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Blandede bolcher Molecular Pathology > Alt det gode > Flashcards

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1
Q

WHat is HNPCC and what causes it?

A

Hereditary non-polyposis cancer. Miscmatch repair

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2
Q

Xeroderm Pigmentosum

A

Excision repair faulty -> can’t repair UV cross linking of pyrimidines

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3
Q

Epithelial and mesenchymal markers

A

Epi: E-cadherin, beta catenin. Mes: Vimentin, fibronectin.

Cell loses epithelial markers, gain mesenchymal markers, and vice versa after metastasis.

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4
Q

How does the metastatic cell travel in the blood?

A

Platelet adhesion for immune escape and escape from anoikis. Called “embolism”

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5
Q

Factors for angiogenesis and lymphangiogenesis?

A

VEGF for angio, PDGF for lymph

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6
Q

What are paraneoplastic syndroms?

A

Tumor tissue produces hormones or hormone-like molecules.
Hypercalceima: Parathyrodea like molecule
Hypoglycemia: Insulin like substance
Hyponatromia: ADH

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7
Q

What causes cancer pain?

A

Bradykinin, prostaglandin, ATP

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8
Q

What opposes angiogenesis? How does the tumor react to anti-angiogenesis treatment?

A 
Avastin
Produce other angiogenic factors
Progenitor cells recruited from bone marrow
Pericytes protect vessels
Tumor migrates to oxygen rich tissue.
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9
Q

Which signature does BRCA have?

A

Signature 3. Treat with cisplatin.

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10
Q

Markers for liver cancer?

A

EpCAM and/or AF protein. 4 combinations: With or without each of the two.

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11
Q

Molecular classes of breast cancer?

A

Luminal A and B. Estrogen receptor positive. Treat with aromatase (prevents estrogen)
Basal like /3x negative. treat with platin
Normal breast
HER2: treat with Ab.

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12
Q

Li-Fraumeni syndrome?

A

Defect p53

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13
Q

Chromothripsis?

A

One event creating several mutations or SVs

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14
Q

Role of androgen receptor in SVs?

A

Androgen receptor creates transcriptional factories which promotes SVs

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15
Q

What is Familial adenomatous polyposis?

A

Caused by defect APC. Several polyps in colon.

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16
Q

What is CUP?

A

Cancer with Unknown Primary

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17
Q

Causes of cellular damage?

A

Loss of ATP -> defect Na/K -> swelling -> burst
Calcium influx -> activation of proteases, phospholipases, dnases. Also makes mitochondria permeable. -> apoptosis.
oxidative stress -> destroys protein, dna, phospholips.

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18
Q

What is phosphatidylserin a sign of?

A

Apoptosis. Flips to extracellular.

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19
Q

Mallory body?

A

Protein accumulation in cytoplasma

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20
Q

Pyroptosis?

A

Inflammatory cell death. Caspase 1 activated. Can be seen with salmonella.

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21
Q

Autophagy?

A

Organelles/proteins in double membrane (ER folds around it). Autophagosome fuses to lysome - autolysosome. Cancer cells use it to gain energy.

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22
Q

Papoptosis?

A

Non caspase apoptosis. No karryolysis. Swelling. Seen in ALS and huntingtons. Maybe early evolutionary apoptosis.

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23
Q

Proteins used for Leukocytes into inflammed tissue?

A

Rolling: L, E and P selektin.
Adhesion: ICAM, VCAM
Diapedesis: PECAM.

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24
Q

Chemotactic factors? Among others…?

A

C5a from complement, IL-8, bacterial debris.

