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Stage 4 > Mechanisms of Disease > Flashcards

Mechanisms of Disease Flashcards

1
Q

Exudative pus if HIGH ? LOW ? on pleural tap

Lights criteria for exudative pleural fluid

A

High acid, LDH, protein >35g/L
Low Glucose

Pleural protein: Serum protein ratio >0.5
Pleural LDH: Serum LDH ratio >0.6
Pleural LDH > 2/3rd of serum LDH

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2
Q

Exudative pus seen in

A

Local disease (High protein). Local factors influence the accumulation or clearance of fluid
Malignancy
Infection

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3
Q

Transudate <25g/L seen in

A

Systemic disease (Low protein <25g). Imbalance between oncotic and hydrostatic pressures
HF
Hypoalbuminaemia
Meig’s syndrome (Ascites, pleural effusion, ovarian tumour)

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4
Q

Bacteria that don’t gram stain

A

Chlamydia

TB - use Ziehl-Neelsen (Mantoux +ve when vccinated, IGRA -ve if vaccinated)

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5
Q

Bacteria that gram stain positive

A 
Strep pyogenes + pneumoniae
Staph aureus (coagulase +)
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6
Q

Bacteria that gram stain negative

A

E.coli

Neisseria Meningitides

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7
Q

Penetrance is

Expressivity is

A

Penetrance is how many develop it

Expressivity is how it manifests

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8
Q

This genetic test only detect gains and losses of chromosomes such as in Downs

A

Virtual karyotyping

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9
Q

Which genetic test can highlight subtle alterations to chromosomes

A 
FISH
Williams syndrome (7q11.23 deletion) - congenital heart disease, periorbital fullness, long smooth philtrum, super happy
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10
Q

Which test takes DNA sample and compares genes to a control to detect mutations

A

Microarray-based Comparative Genomic Hybridization (aCGH)/DNA sequencer

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11
Q

What tests for - Tumour markers e.g. AFP

A

Antibody-based: Immunohistochemistry

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12
Q

Trauma investigation after car crash with suspected subdural

A

CT SCAN or MRI

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13
Q

Pathophysiology of haemorrhage

A
  1. Increased sympathetic response - constriction and inotropy - due to reduced pressure detected by arterial baroreceptors
  2. Adrenaline and cortisol released
  3. Reduced renal perfusion - RAAS activated - more Na thus water retention
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14
Q

Early trauma induced coagulopathy

A
  1. Severe hemorrhage diminishes o2 delivery and causes hypothermia this in turn halts the coagulation cascade, preventing the blood from clotting (coagulopathy).
  2. In the absence of blood bound o2 and nutrients due to hypoperfusion, the bodys cells burn glucose anaerobically for energy, causing the release of lactic acid, ketone bodies, and other acidic compounds into the bloodstream, which lowers the bloods pH, leading to metabolic (acidosis).
  3. This increase in acidity damages the tissues and organs of the body and can reduce myocardial performance, further reducing oxygen delivery and thus (hypothermia).
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15
Q

How does mild acidosis help during trauma

A

Helps unload oxygen at the peripheral tissues

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16
Q

What tests and what results during trauma

A

ABG - acidosis, low HCO3- as its used up (low base excess), low CO2 as patient blows off CO2 to compensate for acidosis
HB - Low
Lactate - High due to anaerobic respiration

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17
Q

Treat trauma bleeding with

A

1Whole blood (all the clotting factors etc)

Resus would only dilute clotting factors

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18
Q

Pathophysiology of Disseminated Intravascular Coagulation

A
  1. Vascular damage/cytokines expose TF
  2. TF stats extrinsic pathway > Thrombin + Fibrin
  3. Excesss Thrombin cleaves fibrinogen into fibrin resulting in clots which trap plateletes (thrombocytopenia)
  4. Fibrin degradation prodcuts convert plasminogen into plasmin = fibrinolysis
    Tissue factor builds up clots of fibrin and traps platelets (low platelets) AND then plasminogen in converted into plasmin to counteract the clotting thus bleeding occurs.
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19
Q

