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Mock exam Qs > ESA1 Mock Exam Qs > Flashcards

ESA1 Mock Exam Qs Flashcards

1
Q

Describe the metaplastic change that occurs in the airway epithelium of long term smokers

A

Mucus secreting pseudostratified ciliated columnar respiratory epithelial cells
To stratified squamous epithelium

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2
Q

What is the most likely gram positive organism to cause chest infection

A

Streptococcus pneumonia

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3
Q

Describe the process of gram staining

A

Cells stained with crystal violet dye
Iodine added & forms large molecular complex with crystal violet
Acetone or methanol added; acts as a decolorizer
Crystal violet trapped by thick peptidoglycan layer of gram +ve bacteria
Acetone/methanol degrades thinner peptidoglycan layer of gram -ve bacteria, so decolourizes it
Red dye (safranin) used to stain bacteria (unstained gram -ve cell) red

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4
Q

A 27 year old female with appendicitis is placed under general anaesthetic. Her heart rate & temperature begin to increase, as does her pO2

What do you suspect has happened?

Her muscles also become rigid. What drug would you administer to correct this & what is the mechanism of action

A

Malignant hyperthermia

Dantrolene: a muscle relaxant preventing calcium release

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5
Q

What enzyme is inhibited by the action of penicillin

A

Transpeptidase

Involved in formation of peptidoglycan cross-links in bacterial cell wall. No cross linking means bacterial cell dies

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6
Q

Explain the pathophysiology of rigor mortis

A

No respiration results in no ATP being produced
Actin-myosin complex remains unbroken
Muscles remain contracted

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7
Q

What are the layers of the meninges, starting from outermost layer

A

Dura mater
Arachnoid mater
Pia mater

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8
Q

Name the cells responsible for myelination in the CNS

A

Oligodendrocytes

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9
Q

Explain how anti-pyretic drugs work

A

Inhibit cyclo-oxegenase enzyme

Reduce levels of prostaglandins (PGE2) within the hypothalamus

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10
Q

How do you work out incidence rate

How do you work out incidence rate per X number of people

A

No of new events / no of people x time (yrs)

IR x no of years

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11
Q

Outline the process of fracture (long bone) healing

A

Haematoma formation
Fibrocartilage callus formation
Bony callus formation: calcified to secondary bone
Bone remodelling

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12
Q

Explain how the body keeps calcium levels constant, with respect to bone

A

Parathyroid gland senses low free calcium
This stimulates PTH secretion
PTH increases serum calcium by stimulating oesteoclast activity

(PTH also increases activity of enzyme creating active form of Vit D)

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13
Q

What is a keloid?

A

Excessive scarring on the skin caused by abnormal amounts of collagen
Usually occurs at sites of surgical incision or trauma

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14
Q

What types of immune cells would you expect to see at the site of a wound and what are their respective functions?

A

Neutrophil: phagocytosis
Monocyte/macrophage: phagocytosis, remove cell debris
Basophils: mediate acute inflammatory reactions, using heparin & histamine
B lymphocytes: make antibodies against antigens
T lymphocytes: assist other WBCs (helper) / destroy virus-infected cells (killer)

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15
Q

What are the functions of the skin

A 
Barrier to infection
Psychosexual communication
Sensory
Thermoregulation
Produce Vit D
Control of evaporation
Barrier against mechanical/thermal/physical injury
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16
Q

Outline the process of renewal of the epidermis

A

Keratinocytes multiply (mitosis) in stratum basale & move up to stratum spinosu
Keratinocytes undergo apoptosis in stratum granulosum & loose nucleus
Keratinocytes terminally differentiated by time stratum corneum
Dead cells shed from stratum corneum

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17
Q

Outline the steps of collagen synthesis

A

Synthesis & entry of chain into RER
cleavage of signal peptide (by signal peptidase)
Hydroxylation of selected proline & lysine residues (by prolyl hydroxylase, which requires Vit C + Fe2+)
Addition of N linked oligosaccharides + galactose to hydroxylysine residues
Chain alignment, formation of disulphide bonds (by disulphide isomerase)
Formation of triple helical procollagen from C to N terminus
Completion of O linked oligosaccharide chains by addition of glucose
Transported in vesicle & released by exocytosis
Removal of N & C terminal peptidase (by procollagen peptidase)
Forms tropocollagen
Covalent cross linking & aggregation of fibrils by lysyl hydroxylase