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25
Macrophage actication?
INF-gamma activates to M1. Phagocytic. ROS. Produces TNF and IL1. M2: angiogenic.
26
What is LOX?
LOX crosslinks elastin and collagen -> stiffening of tissue
27
Factors responsible for fibroblast activation?
TGF beta crucial. Activates SMAD2/3 pathway and also MAPK pathway. Mechanic stress opens Ca2+ pores -> calcineurin. Target TGF beta signalling. ab's against receptor, inhibitor against SMAD3 or RTK.
28
Rheumatoid arthritis pathogenesis?
1) Provocation (eg. smoking) causes apoptosis/necrosis and activation of PAD, which makes citrullinated protein (CCP). Can be presented on MHC II, especially by DR1 and DR4 allells. Antibodies produced against CCP. 2) PAD reaches joint with provocation? CCP made. Antibodies react to CCP -> immune complexes 3) Chronic rheumatoid arthritis. Plasma cells produce abs against immune complex. These abs are called Rheumatoid factors. DR1 and DR4 allels of MHCII may be important for ag presentation
29
Classification criteria RA?
Swollen/tender joints, synovities. Rheumatoid RF or anti-CCP. Acute phase reactants ESR or CRP. Can be seen on MR, often not X-ray
30
Cells in RA?
In pannus: T, Mø, fibroblasts, plasma cellls | In synovial fluid: Neutrophils, immune complexes.
31
RA outside of joints?
Nodules: Skin, lungs, heart Vasculitis: Skin, PNS Pericarditis.
32
Risks in ostearthritis?
``` Age (strongest factor) Female Joint alignment (crooked back etc) Hereditary (collagen dysfunction) Joint injury Obesity ```
33
Symptoms osteoarthritis?
Pain, crepitus, swelling, tenderness, stiffnes. Thickening of bone in subchondral layer. Bone spurs Fluid filled sacs in bone Articular cartilage broken down. Cartilage fibrillation. Proteoglycan loss -> can't hold water
34
Cytokines in osteoarthritis?
TGF beta: Cartilage hypertrophy, bone spurs. | TNF a and IL1 -> IL6 + IL8 -> MMPs. IL6 promotes IL1. IL1 also promotes MMPs. Break down proteoglycans.
35
Platelet coagulation:
vWF. Platelet bind, release granules, attract platelets via Gplb receptor. Ca2+ release from platelets important for coagulation cascade. Collagen negative charge activates. Phosphatidylserin flips on platelets -> CC. Complexes on platelets -> faster CC.
36
Inhibition of CC:
Protein C and cofactor protein S inhibit factor V.
37
Thrombofilia
Increased blood clot risk. Factor V leiden: Highter risk of DVT. V can't be inactivated by ATC.
38
Origin of osteoclasts and osteoblasts?
Mesenchymal stem cells -> osteoblasts. Stimulated by m. stress, sex steroids, wnt.Wnt inhibits inhibitors of B-catenin. Sclerostin inhibits Wnt. Hematopoietic stem cels -> osteoblasts. RANK/RANK-ligand interaction (inhibited by posteoprotegrin) M-CSF/M-CSF receptor interaction Menopause: INcreased RANK expression Treatment: ^osteoblasts teriparatide, down osteoclasts with bisphosphonates. H8 promotes osteoblast diff and bone mass.
39
Layers of the heart
``` Fibrous layer Parietal pericardium Pericardial cavity Visceral pericardium Myocardium Endocardium (Endothelium, dense connective with smooth muscle, connective tissue) ```
40
Conduction system of the heart:
Sinoatrial node -> AV node -> right and left bundle branches -> purkinje fibers
41
Layers of vascular system
Intima: Endothelium, basal membrane, loose connective tissue (internal elastic membrane) Media: Smooth muscle cell with elastin and reticular fibers Adventitia: Vaso vasorum + nervi vascularis
42
Layers of skin:
Epidermis: Stratum corneum, granule, spinosum, basale. basal membrane. Dermis: Papillary layer, reticular layer.
43
Respiratory system
``` Conductictive system (down to bronchi): Goblet cells (mucus) Ciliated columnar epithelium. ``` Bronchioles: Simple columnar/cuboidal Clara cells (surfactant) Terminal bronciole, respiratory bronciole, alveolar duct, alveolar sack, alveole
44
How do pathogens escape/fight immune system
Inhibit phagocytosis, phagosome/lysosome fusion, recognition. Viral latency, antigen display. Antigenic variation. Resistance to anti microb peptides Change net surface charge Carbohydrate capsule Neutrophil make NETs Manipulate immune system: Virus can remove MHCII, modulate cellular behaviour. Regulation of apoptosis.. Hide.
45
Exotoxins of bacteria
Enzymes. Coagulase, hyaluronidase.
46
Examples of infections
Legionella. In water in amoeba. Hot water tanks. zika virus: Placental/fetal, birth + breastfeeding spread. Microcephaly. Novobiocin. HIV utilizes CD4 receptor on T-cell. Influenza uses Sialic acid to get into the cell. Pathogen uptake via M cells (salmonella)
47
Recognition of microbes
Recognise PAMPS, LPS, flagellin. TLR, Intracellular: NOD like: peptidoglycan RIG-like: Viral RNA