PT test is which pathway and which conditions result in prolonged time

A

Extrinsic

Vit K def (2, 7, 9 and 10) or Warfarin use (7)

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20
Q

APTT test is which pathway and which conditions result in prolonged time

A 
Intrinsic
Von WIllebrand (often comes with reduction in factor 8), Hemophilia A (factor 8), Hemophilia B (factor 9), Hemophilia (factor 11) or Heparin use (activates anti-thrombin which inhibits factor II, IX, X and XI) or Lupus anticoagulant (actually prothrombotic in vivo, but prolongs aptt time when tested in vitro)
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21
Q

Bleeding time refers to

A

Platelets thus Thrombocytopenia if prolonged

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22
Q

Haemorrhage and DIC: After excessive activation of coagulation runs out fibrinolysis occurs, what is used to treat this

A

Tranexamic acid (prevents plasmin from degrading fibrin)

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23
Q

Cerebral perfusion pressure = BP - ICP

What happens as ICP increases

A

as ICP increases, CPP decreases, body responds by raising BP and dilating cerebral blood vessels = increased cerebral blood volume thus even higher ICP! Vicious cycle!

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24
Q

How to compensate for high ICP

A

Brain empties CSF from ventricles into spine and into venous blood

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25
Q

Increased ICP causes

A

Projectile vomiting, headache, decreased LOC, dilated pupils, wide pulse pressure, CN6 palsy (no lateral), papilledema and Cushing’s triad reflex

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26
Q

What is Cushing’s triad reflex

A
  1. Increase in BP and heartbeat to raise cerebral blood flow
  2. Baroreceptors in aortic arch detect high BP and induce BRADYCARDIA
  3. Increased pressure on brainstem causes irregular respiratory pattern
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27
Q

Brainstem herniation causes

A

CN3 palsy (down and out and dilated), motor posturing, lower extremity rigidity, hyperventilation

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28
Q

Treatment of increased ICP

A
  1. Remove mass or allow brain to swell out by opening skull
  2. Reduce CSF via ventricular drain
  3. Mannitol to draw out water
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29
Q

Sepsis 6

A 
BUFALO
Blood cultures before giving antibiotics
Urine output monitor
Fluids
Antibiotics
Lactate
Oxygen
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30
Q

Pathophysiology of amyloid beta plaques and Tau/NFTs in Alzheimers

A

b and gamma secretase cleave amyloid precursor protein (APP) into hydrophobic AMYLOID BETA PLAQUES which aggregate. Chromosome 21 implicated in excess APP thus Downs = Alzheimers

Mutations can lead to HYPERPHOSPHORYLATION of Tau which disassembles microtubules and sequesters normal tau into tangles of NFT which then interferes with axonal transport and causes cell death.

Amyloid beta plaques are extracellular and due to degradation of APP

Tau is intraneuronal due to hyperphosphorylation.

Neuritic plaques are combination.

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31
Q

Pathophysiology of Parkinson’s

A

a-synuclein aggregates via phosphorylation into Lewy bodies which decrease dopmaine uptake in the substantia nigra in the midbrain (pale on imaging)

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32
Q

Generally Lysosomal storage disorders have what inheritance and cause what?

A

Autosomal recessive
Deficiency of enzyme results in buildup of metabolite in lysosomes of macrophages and phagocytes and extralysosomally. The reticuloendothelial system is often destroyed, and an enlarged liver and spleen and bone issues are common.

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33
Q

Pathophysiology of Gaucher disease

A

Deficiency of B-glucosidase.

