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BIOL 135 Flashcards

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1
Q

How to T-helper cells activate the accuired immune response?

A

When helper cell activated it in turn activates Cytotoxic T cells and B cells which kill infected cells and produce antibodies

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2
Q

How does HIV virion enter T cells?

A

GP120 binds to CD4
GP41 binds to CXCR4
Viral membrane fuses with T cell membrane
Capsid enters

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3
Q

How is HIV infection detected?

A

Antibodies to HIV
Viral RNA
Fall in T helper cell number

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4
Q

What is an ELISA and what are the steps?

A

Enzyme-Linked-ImmunSorbent Assay

1) Antigen bound to well
2) Pateint serum added
3) Anti-human antibody binds to target antibody (enzyme linked)
4)substrated added and converted into coloured product by the enzyme

Absorbances measures in spectrophotometer

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5
Q

What is latex particle agglutination?

A

Latex particles covered in HIV antigen clump when anti-HIV containing blood added

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6
Q

What methods can be used to detect HIV RNA beforr anibodies are detectable?

A

RT-PCR (using reverse transcriptase due to HIV being retrovirus)

Monitoring of infection via T helper cell numbers using Flow cytometry and flurescence activated cell sorting (FACS)

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7
Q

How does flow cytometry/FACS work?

A

Antibodies with a flourescent label attatched are mixed with target cells and passed through a flow cell with a laser pointed at it.
Fluorescent cells release light in response to the laser and photomultiplier tubes detect this.
This can be used to count number of cells and multiple labels can be used to count more than one type at a time.

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8
Q

What is multiple myeloma?

A

It is a cancer of immunoglobulin producing plasma cells in the bone marrow. Result in a large ammount of immunoglobulin produced which can be detected via cellulose acetate electrophoresis.

The malignant plasma cells in the bone marrow activate osteoclasts which break down the bone.

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9
Q

What is pernicious anaemia?

A

Autoimmune disorder against the gastric parietal cells which take up B12

B12 is used in RBC so less RBCs made and less 02 transported therefore fatigue

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10
Q

What are the main structures in the stomach?

A

Fundus, cardia and the body
Without being filled it has Rugae (folds) allowing for it to expand.

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11
Q

What are the strucural layers of the stomach wall?

A

Mucosa (surface mucus layer with gastric pits in it)
Sub mucosa
Muscularis
Serosa

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12
Q

What cell types are in the gastric pit?

A

Surface mucus cells
Mucous necks
Parietal cell (H+, Cl- and intrinsic factors
Chief cell (secretes pepsinogen and gastric ipase)
G cell (secretes gastrin into blood)

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13
Q

How is HCl produced by parietal cells?

A

Carbonic anhydrase syntehsisses it using water and carbon dioxide into H+ and HCO3-

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14
Q

What is the strucute of a villus?

A

Is has a mucosa layer comprised of asorptive cells, goblet cells, endorendocrine cells and paneth cells.

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15
Q

How is H. pylori able to survive in the gut and how it forms ulcers?

A

An ulcer is a break in the gut lining that fails to heal. H. pylori disrupts the mucus layer in the stomach and pepsin and HCl causes the damage to unprotected tissues. Antibiotics and proton-pump inhibitors can be used to reduce HCl formtaion.

H. pylori can produce urease enzyme which converts urea into ammonia + carobn dixoidoe which neutralises the acidic conditions.

H. pylori can be diagnosed using radioactively labelled urea which gets converted to co2 and exhaled where it can be detected.

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16
Q

What is coeliac disease?

A

Sensitivity ot gliadin (component of gluten) that can cause diarrhoea and weight loss

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17
Q

How does the jejunum differ for coeliac sufferers

A

The villi become flattened and the lamina propria expands.

The mucosa is inflitrated by lumphocytes

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18
Q

What is coeliac disease caused by?

A

Tissue transglutaminase attatching to gliadin peptides triggers an mmune response which destroys the intestinal mucosa.

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19
Q

How is coeliac disease identified?

A

Either by biopsy or and ELISA test for anti-TTGA

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20
Q

What is Crohn’s disease?

A

Chronic inflammation affecting the small intestine (sometimes large)
This results in a thickened submucosa
It has a patchy distribution with healthy areas of GI tract inbetween lesions.

No known cause

Symptoms include:
Diarrhoea (sometimes bloody if lesions deep enough)
Abdominal pain
Tiredness (nutrients not absorbed)
Weight loss

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21
Q

How is Crohn’s diagnosed?