48
Antigenic variation
High mutation rate: HIV, influenza Genetic reassortment Change of phenotypes, eg. HxNx influenza Genetic rearrangement .Trypanosoma. Variant surface glucoprotein. Changes which one it expresses.
49
Injury
Bacterial: Stress cell with ROS -> necrosis -> inflammation Viral: Toxins. Shut down cell function. ACtivate cas. Oncogenic transformation.
50
Warburg effect
Only glycolysis, no oxidative phosphorylation. Causes acidic environment. Extra metabolites for DNA, protein
51
How does inflammation attribute to cancer?
``` Strom cells + leukocytes produce growth factors and proteases (breakdown of cell-cell contact -> movement and growth) Mø integrins -> no anoikis. VEGF for angiogenesis. TNF + EGF -> mobiolity. TGF beta -> epithelium => mesenchymal ```
52
Diagnose of diabetes? Tests?
7/11 - resting over 7 mmol, after 75 g glucose over 11. Glycated hemoglobin over 6,5% Symptoms: Drink water, eat a lot, pee a lot... Glucose tolerance test (75 g) Insulin tolerance test. +/- labelled glucose, see how much is taken up with insulin. Clamp test: Constant insulin, variable glucose. How much glucose for constant blood sugar? Type 1: loss of beta cell mass. Absolute insulin deficiency. Type 2: Insulin resistasnce and failing Beta cell compensation progressive loss of beta cell mass.
53
Diseases as consequence of diabetes?
Retinopathy, neuropathy, cerebrovascular disease, coronary heart disease, nephropathy, foot ulcers
54
Other types of diabetes?
Gestational diabetes: Mother has high glucose in blood during pregnancy for sake of child -> diabetes. MODY 3: Maturity onset of diabetes of the young. Type 3: Genetic mutation in HNF1 alpha -> reduced Beta cell function. Treat w sulfornytureas
55
Tissue regulation of blood sugar?
Adipose, liver and muscle have uptake. Glucogenesis. Lipogenesis in adipose and liver.
56
Molecular mechanism of insulin resistance?
TNF alpha w. receptor or lipotoxicity -> TRAF -> inhibitory kinases of insulin pathway. Glucotoxicity -> RAGE receptor -> inhibitory kinase of insulin pathway.
57
Inflammatory response in diabetes?
Type 1: CD8 kills beta cells through FAS or granzymes. INF gamma and TNFa -> apoptosis + Th4 and Mø activation. Blockage of TNFa -> better. Inhibitor of IL1 -> type 1 better. IL1 induce apoptosis in Beta cells. Produced by inflammasome. Produced by leukocytes?. Type 2: Mø: IL-1 production. Glucose also induces IL-1 production? Only low grade insulitis.
58
Stages of brain development and their diseases
Proliferation - Microcephaly, megalencephalis Migration - Heterotropic, lissencephaly (agyric) Apoptosis/Maturation - Polymicrogyric, focal cortical dysplasis, post mig microcephaly Methamphetamin mestrer to telefoner.
59
Diseases
Stroke: Hemorrhagic or ischemic. Prion: AD (Abeta fibrils), Parkinsons (lewy body formation) ALS (motor neurons)
60
Clinical features of MS?
Clinical features: Time and space dissociation, multiple areas, attack = sudden appearance and worsening (minimum 1 month apart) Forms: Relapse remitting, progressive 1 and 2, progressive relapsing.
61
Mechanisms of MS?
``` Autoreactive T-cells -> Mø activation -> myelin degradation. HLA association Myelin basic protein one antigen. EAE scores (mouse model) Treatment -Attacks: Steroids -Immunosuppresive: INF-beta ```
62
Histology and function of liver?
Central vein, portal triad, bile canaliculi, sinusoids, fenestra w/o diaphragms, space of disse. Bile salts, gall bladder
63
Histology and function of pancreas?
Exocrine: Acini, intercalated ducts (squamous), lobular ducts (columnar) Endocrine: aplha, beta and delta cells (somatostatin)
64
Histology and function of kidney?
``` Podocyte on glomerulus -> filtration slits Bowmans capsule (parietal layer, visceral layer) Proximal tubule -> most exchange Arteriole ```
65
Thyroid gland
C cells secrete calcitonin. Colloid > glucoprotein
66
GI tract
Mucosa: Lining epithelium, lamina propria, muscolaris mucosae Submucosa: Connective tissue, glands Muscularis externa Serosa/adventitia
67
Stomach
``` Cardiac, fundic, pyloric glands. Chief cells (pepsinogen), parietal cells (HCl), Mucous cells ```
68
Small intestine
Crypts of lieberkuhn + villi | Goblet cells, paneth cells (antimicrobial), M-cells (immunological)
69
Colon and appendix
Colon: No villi Appendix: Lots of lymph tissue
70
Uterus
Endometrium (stratum funcionale, stratum basale). Recoil of arteries leads to ischemia and menstrual phase. Myometrium Perimetrium (serosa)
71
Cervix
Endometrium. Transition zone.

Blandede bolcher Molecular Pathology (2 decks)

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