It no longer cleaves the ceramide lysosomal enzyme and so accumulation of Glucocermaide occurs in the lysosome of macropahges

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34
Q

Pathophysiology of Niemann-Pick disease

A

Deficiency of Sphingomyelinase and this results in build up of Sphingomyelin

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35
Q

Pathophysiology of Haemochromatosis

A

Decreased hepcidin synthesis
Low hepcidin results in no inhibition of ferroportin which transports iron from GI cells and marrow macrophages into the blood, thus higher iron enters the blood (high hepcidin in infection normally sequesters iron from bugs)
Iron causes liver fibrosis and pancreas destruction > diabetes

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36
Q

Iron panel in Haemochromatosis

A

Raised iron
Raised ferritin
Raised transferrin saturation (as lots of iron)
Low TIBC (aka transferrin, low as dont need it as iron is already high)

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37
Q

Pathophysiology of Wilsons disease

A

Or ATP7B releases copper and produces ceruloplasmin – defect = low copper in serum (high in tissue) and low ceruloplasmin

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38
Q

Diagnostic features of Wilsons

A

Autosomal recessive, 30s, Liver disease, Psychiatric changes, Tremor, Kayser-Fleischer rings

Low ceruloplasmin
Low serum copper
High urine copper
Biopsy to diagnose

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39
Q

Pathophysiology and features of Menkes

A

ATP7A absorbs copper from small intestine, defect = low copper

Strikingly peculiar hair, which is kinky, colorless or steel-colored, and easily broken

Ceruloplasmin and copper (serum and urine) LOW

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40
Q

Example of a Direct-ligand-gated channel

A

Multidrug resistance ATPase pumps out foreign chemotherapy agents thus causes resistance

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41
Q

Examples of G-protein-coupled receptor

A

involved in many diseases and target of 40% of all drugs including Hydrocodone and Lisinopril.

Beta-adrenergic receptors, prostaglandin E2 receptors

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42
Q

Example of Tyrosine kinase-linked receptor

A

insulin receptor
VEGF
EGFR - block this and block cancer

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43
Q

Pathophysiology of Von Hippel-Lindau disease

A

Under normal oxygen conditions VHL protein causes degradation of hypoxia inducible factor (HIF).

But under low oxygen conditions OR where VHL is mutated HIF is free to activate transcription factors which upregulate vascular endothelial growth factor = angiogenesis and cell proliferation = VHL disease results in lots of cancers

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44
Q

Rb (tumour suppressor) mutation leads to

A

Loss of restraint from G1 to S phase and results in retinoblastoma

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45
Q

What is contact inhibition

A

Close cell-to cell contact in dense cell populations act as an inhibitory factor on cell proliferation, and is absent in cancer cells.

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46
Q

ACID mnemonic for hypersensitivity reactions

A

Type 1 Allergy
Type 2 Cytotoxic via antibodies and complement
Type 3 Immune complex
Type 4 Delayed

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47
Q

Type 1 Allergy hypersensitivity reaction pathophysiology - atopy, anaphylaxis, asthma

A

Initial exposure to antigen sensitizes the immune system to produce large amounts of IgE

Mast cells become coated in IgE and degranulate on subsequent re-exposure to the antigen

Histamine is released > bronchi contract, vessels dilate = oedema and SoB

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48
Q

Allergy: Early phase reaction of swelling/angioedema/hives within 30minutes which then settles but then WHAT causes late phase reaction which occurs around 4hour mark until 20hours

A

Deterioration occurs later when eosinophils are recruited from bone marrow

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49
Q

Allergy
Ix
Management - ABCF

A

Mast cell Tryptase – released during anaphylactic response with peak after 1hr (or mastocytosis but levels increase after 1hr)

Adrenaline 0.5ml 1/1000 IM
Benadryl Chlorphenamine (antihistamine) 10mg IV
Corticosteroid Hydrocortisone 200mg IV
Fluid bolus 500-1000ml IV

Discharge with antihistamine and 3 days oral prednisolone and 2 adrenaline autoinjector epipens

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50
Q

Type 2 hypersensitivity reactions (Antibody IgM IgG destruction on fixed antigen)

