Q

Discuss 3 factors that aid cellular regeneration?

A
  1. Growth factors
  2. Cell-cell contact inhibition via cadherins preventing intact cells from proliferating and stimulating proliferation in damaged cells due to the loss of contact inhibition (damaged cells proliferate until they touch neighbouring ‘normal’ cells)
  3. Electric currents + nerve impulses
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37
Q

Name 3 cells that produce growth factors

A

MEP

Macrophages

Endothelial cells

Platelets

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38
Q

Name 2 examples of labile tissue

A

Columnar epithelia of GI tract (surface epithelia) and haematopoietic stem cells

39
Q

Name an example of stable tissue

A

Parenchyma of liver (turn into cells from their origin)

40
Q

Name 3 types of permanent cells

A

Neurones, skeletal muscle, cardiac muscle

41
Q

What is asymmetric replication and when is it typically seen?

A

In stem cell replication, there is always 1 daughter cell that remains as a stem cell, whereas the rest of the daughter cells turn into the end (non-diving) cell.

42
Q

At what rate do the sprouting axons of the peripheral nervous system grow at?

A

1-3 mm/day

43
Q

What are 3 effects of growth factors in cellular regeneration?

A

Locomotion

Angiogenesis

Inhibition of cell division

44
Q

Name 2 growth factors

A
  1. Vascular endothelial growth factor

2. Epidermal growth factor

45
Q

Discuss 3 scenarios where you would get fibrous repair (a scar) instead of normal regeneration?

A
  1. Necrosis of permanent tissue
  2. Loss of collagen framework of necrotic stable and labile tissue
  3. Chronic inflammation of necrotic stable and labile tissue
46
Q

Describe the pathophysiology of fibrous repair

A
  1. Blood clots
  2. Neutrophils infiltrate and digest clot
  3. Macrophages and lymphocytes infiltrate
  4. Angiogenesis due to proliferation of endothelial cells + myo/fibroblasts make collagen, a GLYCOPROTEIN (THIS IS GRANULATION TISSUE)
  5. Vessels, and other cells regress a part from collagen myofibroblats leading to the scar contracting as a result of the contraction of the fibrils in the myofibroblasts
47
Q

Describe the formation of Type 1 fibrillar collagen

A
  1. Alpha chains produced in ER of myo/fibroblasts
  2. Vit C hydroxylation - proline and lysine to hydroxylysine and hydroxyproline
  3. Procollagen x3 helix
  4. Procollagen secreted out
  5. Cleavage of procollagen to tropocollagen
  6. Polymerisation of tropocollagen to microfibrils
  7. Microfibrils -> fibrils -> (collagen) fibres
48
Q

Describe some signs seen in Ehlers-Danlos syndrome and what is the cause of this?

only need 3 but I’ve written a whole list

A

Collagen Type V mutation thus collagen lacks TENSILE STRENGTH so:

  • hypermobile joints, more prone to dislocation
  • poor wound healing
  • colon, large artery and corneal rupture
  • hyperextensible skin
49
Q

In osteogenesis imperfecta, why do they have:

A) blue sclera
B) fragile skeletons

A

A) not enough collagen in the sclera so it is translucent

B) too little bone tissue so not enough collagen

50
Q

Alport’s syndrome is an X linked mutation mostly affecting males.

What effect does this mutation have?

What triad of signs are typically seen?

A

Type IV collagen is abnormal leading to:

Dysfunction of the:

  • GBM (so have haematuria in childhood then get Chronic renal failure)
  • cochlea of ear (sensorineural hearing loss)
  • lens of eye

Side note:
‘A comes before E like 4 comes before 5’
A - Alport syndrome, 4 - type IV collagen malfunction
E - Ehlers Danlos syndrome, 5 - type V collagen malfunction

51
Q

Bone remodelling process

A

Hot - Haematoma forms
Teacher - Tissue dies
In -Inflammation
A - Angiogenesis
School - Soft callus forms - trabeculae of spongy bone
Can - Hard callus forms - bony callus of spongy bone
Love -Lamellar bone
Reece - Bone remodelling - Conversion of spongy/cancellous bone to cortical/compact bone

52
Q

In primary intention wound healing, what tissue dies before the wound healing can occur?