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18
Q

Describe the structure of myoglobin & haemoglobin

A

Mb:
Single subunit protein that contains one Harm grp for binding & transport of oxygen
Can bind one molecule of oxygen
Hyperbolic O2 binding: no cooperativity

Hb:
Tetrameric protein (2 alpha, 2 beta subunits), containing 4 Haem grps
Can bind 4 molecules of oxygen
Sigmoidal O2 binding. Cooperative binding

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19
Q

Describe the effects of 2,3 BPG on binding of oxygen on Hb & the physiological significance of this

A

Decreases affinity of Hb for O2
Curve shifts to the right

BPG conc increases at high altitudes, promoting O2 release at tissues
BOG also produced during metabolism, so O2 released more readily in areas performing high amts of metabolism

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20
Q

Describe the structural differences between oxygen & deoxygenated Hb

A

Oxygenated:
Binding of O2 promotes stabilisation of R state, which allows for cooperativity

Deoxygenated:
Can exist in low affinity T state

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21
Q

Describe the pathophysiology of sickle cell anaemia

A

In deoxygenated state, rbc’s take up sickle shape & polymerise
When oxygenated, rbc’s return to normal biconcave shape

Repeated cycle of deoxygenation & oxygenation = rbc looses elasticity
Stays in sickled state
Unable to pass thru narrow capillaries, causing occlusion & Ischaemia

Shape also predisposes cell to early destruction by haemolysis (30 days rather than 120)
Causes anaemia

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22
Q

Why can cole weather, being ill & being dehydrated make sickle cell disease worse?

A

Cold: causes vasoconstriction, passage of already distorted rbc’s more difficult & ore prone to lysis

Dehydration: contraction of extracellular vol, increases blood viscosity, increases likelihood of vaso-occlusive crisis

Ill: increases no of WBCs, which increases viscosity of blood. Makes it difficult for rbc’s to pass thru capillaries

Sickle cell disease = functionally asplenic
Less able to fight off bacteria & risk of being overwhelmed by infection

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23
Q

What is a sickle cell crisis?

A

Lack of perfusion to an area causing ischaemic injury & subsequent pain

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24
Q

Describe the process of DNA replication

A

Initiation:
Recognition of / binding to an ‘origin of replication’
DNA helicase unravels DNA double helix
RNA primase lays down primers

Elongation:
Replication from 5’ to 3’ in both leading & lagging strands
Lagging strand replaced discontinuously (Okazaki fragments)

Termination:
RNA primers removed
Discontinuous fragments joined up by DNA ligase

Semi conservative replication:
2 daughter helices have 1 strand comprised of parental DNA from original & one newly synthesised strand

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25
Q

Describe DNA gel electrophoresis

A

Used to separate diff sized DNA fragments:

Agarose gel submersed in tank of buffer solution (conducts electricity)
DNA fragments added to agarose gel

Dye added for better visualisation of DNA

DNA negatively charged & moves to positive electrode when electric current present

Larger fragments move slower

Fragments of known size used as a reference

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26
Q

Explain PCR & describe its uses

A

Amplified DNA segments by repeated copying of target DNA using thermo-stable DNA polymerase & pair of primers that uniquely define region to be copied

Denaturation: high temp (94-96)
Double stranded DNA becomes single stranded

Annealing: lower temp (50-65)
Primers bind to strands

Renaturation/DNA synthesis: medium temp (75-80)
DNA Taq polymerase synthesises complementary DNA strand

Used to:
Amplify specific DNA fragment
Investigate single base mutations

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27
Q

State the 3 layers of the adrenal cortex & their respective secretions

A

Zona reticularis: androgens, cortisol

Zona fasciculata: glucocorticoids

Zona glomerulosa: mineralocorticoids

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28
Q

Why is a patient with Addisons hypotensive?