  1. RBC surface antigen
  2. Platelet integrin
  3. Collagen type 4 basement memebrane
  4. Streptococcal cell wall antigens (cross react with cardiac muscle)
  5. AcH receptor
  6. TSH receptor
  7. IF
A
  1. Autoimmune hemolytic anaemia
  2. Autoimmune thrombocytopenic purpura (abnormal bleeding)
  3. Anti-GBM disease (Goodpastures = glomerulonephritis + pulmonary hemorrhage)
  4. Acute rheumatic fever (myocarditis + valvular damage + arthritis)
  5. Myasthenia gravis (muscle weakness)
  6. Graves (hyperthyroidism)
  7. Pernicious anaemia
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51
Q

Test for autoimmune hemolytic anaemia

A

Direct coombs test (RBCs are separated from plasma and mixed with coombs regent which is an antihuman globulin or an antibody against human antibodies, if the RBCs agglutinate or clump up then they probably had antibodies on their surface)
Indirect coombs is used for blood group incompatibility

52
Q

Type 3 hypersensitivity (IgG Antibody + complement destruction on soluble travelling antigen) examples

A

Foreign proteins/drugs > Serum sickness > Fever, rash, joint pain, lymphadenopathy
Nuclear antigens > SLE > Glomerulonephritis + Vasculitis
Hep B antigen > Polyarteritis nodosa > Vasculitis
Streptococcal antigen > Post-streptococcal glomerulonephritis > Glomerulonephritis

53
Q

Difference between type 2 and type 3 hypersensitivity reactions

A

In type II hypersensitivity the antibody binds to an antigen on say RBCs or receptors, but in type III hypersensitivity it binds to soluble antigens forming an antibody antigen.
Complement is used in large amounts, compared to type 2, thus complement levels can be used to track disease status
Type II corresponds to the tissue where antibodies attach. Type III is where immune complexes are deposited not made

54
Q

Type 4 hypersensitivity (Delayed T cell mediated destruction) examples

A

Contact dermatitis

Hashimotos thyroiditis - Hypothyroidism after initial hyperthyroidism

55
Q

Coroner if

A
  1. Cause of death is unknown
  2. Death was violent or unnatural
  3. Death was sudden and unexplained
  4. Deceased was not visited by medic during their final illness
  5. Medical certificate isn’t available
  6. Deceased was not seen by doctor who singed medical certificate within 14 days before death or after they died
  7. Death occurred during operation
  8. Medical certificate suggests death via industrial disease or industrial poisoning
56
Q

Endothelium relaxing factors

A

NO - antithrombotic
Bradykinin
PGI2

57
Q

Endothelium contracting factors

A

Endothelin
Angiotensin II
Thromboxane 2

58
Q

Von Willebrand factor has what affect on platelets and thrombosis

A

Platelet aggregator and prothrombotic

59
Q

3 stages of atherosclerosis

A
  1. Fatty streak development - Monocytes engulf the oxidised LDL and become fom cells
  2. Plaque progression - Fibrous capsule causes luminal narrowing = claudication and angina
  3. Plaque disruption - unstable capsule leads to emboli
60
Q

Multiple nodular lung shadowing is seen in

A

Wegeners granulomatosis
Lung mets
Infection

61
Q 
Vasculitis
Under 5
Under 10
Over 30s
OVer 50s
A

Kawasaki (MI, coronary aneurysm)
HSP
Primary systemic vasculitis
GCA

62
Q

Far eastern under 50s vasculitis affecting the aortic arch

A

Takayasus

63
Q

Microscopic polyangiitis autoantibodies

A

pANCA and anti-MPO

64
Q

Eosinophilic granulomatosis with polyangiitis or Churg-Strauss autoantibodies

A

pANCA with anti-MPO and High Eosinophils

65
Q

Granulomatosis with polyangiitis or Wegener’s granulomatosis autoantibodies

A

cANCA with anti-proteinase 3

66
Q

Small vessel with late onset asthma, hypereosinphilia and nasal polyps vasculitis

A

Churg-Strauss

67
Q

Lower resp tract infection and kidneys affected

A

Wegener’s

68
Q

IgA vasculitis in children – small vessels, joint pain, palpable purpura, abdo pain, nephritis

A

HSP

69
Q

WBCs in CTD are?