A

(A low number of) epithelial cells and connective tissue

Collagen and elastin are both examples of connective tissue

53
Q

What triggers the extrinsic pathway?

A

Thromboplastin released from damaged cells next to the haemorrhage

(Thromboplastin/Factor III/Tissue factor (all the same thing, just different names) is an enzyme released from platelets and other damaged cells and it converts Prothrombin -> Thrombin)

54
Q

Im haemostasis, what does the platelet bind to?

A

Subendothelium

55
Q

What makes up the subendothelium?

A

Basement membrane, collagen

56
Q

Measuring fibrinogen levels and TT thrombin time includes which pathways?

A

Both include the common pathway

57
Q

How are Haemophilia A and B inherited?

What is the primary biological effect of the mutations?

What clotting test will be affected and how would it be effected?

A

X linked recessive (so mostly only affect men)

Haemophilia A has a factor VIII (8) deficiency
Haemophilia B has a factor IX (9) deficiency

As both of these coagulants are involved in the intrinsic pathway, the PTT time will be longer

58
Q

What is the pathogenesis of von Willebrand disease?

A

Autosomal dominant disease leading to von Willebrand factor deficiency so get reduced platelet aggregation and reduced factor VIII stabilisation

(Thus PTT increases - more factor VIII broken down in intrinsic pathway)

59
Q

What does your platelet count have to be (at a minimum) for you to be classed to have thrombocytopenia?

What does the bleeding appear as?

A

100 x 10^9/L

Petechiae (bleeding from capillaries)

60
Q

Name 3 abnormalities in clotting in Thrombophilia

Discuss if they are high or low

A
  • low Antithrombin III
  • low Protein C
  • high factor V Leiden (in common pathway)
61
Q

Which thrombi is pale, granular, with lines of Zahn

A

Arterial thrombi

62
Q

How does a fat emboli come about?

A

Bone fracture then bone marrow fat breaks up and releases oil. The oil then coalesces and enters a gaping venule

63
Q

Macroscopically, what do you see in atherosclerosis?

A

Fatty streaks (in the intima)
Simple plaque
Complicated plaque

64
Q

Give 3 examples of complicated plaque

A

Ulceration

Calcification

Aneurysm into plaque

65
Q

Name 4 later microscopic changes seen in atherosclerosis

A

Fibrosis

Necrosis

Cholesterol clefts

Plaque fissuring

66
Q

What is the pathophysiology of homozygous familial hyperlipidaemia?

A

Low LDL-R so high circulating LDL so more atherosclerotic plaque so a lot of them have a MI before 20

67
Q

Discuss 4 reasons why obesity can lead to atherosclerosis

A
  1. Reduced HDL - less LDL metabolised by liver
  2. Prone to DM - leads to hypercholesterolaemia
  3. Prone to hypertension - damages endothelial cells leading to LDL oxidation
  4. Hypertriglyceridaemia
68
Q

Thrombomodulin function

A

Activate protein C

69
Q

What does CDK stand for?

What activates CDKs?

What is the function of CDKs?

A

Cyclin-dependent kinase

Cyclin activates them

They phosphorylase retinoblastoma proteins. Typically RB proteins (a tumour suppressor gene) keep cells at the R point (G1 end) but when the cell is ready to divide, RB is phosphorylated by activated CDK

70
Q

Stable, labile and permanent tissue.

Which one under goes hypertrophy and hyperplasia?

A

Hypertrophy:
Permanent

Hyperplasia:
Stable
Labile

71
Q

Give an example of compensatory hypertrophy

A

When you have one kidney removed, the kidney remaining will undergo hypertrophy

72
Q

Anaplasia definition

A

Very poor cell differentiation

73
Q

What are myelomas?

A

Malignant neoplasms of plasma cells

74
Q

Describe the process of malignant metastasis

A
  1. Growth and invasion of basement membrane at primary site
  2. Transport via, blood, lymph of transcoloemic spread to secondary site and lodge there
  3. Grow at secondary site to form new tumour (colonisation)
75
Q

Discuss 3 factors that are needed for proper malignant invasion?