A

Intestinal biopsy, fecal tests, barium meals, CT/MRI scans

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22
Q

How is Crohn’s treated?

A

No cure but symptoms can be treated with surgery, corticosteroids and antibiotics if caused by infection

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23
Q

What is cystic fibrosis?

A

A mutation in the Cystic fibrosis transmembrane conductance ragulator gene (CFTR) which prevents chlorine, sodium and water leaving the cell into mucus.

This results in viscous mucus accumulating in lungs and GI tract (blocking exocrine ducts in pancreas)

This results in chest infections, inflammation and structural change in the lungs and malabsorption in the GI tract

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24
Q

What are symptoms of cystic fibrosis?

A

Child tastes salty (due to CFTR mutation preventing absorption of chloride and sodium ions out of the sweat into the cell)
Respiratory disease
Failiure to thrive due to malabsorption and steatorrhea (fat in stool)

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25
How can cystic fibrosis be identified?
Pilocarpine Iontophoresis sweat test with high chloride/sodium levels in sweat test being a positive result. Or detection of gene mutations directly (over 1300 known mutations) using PCR with specific primers to detect mutation (CF has 95 bases normal has 98 in most common mutation)
26
What is lactase deficiency (lactose intolerance)
Insufficient lactase Undigested lactose causes fluid retention in faeces Bacterial fermentation of lactose produced H2 detectable in breath via mass spec
27
How can lactose intolerence be detected?
By giving a lactose meal and then doing a blood glucose test over 3 hours
28
What is the thyroid negative feedback loop?
Hypothalamus produces TRH which stimulates the anterior pituitary to make TSH which stimulates the Thyroid to make T3 and T4 T3 and T4 then stop both the hypothalamus and the pituitary from producing anymore.
29
How do you determine the difference between Inactive thyroid histology and active?
Active form has Free T4/T3 that isn;t bound to protein and is undergoing endocytosis
30
What is the difference betwwen 2-site ELISA and 2 step competitive ELISA?
2-Site is where the patients serum TSH attatches to antibody bound to the well and another antibody with HRP enzyme attatches to any bound TSH to produce a colour. Competitive involves adding both patient serum T4 and HRP bound T4 so they compete for the same antibodies bound to the well. More colour means HRP T4 outcompeted and patient has lower T4 levels and vise versa.
31
How does the Anti TSH receptor cell assay work?
Cells express TSH receptor and contain luciferase gene + promoter When patient serum added and if there is autoantibody TSH cAMP activates luciferase gene which produces light with luciferin which can be detected for a positive result. In a negative result where TSH receptor isn't bound cAMP doesn't rise and no light is produced.
32
What is Anti-TPO ELISA?
ELISA wells coated with TPO antigen Patient serum added and any anti-TPO antibodies bound HRP anti-human antibody added Colour produced in presence of anti-TPO
33
What is graves disease?
An increase in FT4/FT3 with low/absent TSH (due to Anti-TSH receptor autoantibodies) Symptoms: hyperthyroidism symptoms and staring eyes as well as thyroid swelling
34
How does thyroid histology differ in graves disease?
Thyrotoxic hyperplasia (all thyroid follicles active) opposed to normal where most are inactive.
35
What are conditions where T4/T3 can be overproduced?
Graves disease Thyroid adenoma (single benign lump that can form thyroid hormones occasionally) Multinodular Goitre
36
What are treatments for Hyperthyroidism?
Antithyroid drugs (prevent iodine bindin to tyrosine) Sub-total thyroidectomy (usually results in hypothyroidism eventually requiring T4 supplements) Radioactivie Iodine (similar results to thyroidectomy but over longer time)
37
What are treatments for hypothyroidism?
Replacement T4 given and thyroid hormone + TSH monitoring
38
What is Hashimoto's thyroiditis?
Autoimmune destruction of the thyroid Increased TSH Lower T4 Autoantibodies (usually anti-TPO) sometimes other autoimmune conditions
39
What is congenital hypothyroidism?
Underdeveloped thyroid / wrong location. Causes brain damage if not treated early. Symptoms: Growth failure Delayed puberty Impaired development (mental/physical)
40
What happens to the thyroid without sufficient iodine?
Enlargement of thyroid and hypothyroidism
41
What are the two sections of the adrenal gland?
Medulla and cortex
42
How does adrenal gland negative feedback work?
Hypothalamus makes CRH which promotes ACTH production from anterior pituitary which promotes corticosteroid production from adrenal glands which inhibit hypothalamus and pituitary
43