A

Low

70
Q

Duplex scanning reveals 1? in GCA but definitive diagnosis is by 2?

A
  1. Arterial wall thickening

2. Positive temporal artery biopsy showing granulomatous vasculitis (+ve in PMR and skip lesions)

71
Q

GCA treatment

A

High dose steroids and aspirin

72
Q

Pathophysiology of pulmonary hypertension

A

Endothelial cell mutations (BMPR2) +
increased pulmonary artery flow (eisenmenger syndrome) +
Alveolar and arteriolar hypoxia =
Vasoconstriction, smooth muscle hypertrophy and fibrosis from fibroblast cells via proliferative signalling

73
Q

Pathophysiology of Eisenmenger syndrome

A
  1. Systemic (LV) to pulmonary (RV) circulation connection (VSD)
  2. Left to right shunting of blood
  3. Increased pulmonary blood flow
  4. Irreversible pulmonary vascular injury
  5. Irreversible pulmonary vascular resistance
  6. Right to left shunting of blood
  7. Hypoxia and erythrocytosis
74
Q

NAFLD spectrum

A
  1. Simple steatosis (fatty liver) features fat but no inflammation or hepatocellular injury
  2. Non-alcoholic steatohepatitis (NASH) features fat, inflammation and hepatocellular injury
  3. Cirrhosis
75
Q

AST:ALT ratio indicating cirrhosis?

A

Higher AST = cirrhosis

Low platelets is also a hallmark

76
Q

Hepatic vein transit time (HVTT) threshold of more than ? can distinguish mild to moderate from advanced fibrosis

A

24 seconds

77
Q

Alpha2-macroglobulin

A

High: Nephrotic syndrome (cannot be excreted due to its large size, however many other proteins do leak through, so increased production of all proteins occur but now alfa2-macroglobulin is extra high) and cirrhosis
Low: Pancreatitis

78
Q

Haptoglobin

A

Mops up haemolysed RBCs and so is low during haemolytic anaemia. However it is also low if the liver is not producing enough

79
Q

GGT

A

Raised ALP can be due to bone or bile duct disease, but if there is also a raised GGT then it pints to a liver/biliary reason. Also raised in alcohol

80
Q

Bilirubin

A

Raised from day 1 of birth = haemolytic disease of newborn. Raised from day 2-7 is physiological due to liver maturing and RBC breakdown time. Unconjugated can be due to = haemolytic, sickle cell, pernicious anaemia, transfusion reaction. Conjugated = Liver or bile duct blockage, hepatitis, liver trauma, cirrhosis

81
Q

CPA (collagen proportionate area)

A

Special stain and then measure the amount of red = fibrosis. Quantitative method of measuring fibrous tissue, using digital image analysis of the proportion of collagen in liver tissue, namely collagen proportionate area (CPA).

82
Q

Liver stiffness correleates with…

A

Cancer

83
Q

Biomarkers and imaging help but gold standard is

A

BIOPSY

84
Q

Ursodeoxycholic acid mechanism

A

Dissolves gallstones by thinning down bile and flows through liver better so jaundice may improve

85
Q

Anaesthetic drug known to cause fulminant hepatitis

A

Halothane

86
Q

In normal cells there is contact inhibition which switches off division after reproduction. Recognition of like cells which stay together and do not stray to other part of the body are due to the presence of WHAT? on the cell surface.

A

Glycoproteins

87
Q

The mutagens that predispose cells to develop tumours are called

A

Initiators

88
Q

Non-reactive compounds that stimulate tumour development are called

A

Promoters

89
Q

Those that both initiate and promote are termed

A

Complete carcinogens

90
Q

Initiation

A

Produces a permanent mutation change but does not itself cause cancer.