A

Altered:

Proteolysis - more matrix metalloproteinases so connective tissue, basement membrane and stroma can be broken down

Adhesion - less E-cadherins binding malignant cells to each other and less integrins binding malignant cells to stomal proteins

Motility - actin cytoskeleton changed

76
Q

Name 5 cancer sites that are most likely to spread to the bone

A 
Lungs (Bronchus)
Thyroid
Breast
Prostate
Kidney
77
Q

How can human papilloma virus lead to cervical carcinoma?

Discuss fully

A

E6 (released from HPV) can inhibit p53 so DNA repair and apoptosis, of faulty genes and cells, does not occur

E7 (released from HPV) can inhibit RB protein so faulty cells push past the restriction point and start dividing

(p53 and RB proteins are tumour suppressor genes)

78
Q

Name 2 oncogenes

A

ras

HER-2

79
Q

What is the function of ras?

A

Encodes for G proteins which forces the cell past the restriction point

80
Q

What alterations in growth control are made in tumour growth?

A
  1. Growth signals
  2. Resistance to anti-growth signals
  3. Cell immortalisation
  4. Angiogenesis
  5. Apoptosis resistance
  6. Invasion and metastases
81
Q

What is genetic instability?

A

High frequency of mutations in the genome of the cell lineage

82
Q

The care taker gene is a tumour suppressor gener

What is its main function?

A

DNA repair

83
Q

Describe the grading system for breast carcinomas?

A

Bloom Richardson system:

  1. Tubular formation
  2. Pleomorphism
  3. High mitotic no.
84
Q

Pleomorphism definition

A

Variation in shape and size of nuclei

85
Q

CA 125 levels will be high in what cancer?

A

Ovarian cancer

86
Q

What are the 3 main categories of opsonins?

Give 2 examples of each

A

Acute phase proteins:

  • MBL
  • CRP

Antibodies:

  • IgG
  • IgM

Complement proteins:

  • C3b
  • C4b
87
Q

How do anti-oxidants neutralise ROS?

A

Donating an electron

88
Q

Name 2 proteins that are involved in the neutralisation of ROS by sequestering iron and copper.

Which protein does what?

With the removal of iron and copper, what does this now mean?

A

Ceruloplasmin sequesters (takes away) copper

Transferrin sequesters iron

So iron and copper are unable to catalyse the production of new free radicals

89
Q

Diapedesis definition

A

Entry of RBC through intact endothelial cells lining a blood vessel wall

(Neutrophil:
Chemotaxis -> Migration -> Diapedesis -> Phagocytosis)

90
Q

Describe the pathophysiology behind Achondroplasia

A

FGF3 receptor gene mutation so FGF cannot fulfil its normal function of promoting collagen formation from cartilage.

Endochondral ossification is affected.

91
Q

Factor VIIa and Factor VIIIa both convert Factor X to Factor Xa in the common pathway.

State what pathway, intrinsic or extrinsic, Factor VIIa and Factor VIIIa belong to.

State what triggers each pathway and what tissue factor is initially released.

A

Factor VIIa - Extrinsic pathway

Factor VIIIa - Intrinsic pathway

Extrinsic pathway is triggered by trauma leading to the release of tissue factor VII.

Intrinsic pathway is triggered by endothelial damage of blood cells promoting the release of tissue factor XII.

92
Q

What are 4 possible outcomes from acute inflammation

A
  1. Complete resolution
  2. Fibrosis and scarring (occurs when there is significant inflammation)
  3. Chronic inflammation (due to repeated insult)
  4. Abscess formation

(An abscess is a localised collection of pus surrounded by granulation tissue. Pus contains necrotic tissue with suspended dead and viable neutrophils and dead pathogens. It forms when the primary insult is a pyogenic bacterium and extensive tissue necrosis occurs.)

93
Q

If an abscess is not drained, what will happen to it?

A

It will be replaced by scar tissue

Pathological Processes (2 decks)

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