What hormones does each part of the adrenal gland produce and what do they do?
Cortisol (zona reticularis) Raises blood glucose, increases lipid and protein breakdown, stress resistance, immune response depression Aldosterone (zona fasiculata) regulates Na and K homeostasis (promotes reabsorption of these in kidney) DHEA (zona glomerulose) converted to testosterone in circulation and responsible for secondary sexual characteristics. (all based on structure of cholesterol) adrenaline, noradrenaline (from chromaffin cells) for for fight/flight response
44
How are adrenal hormones (including adrenal affecting hormones) diagnosed (what test)?
All but ACTH is competitive ELISA Plasma ACTH is 2 site ELISA
45
What is the dexamethasone supression test?
Tests if cortisol production is being regulated by negative feedback. Dexamethasones inhibits ACTH so cortisol levels should decrease.
46
What is the synacthen test>
Synthacthen added (ACTH analogue) Expect increase in cortisol levels.
47
What is adrenal cortical insufficiency and how is it diagnosed?
Destruction of both adrenal glands (addison's disease) Symptoms - muscle weakness, fatigue, pigmentation, sweating, hypertension, low Na levels Diagnosis: High plasma ATCH low cortisol little increase in cortisol in synacthen test.
48
What is hyperadrenalism (cushing/conn)?
Cushing's syndrome (glucocorticoid hypersecretion) Muscle weakness, hypertension, hirsutism, central obesity, osteoperosis Conn's syndrome aldosterone hypersecretion, polydipsia, polyuira, elecrolyte disturbances Caused by adrenal cortical hyperplasia (raised cortisol in dexamethasone test), cortical adenoma (cushing/conn's appearing yellow without detectable ACTH) or cortical carcinoma (yellow/white tumor which often secretes cortisol and androgens diagnosed by increase in those)
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51
How might the toxicity of a molecule derive from a metabolite?
For instance heroin is quickly broken down into morphine and morphines products can be identified in urine and these metabolites can be more toixc than the initial molecule.
52
Why does alcohol affect vision?
Opsin is used up on the breakdown of methanal rather than of retinal.
53
How does alcohol detection in breath work?
If alcohol is present in blood it will be exchanged in lungs and exhaled where it can be detected and concentration determined. Modern detection methods use infrared light (ammount of IR light absorbed is directly proportional to alcohol conc) or fuel cells can react alcohol and oxygen to produce an electric current.
54
What are the effects of aspirin toxicity?
After 10-30g in adults or 3g in children aspirin can be fatal with symptoms of nausea, vomiting, raised temperature and central system balance impacts and tinnitus. Severe toxicity can bring more sever impacts and lead to comas and death.
55
How do you measure aspirin toxicity in people?
Aspirin undergoes metabolism to produce biologically active compound. It breaks down into salicylic acid and acetate. Salicylic acid can be detected in blood after 1 hour and you should measure salicylate conc 4 hours after consumption and then every 2 hours after until levels fall.
56
How to treat aspirin toxicity?
Treatment of sodium bicarbonate to increase pH and reduce uptake IV fluids to simulate renal clearance Serious cases require hemodialysis
57
Where does the toxicity of paracetamol come from?
It comes from the metabolite NAPQI which is normally conjugated to gluthathione to form non-toxic compounds that are excreted in urine If GSH levels fall NAPQI rises and becomes toxic. To treat it GSH should be elevated to remove the NAPQI In excess NAPQI binds to SH- groups in celluar proteins
58
How is the risk of paracetamol toxicity determined?
It is determined by serum examination over time after ingestion (if over 100mg/l in 8 hours is toxic in normal patients
59
What samples can be analysed for presence of drugs and metabolites?
Blood (invasive) - needs permission but difficult to add adulterants to. Urine (non-invasive) 0 need cooperation, easily adultered Saliva (non-invasive) 0 need cooperation (limited number of analytes) Hair (non-invasive) ^^
60
What are the main differences between screening tests and confirmatory tests?
Screening are more easy tests to do that can be done on site, cost less and have quick results at the expense of being less useful due to being presumative, lacking specifiity and having high cut off limits. Confirmatory tests are done in the lab and give better results but take a longer time.
61
How to identify a compound (drug) and its ammount in a sample?
Main tests for identity of drugs are chromatography, mass spec, sectrophotometry-infrared Main abundance tests are chromatography and spectrophotometry UV-Visable
62
What is randox biochip technology?
