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PATH20001 Exploring Human Disease > Gaps > Flashcards

Gaps Flashcards

(65 cards)

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1
Q

What is invasive carcinoma?

A

Cancer that has spread beyond its original tissue layer into nearby tissues. It can invade lymphatics, blood vessels, or organs.

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2
Q

What is squamous cell carcinoma?

A

A cancer arising from squamous cells in the skin or mucous membranes. Often caused by UV exposure.

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3
Q

What is the role of E6 and E7 in HPV and cervical cancer? How do they disrupt cell cycle checkpoints?

A

HPV’s E6 protein degrades p53, and E7 inactivates Rb protein. This disrupts cell cycle control, leading to uncontrolled cell division and potential cancer development.

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4
Q

What is the role of vWF in primary hemostasis?

A

Von Willebrand factor (vWF) helps platelets adhere to damaged blood vessels, forming an initial plug to stop bleeding

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5
Q

HPV oncoproteins

A

HPV’s E6 and E7 proteins interfere with tumor suppressors p53 and Rb, promoting uncontrolled cell growth and potential cancer formation.

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6
Q

Role of vWF in Primary Hemostasis

A

• Vascular injury → collagen exposed
• vWF binds collagen → conformational change
• Exposes binding site for GPIb on platelets
• Platelets tether to injury site via GPIb–vWF–collagen
• vWF also stabilises factor VIII in plasma

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7
Q

Steps in Secondary Hemostasis

A

• Initiation: TF + FVIIa → activates FX → FXa
• Amplification: Thrombin (FIIa) activates FV, FVIII, FXI
• Propagation: Activated factors assemble on platelets → more thrombin
• Fibrin formation: Thrombin cleaves fibrinogen → fibrin
• Stabilisation: FXIIIa cross-links fibrin → stable clot

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8
Q

Tubular Epithelial Cell Necrosis (Ca²⁺ overload)

A

• Ischaemia/toxins → ↑ cytosolic Ca²⁺ in tubular cells
• Activates phospholipases, proteases → membrane damage
• Ca²⁺ impairs mitochondria → ↓ ATP
• Loss of membrane integrity → necrosis
• Seen in acute tubular necrosis (ATN)

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9
Q

List the steps in scar formation

A
  1. Inflammation
  2. M2 MPs replaces M1
  3. Angiogenesis
  4. FB recruitment and prolif
  5. Connective tissue deposition
  6. Connective tissue remodelling
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10
Q

Outline angiogenesis

A

New BVs development from existing ones
Key cells: pericytes, M2 MPs, endo cells

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11
Q

Outline fibroblasts

A

Fibroblasts: secrete collagen

MyoFBs: wound contraction during 2* intentional healing

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12
Q

What is the role of the ECM in wound repair?

A

Mechanical support - scaffold

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13
Q

What are the forms of ECM in wound repair?

A

Basement membrane
Interstitial matrix

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14
Q

What are the ECM components involved in connective tissue deposition?

A

Collagen, laminin, proteoglycans, glycoproteins, elastin

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15
Q

What are the cells involved in connective tissue deposition

A

M2 MPs
FBs - migrate to injury site + produce collagen

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16
Q

Describe granulation tissue

A

Initially weak, soft scar tissue
Type III collagen

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17
Q

Describe scar remodelling

A

Collagen I replaces collagen III - stronger
MMPs = matrix metalloproteases also facilitate remodelling
MyoFBs bring wound edges together

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18
Q

Outline scar formation after MI

A

Troponin 1 released from cardiomycotes - plasma indicator of MI
Repair = fibrosis
Inflammation (Ns, M1 MPs) → gran tissue (M2 MPs, FBs, endo cells) → collagen rich scar
Mediators:
- TGF-b → fibrosis
- VEGF → angiogenesis
- MMPs → ECM remodelling

Outcome = structural integrity resolved but weakened contractility → heart failure risk