A

Aldosterone stimulates reabsorption of sodium and hence water
Therefore no aldosterone = less water retention by kidneys = hypovolemia, hypotension

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29
Q

Why is an Addisonian patient’s skin pigmented?

A

Adrenal gland dysfunction = low cortisol
Negative feedback = more ACTH released from pituitary gland
ACTH & MSH both derived from POMC
MSH stimulates melanocytes to produce melanin, therefore skin pigmentation

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30
Q

If a patient is suffering with Addisons, what would the Synacthen test show & why

A

Low cortisol/doesnt rise above 540 nmol/l
Despite admin of synthetic ACTH
suggesting primary adrenal insufficiency

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31
Q

What would the blood test of a patient with Graves disease show & why

A

High T3 & T4: autoantibodies stimulate TSH receptors

Low TSH: negative feedback from high T3/T4, to reduce TSH production

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32
Q

Describe the steps involved in synthesis of T3 & T4

A

Stimulated by TSH
thyroglobulin synthesis in thyroid epithelial cells
Exocytosis of thyroglobulin into colloid
Iodination of tyrosine residues on thyroglobulin
Coupling of 2 x DIT to make T4 & MIT + DIT to make T3
Endocytosis of iodinated thyroglobulin into follicular cell
Proteolytic Cleavage to make free T3/T4
Diffuse from epithelial cells & Exocytosis into bloodstream

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33
Q

Explain the mechanism of action of Carbimazole & what it is used for

A

To treat hyperthyroidism

Metabolised to methionine
Inhibits thyroid peroxidase
Prevents iodination of tyrosine residues

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34
Q

Explain the mechanism by which alcohol causes:
Jaindice
Ascites
Hepatomegaly

A

Jaundice:
Mixed myoerbilirubinaemia from mixture of hepatocellular injury & cholestasis

Ascites:
Reduced protein synthesis e.g. Albumin in damaged liver = reduced oncotic pressure in blood vessels. Hydrostatic pressure greater than oncotic pressure which favours mvmt of fluid out into intestinal space
Also Liver cirrhosis = portal htn

Hepatomegaly:
Lipid deposition in liver (alcoholic fatty liver disease) = hepatomegaly

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35
Q

What is the mechanism of Disulfiram

A

Inhibitor of aldehyde dehydrogenase
Causes build up of acetaldehyde
This is a toxic metabolite causing unpleasant hangover-type symptoms

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36
Q

Why would a patient with alcoholic liver disease display extensive bruising & bleeding

A

Clotting factors are synthesised by liver
Liver damage = reduced synthesis of clotting factors

Malnutrition also common in alcoholics, may = vit K deficiency

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37
Q

What causes the sweet smelling breath of someone in Diabetic kKetoacidosis

A

Absolute lack of insulin
Causes production & build up of ketones in blood
Acetone is one type of ketone & causes acetone smell on breath

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38
Q

State the features of an alpha helix & beta sheet

A

Alpha helix:
Right handed helix
3.6 aa per turn
0.54nm pitch

Beta sheet:
Extended conformation
Parallel or antiparallel
Multiple inter-strand H bonds

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39
Q

What are apolipoproteins & describe their role in lipid transport

A

They bind to lipids to form lipoproteins

Lipids are insoluble in water
Lipoprotein molecules allow for molecule to be transported in aqueous env
Interact with receptors & enzymes so that lipids can be taken up by cells

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40
Q

What is the underlying genetic defect in familial hypercholesterolaemia & explain what the blood test results would be

What conditions would a patient be at risk of

A

Defective LDL receptors

Reduced LDLs uptake by hepatocytes
= increased levels of circulation LDLs

CAD/MI
stroke
Peripheral vascular disease

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41
Q

Explain the following:
95% CI for age & deprivation adjusted IRR for female south asians compared with female non-south asians for all cancers is 0.49-0.79

Why might incidence increase over time amongst SAs?

A 
The 95% CI doesnt contain 1
The null hyp can be rejected (p<0.05)
Unlikely to be due to chance
Stat sig finding
IR of cancers in FSA less than IR of cancer in FNSA

Lifestyle factors e.g. Changes in diet

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42
Q

At which stage if the cell cycle do chromosomes replicate?