A chip containing a arrays of discrete test regions with unique analyte tests on each (up to 49 tests per chip) Analyte binding (similar to ELISA) results in light which can have its intentisty measured to find quantity.
63
What is the problem with antibody-based technologies for drug tests?
They can have cross-reactivity and react to similar compounds as well. Therefore additional confirmatory tests must be done to be sure.
64
How is liquid-gas chromatography used in pair with mass spec to identify molecule presence?
The liquid-gas chromatogrpahy has good resolution and produces measurable peaks but these peaks alone can't determine anylates with certainty The mass spectroscopy is then used to determine locations of peaks to confirm However this can still produce false positives as molecules with similar structure and the same mass they can be confused so the fragmentation ion signatures of IR spec is used to ultimately confirm
65
Why is serum protein separation useful in practice?
Disease can cause over/underproduction of proteins Identification of particular isoenzme may indicate what part of body is effected (e.g creatie kinase for Myocardial Infarction)
66
How much of the plasma consists of protein and what are they?
7-9% (65-90g/L) Albumins (45g/L) Globulins (27g/L) Fibrinogen (3g/L)
67
What are the functions of plasma proteins?
Anti-proteases e.g anti-chymotripsin Blood clotting e.g fibrinogen Enzymes (function in blood / leakage from tissue) e.g creatine kinase Peptide hormones e.g ACTH, TSH, Insulin Immune defence e.g immunoglobulins Inflammatory response Tumour marker e.g ACTH (quantity) Transport proteins e.g Albumin
68
What are the main problems of the blood circulatory system
Haemorrhage and thrombosis also blood clots, non-haemorrhagic strokes and pulmonay emboli
69
What are the stages of blood coagulation?
1) vascular constriction - fast response to serotonin, endothelins and tissue factor 2) Platelet activation plug formation - temporary platelet plug in seconds 3) coagulation cascade and fivrin clot formation (minutes Clot dissolution - (days)
70
What is the blood coagulation cascade?
Zymogens (enzyme precursors) are activated by proteolutic cleavage of peptide bond. This can result in a cascade of enzymes acting on more/other enzymes. For example factor 1 can activate factor 2 which will activate factor 3 and so on. Negative and positive feedback systems in place. Use diagram on slide 14 of lecture 11 as it will be likely used in exam
71
What are the 2 seperate pathways of the blood coagulation cascade before the common pathway and which is faster?
The intrinsic pathway and extrinsic pathway Intrinsic is longer and slower (inting people are slow) Extrinsic is shorter and faster
72
Describe the intrinsic pathway
Activated when blood exposed to collagen it activtes factors in a chain (which you need to know) until it gets to thrombin which when activated produces fibrin which clots it acts more slowly but produces large ammount of thrombin.
73
Describe the extrinsic pathway
It starts in the blood vessel wall when endothelial cells are damaged releasing factor 3 which activates 7 then 10 to make thrombin to respond with firbrin It acts very quickly but produces less thrombin
74
What are gla domains and why are they important?
Factors VIIm VIII, IX, X and prothrombin contain gla domain (10 -carboxyglutamate) Vitamin K-dependent carboxylation serves as calcium ion binding sites attatching to phospholipids on the outside of platelets causing the reaction to become localised to the injury site (where the platelets are)
75
What is prothrombin and how does it convert to thrombin?
Prothrombin contrainns two parts one of which has 10-12 glutamic acid residues which are carboxylated with vitamin K and attatch to the cell. This causes the rest of the prothrombin molecules to detach (hydrolysed) leaving thrombin behind.
76
What are the 3 types of haemophilia?
Type A - most common and severe factor 8 deficiency (basically only extrinsic producing thrombin) It is hereditary and sex linked recessive disease that causes pronounced tendency to bleed. Type B - Factor IX deficiency similar to type A Type C - rare and mild - factor XI deficiency still produces enough thrombin just slowly.
77
What is factor V leiden?
Factor 5 gets activated by thrombin and increases the rate of clotting. This clotting is reversed by protein C degrading activated factor 5. In people with factor V leiden a single point mutation results in resistant factor 5 and manifests as abnormal bloot clots in the legs and lungs.
78
What is vWF deficiency?
GP1b receptors trigger activation of platelets when it becomes exposed due to damage. Symptoms include: large bruises and easy bruising, bleeding gums, heavy menses/partuition haemorrhage, frequent long lasting nose bleeds, heavy bleeding from cuts, heavy long lasting bleeding from tooth extraction