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19
Q

Outline the steps in the cell cycle

A

G1: prep for dna rep
S: dna synth
G2: prep for mitosis
M: mitosis
G0: resting

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20
Q

Outline healing of a skin wound by 1st intention

A
  1. Coagulation → clot forms
  2. Acute inflammation → tissue debris removal
  3. Regeneration → epithelial renewal (labile) → connective tissue deposition
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21
Q

List factors affecting healing

A

Mechanical stress
Location
Infection
Nutrition
Blood supply

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22
Q

Outline liver regeneration

A

Hepatocytes proliferate after a) resection (60% removed → regrow they 4-6 wks) and b) necrosis
BUT requires intact ECM - chronic inflamm/infxn → fibrosis

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23
Q

Outline alcoholic liver disease

A

Steatosis → inflamm → fibrosis → cirrhosis
= Nodular liver structure w disrupted fn

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24
Q

General mechanisms of xenobiotic metabolism

A

Mainly metabolised in liver → makes X more h2o soluble → easier to excrete

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25
Outline phase I metabolism
Functionalisation Oxidation/reduction/hydrolysis intros/uncovers reactive grips Cytochrome P450 enzyme family (CYPs) converts lipophillic toxins → reactive metabolites = can be more toxic :( E.g. benzo[a]pyrene from cig smoke → oxidised by CYPs → forms dna adducts = carcinogenic E.g. paracetamol → sml % metabolised into toxic intermediate NAPQI
26
Outline phase II metabolism
Conjugation - conjugates reactive metabolites from phase I w polar grps - GSH, glucuronic acid, sulfate, AAs Enzymes = transferases Converts reactive intermediates → non-toxic h2o soluble forms E.g. NAPQI → conjugated w glutathione = safe But overdose → glutathione depletion → depatotoxicity
27
Outline phase III metabolism
Transport Ps expel conjugated, h2o soluble toxins from hepatocytes → bile/urine q
28
Why is CO a toxin
Binds Hb x200> O2 → systemic hypoxia
29
Why is SO2 a toxin?
Forms sulfuric acid → mucosal irritation
30
Why is ozone a toxin
Free radical generator → lung inflamm
31
Why is fine particulate matter a toxin
PM < 10um Phagocytosed by alveolar MPs → Ck release → chronic inflamm
32
Explain genetic susceptibility to toxins
Polymorphisms in CYP genes impacts phase I metabolism
33
Outline how asbestos causes disease
Asbestos = fibrous silicon - inert + indestructible → chronic inflamm + ros production → mesothelioma + lung cancer E.g. Wittenoom WA = words highest mesothelioma rates during blue asbestos mining
34
Outline tobacco as a toxin
> 4000 chems incl 60 carcinogens → dna dmg Bronchitis → emphysema → lung CX Crosses placenta → miscarriage
35
Outline heavy metal incl. lead as toxins
Promos ox stress → damages nervous system. Kidneys, bones, and GI tract Chronic exposure → cognitive impairment in kids
36
Outline alcohol as a toxin
Phase I metabolism produces acetylaldehyde = toxic → protein/dna dmg ROS → lipid peroxidation → fatty liver, hepatitis, cirrhosis → crosses placenta → fetal alc syndrome
37
Describe radiation in daily life
Constant low lvl - naturally occurring and manmade e.g. luminous watches
38
Outline the 2 types of radiation
Non ionising = UV, IR, microwaves, sound - low E - moves atoms w/in mols but X remove e- - still can cause cell dmg e.g. UV Ionising = x-rays, gamma rays, high E neutrons, a/b particles - high E - can displace e- (ionising) - dna dmg → cell death
39
Mechanisms of radiation injury
Ionisation → direct dna strand break Radiolysis of h2o → forms ROS → - dna dmg - P dmg - membrane dmg
40
Outline the cellular targets of radiation