91
Q

Promotion

A 
Initiated cell can then undergo promotion via repeat dose-responsive exposure to a special class of incomplete carcinogens (known as promoters), which selectively enhance the growth of initiated cells. This stage is reversible and the disappearance of the promoter results in the disappearance of the proliferated cells.
For example, patients who have smoking Hx plus exposure to asbestos, will amplify their risk of developing mesothelioma.
92
Q

Progression

A

Irreversible and involves multiple complex DNA changes (due to the instability brought about by promotion), such as chromosomal alterations and morphological cellular changes, which are detectable by microscopy. Here, the multiplying cells undergo a genetic event that causes a permanent growth advantage.

93
Q

Smoking is a risk for which cancers

A

Breast
Cervical
Bladder

94
Q

Smoking is protective against which female cancer

A

Endometrial

95
Q

Which disease involves a defect in Nucleotide Excision Repair (NER) pathway resulting in UV induced skin malignancies

A

Xeroderma Pigmentosum

96
Q

Infections/inflammation causing cancer

  1. HIV
  2. EBV
  3. HPV 16 18 31 45
  4. Hep B and C
  5. Sclerosing chlangitis
  6. Chronic pancreatitis
  7. UC
  8. Helminth schistosomiasis
  9. H.pylori
A
  1. HHV8 > Kaposi sarcoma
  2. Hodgkins lymphoma / Burkitts lymphoma
  3. Cervical cancer
  4. Hepatocellular carcinoma
  5. Cholangiocarcinoma
  6. Pancreatic cancer
  7. Colon cancer
  8. Bladder cancer
  9. Gastric cancer / lymphoma
97
Q

Breast cancer hormone risk factors

A

The more estrogen exposure the higher the risk of breast cancer:
Early menarche to late menopause (prolonged with HRT) increases risk.
Low parity as estrogen decreases during pregnancies.

COCPs do not increase the risk as the amount is small, its offset by progesterone and its taken when estrogen should be present anyway!

98
Q

Ovarian cancer hormone risk factors

A

Related to the number of ovulations:
Risk increased by nulliparity (lots of egg cycles).

COCP reduces risk as these prevent ovulations/epithelial ruptures!

99
Q

Endometrial cancer risk factors

A

Risk increased by unopposed estrogen:
Estrogen increases risk and so low parity and HRT increase risk

COCP reduce risk as it contains protective progesterone
Smoking is protective.

100
Q

Cervical cancer risk factors

A

Smoking is risk factor!
Increased by HPV exposure
Not related to estrogen. However COCP may go hand-in-hand with HPV exposure.
For once nulliparity may reduce the risk as pregnancy can damage the cervix

101
Q

Number 1 aetiological risk factor of all cancers?

A

DIET (but smoking for the exam?)

102
Q

Germline mutations

Somatic mutations

A

Abnormality is in every piece of DNA, present from embryogenesis, may not have been passed from parents but can be passed onto offspring. Responsible for hereditary cancer syndromes

Mutation occurs within DNA of an individual cell. So within the germline there is no mutation but within the tumour there is. Thus you cannot pass this on unless it occurs in a germ cell. Non-inheritable. Sporadic cancers

103
Q

Gene which gives rise to both sporadic (somatic) colorectal cancers AND familial (inherited germline) colorectal cancer

A

APC

Familial Adenomatous Polyposis FAP

104
Q

HER2 breast cancers

A

Resistant to normal taxane chemo

Sensitive to monoclonal antibody Herceptin (trastuzumab)

105
Q

Hereditary retinoblastoma - 1 hit

Sporadic retinoblastoma - 2 hits

A

Since you are born with one mutation you only need one more for a tumour

Normal Rb gene first, so first somatic mutation does not cause cancer, but second mutation will cause a tumour – 2 hit model - rarer

106
Q

Mis-segregation and mitotic recombination

A

Defect becomes present in both chromosomes (homozygous). So errors can occur in replication that mean that mutations can go from heter to homo simply in cellular replication

107
Q

Philadelphia chromosome

A

The BCR gene of chromosome 22 undergoes reciprocal translocation with the ABL gene of chromosome 9 resulting in BCR-ABL fusion gene that codes for a tyrosine kinase protein that causes uncontrollable division of CML cells

108
Q

Burkitt’s lymphoma chromosome/gene

A

Burkitt lymphoma results from chromosome translocation (8 and 14)