79
What is thrombocytopaenia?
A platelet deficiency which causes increased bleeding times from 5 to over 30 minutes.
80
What is the purpose of thrombomodulin?
It binds to thrombin modules and allows for the binding of protein C and S which act on factor 5 and 8 reducing comon pathway activity (5) and intrinsic pathway activity (8)
81
What are protein C and S deficiencies?
they are autosomal dominant inheritnce Type 1: quantity issue Type 2: quality issues They can also occur in patients with liver disease, taking warfarin or with nephrotic syndrome (enlarged glommerelus pores loosing proteins in urine). as age progresses production decreases resulting in elderly people having a harder time coagulating blood (larger bruises)
82
What are coagulation tests?
PT (prothrombin time) measures the extrinsic factor. A high PT corrolates to a low factor VII International normalised value (INR) is the standardised version of PT so a normal value is 1 APTT measures the intrinsic path (factors XII, XI, IX and VIII), High APTT can show bleeding disorders (haemophilliam von villebrand) as well as anti-phspholipid syndrome Fibinogen levels are also measured. High can be caused by inflammation, cancer or trauma. low can be due to DIC, liver disease, (check workshop for more) DIC and LIVER FAILIURE has HIGH PT AND APTT
83
What is the point of mixing studies?
By adding components (or just regular blood) to the blood and checking for coagulation you can find the problem as the component that fixes the issue is the original patients issue. If the issue is not solved then you can determine its likely an inhibitor.
84
What is GFR and what does it measure?
It is the Glomerular Filtration Rate and is an index of kidney function The only ways to measure it are difficult to use routinely so an estimate (eGFR) is used more often.
85
What is the effect of a fall in GFR?
A fall in the GFR results in reduced urea and creatinine excreation as well as the build up of other waste products. However, a significant rise in these levels will only become apparent after about 3/4 loss in kidney function (around 40ml/min opposed to 160)
86
What are the main causes of kidney failure?
Diabeted - 38% High blood pressure - 26% Glomerulonephritis - 16%
87
What are the 2 main tests of glomerular function?
Inulin test is ideal but difficult to use Creatinine clearance is used more but still has problems with: urine collection only detects change difficult to use in clinical practice. Creatinine clearance can only be used to determine an estimation of GFR.
88
How does eGFR relate to measured GFR?
Similar results around physiological levels but risk of false positive in high levels (establising early disease)
89
How does GFR relate to rate of death and rate of cardiovascular events?
Both rate of death and cardiovascular events increase dramatically with lowered GFR levels.
90
What are the structural changes in a diabetic glomerelus?
Basement membrane thickening, foot processes fusion, podocyte loss and mesangial matrix expansion.
91
Why might larger proteins may be present in the urine and what proteins might you find?
Changes in the glomerular basement membrane can create gaps large enough for larger proteins to pass through. these include: Albumin (main plasma protein) Immunigolbulins Lysozymes Myglobin (from muscle tissue) Haemoglobin
92
What are micro and macro-albuminuira?
Less than 30 mg of albumin over 24 hours is normal 30-300mg per 24 is microalbuminuria >300 is macroalbuminuria
93
What is the progression of diabetic kdiney disease?
Before 2 years may exhibit hyperglycemia and high GFR between 2-5 years cellular injury may occur Between 5-10 years microalbuminuria can be observed along with hypertension (ACE inhibtors should be given around this time).
94
What is the corrolation between cardiovascular events and protein content in urine?
They are directly proportional.
95
What are issues with measuring protein in urine?
Different proteins respond differently even with the same methods Proteins can have different results as for different methods as well. there is variable influence of interfering substances There is no standard references.
96
what methods can be used to identify CKD?
Blood pressure eGFR calculation Albumin/creatinine ratio (ACR) Urine sediment dipstick for RBC and WBC (in case of infection)
97
what are the risk factors for atherosclerosis in the general population and what extra risk factors are relevent to CKD patients?
General: Age Male Hypertension Left ventricular hypertrophy smoking diabetes Dyslipidaemia (lipids in blood) Inactivity CKD: Mineral bone metabolism Vascular calcification Uremic toxins Abnormal lipid modifications inflammation oxidative stress endothelial dysfunction
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