DNA = main target Dmg depends on: - Cell prolif rate (rapidly div cells = more vulnerable) - repair capacity (chronic low dose → dna repair vs acute high dose → overwhelms repair capacity)
41
Describe UV radiation
From sun → pyramidine dimers in dna → mutxn in nucleotide excision repair pathway
42
Cancers caused by UV radiation
Basal cell carcinoma Squamous cell carcinoma Melanoma
43
Outline UVA
320-400nm Penetrates dermis Prod ROS → dna dmg
44
Outline UVB
280-320nm Penetrates epidermis Direct dna dmg - main producer of pyramidine dimers
45
Outline UVC
200-280nm Potent mutagen but mostly filled by O3 layer
46
Radiation measurement units
Curie = disintegrations/sec Gray = E absorbed/unit mass of tissue Sievert = equivalent dose adjusted for bio FX
47
Outline acute whole body radiation syndrome
Hematopoietic - 2 wks - neutropenia, thrombocytopenia GI tract - 1-3 wks - nausea, vomit, diarrhoea, desquamation, infxn, bleeding CNS - 14-36hrs - confusion, seizures → death
48
List the types of nutritional diseases
- deficiencies - obesity - EDs
49
Outline malnutrition
- insufficient protein/cal intake - deficiency in ingestion/absorption → general weakness
50
Outline nutritional injury associated with fat soluble vitamins
ADEK Stored but poorly absorbed E.g. coeliac
51
Outline nutritional injury associated with water soluble vitamins
Less storage available → deficiency develops faster
52
Outline vitamin d deficiency
Rickets (children) → cartilage overgrowth in epiphyses Osteomalacia (adults) → unmineralised bone matrix
53
Outline vitamin a deficiency
→ impaire cell differentiation → GI epithelium metaplasia → inc CX risk + inc keratin debris → stone
54
Outline vitamin c deficiency
Scurvy → impaire collagen hydroxylation → weak BVs → bleeding gums + skin petechiae → inpaired wound healing
55
List micronutrient imbalances that cause systemic dysfunction
Iron, calcium, iodine, zinc
56
Explain the role of energy homeostasis in obesity
Pathophysiology: CNS integrates gut + endocrine feedback (leptin, insulin, ghrelin, PYY) → hypothalamus coordinates appetite + metabolism Dysregulation Chronic excess cal intake → - blunted E balance signals → inc body weight “set point” - hormonal resistance (insulin, leptin) Outcomes: - weight gain - T2D
57
What are the cardiovascular risks associated with obesity?
Dyslipidaemia Hypertension Atherosclerosis
58
What are the cancer risks associated with diet?
- exposure to carcinogens e.g. aflatoxins → p53 mutxn → Neu5GC (animal derived food) → chronic inflamm + ROS
59
How does obesity cause chronic inflammation
Adipose tissue = pro inflamm cks
60
Outline plasma derived mediators of acute inflammation
Origin: circulating precursors (mainly liver synth) E.g.: c’ proteins, linings (bradykinin), coag factors Activation: proteolytic cascades Role of AA: none - AAs are not plasma derived
61
Outline cell-derived mediators of acute inflammation
Origin: produced de novo by inflamm cells E.g.: AA metabolites (PGs, LTs, lipoxins), histamine, CKs (IL1, TNF), NO Activation: synth on demand after cell activation Role of AA: yes - AA metabolites key class of cell-derived metabolites
62
Name the 3 main classes of eicosanoid mediators
PGs, LTs, lipoxins
63
Describe PGs
Pathway: cyclooxygenase Main functions: - vasodilation (PGI2, PGD2) - inc vasc perm - pain (PGE2) - fever (PGE2) Other functions: - PGI2 →inhibits platelet aggregation - PGD2 → neutrophil recruitment
64
Describe LTsMain
Origin: Lipoxygenase Main function: - LC chemotaxis (LTB4 - neutrophils) - broncoconstriction (LTC,D,E4) - inc vasc perm (LTC,D,E4)
65
Describe lipoxins
Pathway: Lipoxygenase Main functions: - inflamm resolution - inhibit N recruitment - promo MP-mediated debris clearance E.g.: LXA4, LXB4 → inhibits N adhesion/chemotaxis + promos inflamm res

PATH20001 Exploring Human Disease (30 decks)

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