Myc gene

Common in central Africa and associated with EBV

109
Q

Caretaker genes

A

Control mechanisms to identify errors and repair them like NER

110
Q

Tumour suppressor genes

A

Normally inhibit cell proliferation - cell cycle control, DNA repair, apoptosis

Mutations involve a loss-of-function and both genes need to be rendered ineffective thus recessive

111
Q

Oncogenes

A

Whereas proto-oncogenes merely promote growth, a mutation to them will result in true oncogenes, causing a gain-of-function

This activating nature only one gene copy need be affected for uncontrolled cell growth thus dominant

112
Q

Ataxia telangiectasia

Gene

Cancer risks

A

Automsomal recessive - Only manifests if both maternal and paternal alleles of the gene carry mutation. If both parents are unaffected carriers then 25% risk to offspring.

Caused by mutations in ATM gene which encodes kinase protein essential for p53

Increased risk of haematological and breast cancer

113
Q

Bloom syndrome

A

Leukemia, Wilms tumour, facial telangiectases

BLM gene affects homologous recombination repair

114
Q

Cowden syndrome

A

Breast, thyroid, GI, pancreas cancer

PTEN

115
Q

Li-Fraumeni syndrome

A

Sarcoma, breast, lung cancer

p53 on chromosome17

116
Q

Double strand damage is repaired by

A

Homologous recombination

BRCA1/2 and PALB2 assist with this

117
Q

Fanconi anaemia

A

AML, SCC
Developmental and skeletal deformities
FACA gene affects homologous recombination repair

118
Q

Autophagy

A

Catabolic process during which cellular constituents are degraded by lysosomal machinery within the cell. Radiotherapy and chemo induces high levels of autophagy which are protective, cell become stressed and enter dormancy, now the cell is resistant to chemo… thus timing is important

119
Q

Name the calcium dependent cell-cell adhesion protein which helps prevent invasion. Downregulation of this decreases cellular adhesion strength and increases cell motility. CDH1 mutations can affect this and give rise to metastasis.

A

Cadherin-1

120
Q

VITAMIN C DEF

A 
Vascular
Infection/inflammatory
Traumatic
Autoimmune
Metabolic
Iatrogenic
Neoplastic

Congenital

Degenerative
Endocrine
Functional

121
Q

High urea: creatinine

A

pre-renal, bleed (GI digestion of blood into urea), dehydration, lots of protein (diet or catabolic state), corticosteroids

122
Q

Low urea: creatinine

A

Intrinsic renal damage, liver dysfunction, SIADH, rhabdomyolysis

123
Q 
Which of the following best describes the cell population involved in wound angiogenesis?
Endovascular endothelial cells
Microvascular endothelial cells 
Arterial endothelial cells 
Venous endothelial cells 
Lymphatic endothelial cells
A

Microvascular endothelial cells

124
Q

Which layer differentiates between continuous and fenestrated endothelium versus discontinuous endothelium?

What type of vessels come in continuous, fenestrated and discontinuous forms?

Where does atherosclerosis mainly occur?

How would you describe the pathological effect of modified LDLs on the endothelium ?

A

Basement Membrane

Capillaries

Intima

Inflammatory

125
Q

What structure is responsible for storage of vWF and P-selectin?

A

Weibel Palade body

126
Q 
Example of signalling
Endocrine
Paracrine
Autocrine
Juxtacrine
A

Thyroxine release from thyroid gland

von Willebrand factor + VEGF

Immune cells + cancer cells

Cardiac myocytes + T/B cell activation

127
Q 
Example of receptors
Ligand gated
G protein
Tyrosine kinase
Intracellular nuclear
A

Nicotinic acetycholine receptor = Myasthenia gravis (ice test + autoantibodies + edrophonium test)

Causes vasoconstriction, inotropy change and starts AKT pathway > mTOR (cancer + alzhemiers) + NF-kappa b (cancer)

Insulin receptors

Steroids

Stage 4 (12 decks)

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