A

Synthesis (S)

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43
Q

What study would you use to investigate:

Incidence of rare chronic granulamatous disease in people vaccinated against measles as a baby

A

Case control

Good for rare diseases
Likelihood of dev condition is low, so cant use cohort

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44
Q

What would be seen on an endocrine test for Addisons

A

Hyponatremia ( from lack of aldosterone ) hyperkalaemia (from lack of aldosterone), hypoglycaemia (from lack of cortisol)

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45
Q

Which classification do salivary glands belong?

A

Compound tubuloalveloar

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46
Q

What is the pattern of inheritance of Becker’s Muscular Dystrophy

A

X linked recessive

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47
Q

What is the diagnostic value for diabetes in HBA1C

A

> 10 % (normal 4-6%)

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48
Q

What antigen is found in hyperthyroidism (Grave’s disease)

A

Anti-thyroid peroxidase antibodies (anti-TPO)
Thyrotrophin receptor antibodies (TRA bs)
Thyroglobulin antibodies

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49
Q

What is the lifespan of a red blood cell

A

110-120 days

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50
Q

Outline the mechanisms of erythropoeisis

A

Controlled by partial pressure of O2
pO2 stimulates erythropoietin

Feedback system:
Increased production of erythropoietin from peritubular endothelial cells (kidney) in response to hypoxia
Erythropoietin increases rate of rbc production & release from bone marrow
Increased oxygen carrying capacity of blood

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51
Q

Describe the affect of Hb dissociation curve at high altitudes

A 
HB increases at high altitudes
Reduced affinity of Hb for O2
Curve shifts to the right
Tense state
Less taken up by lungs
More released at tissues

Similar to increased 2,3 BPG

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52
Q

Describe coeliac disease

Explain why patients have a higher risk of fractures

A

Mainly affects small intestine: inflammation
Reaction to gluten
Autoimmune
Destroys villi

Vitamin D deficiency = orsteomalacia
Oesteoporosis

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53
Q

What are the chemical bonds found in glucogen

A

Alpha 1,4 glycosidic bonds: link main stem glucose molecules

Alpha 1,6 glycosidic bonds: link stem & branch

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54
Q

Cellulose:
Describe its function in the GIT
describe its chemical structure

A

Hydrophilic bulking agent for faeces: dietary fibre

Beta 1,4 linked glucose units
Straight chain polymer
Humans don’t have enzymes to digest these bonds

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55
Q

Describe the allosteric regulation of enzymes

A

Regulation of a protein (multisubunit enzyme) by binding effector molecule at a site other than protein’s (enzyme’s) active site

More than one active site for substrate

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56
Q

In the endocrine pancreas:
what 3 types of cells are found
What do they secrete
Where are they found

In the exocrine pancreas:
What types of cells are found
What do they secrete
What are they stimulated by

A

Endocrine:
In islets of langerhans
Alpha cells: glucagon (increase blood glucose)
Beta cells: insulin (decrease blood glucose)
Delta cells: somatostatin (regulates/stops alpha & beta cells)
Gamma cells: pancreatic polypeptide

Exocrine:
Ducts containing acini
Proteases (trypsinogen, chymotrypsinogen), lipases, amylases, bicarbonate ions
Secretin, gastrin, CCK

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57
Q

Describe Nissel body/substance

Where it is found
What it contains

A

large granular body found in neurons

granules are RER with rosettes of free ribosomes

are the site of protein synthesis

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58
Q

What are the classifications of muscle & describe their features

A 
Skeletal:
Striated
Multinucleated; at periphery
Cells cant divide: regenerate by mitotic activity of satellite cells; increases musc mass
Gross damaged repaired by CT (scar) 
T tubules in line with A/I band

Cardiac:
Striated
1-2 nuclei per cell; central
Branched
Incapable of regeneration: fibroblasts invade & lay down scar tissue
T tubules in line with Z bands
Intercalated discs: Gap junctions (electrical coupling), adherens type junctions (anchor cells) desmosomes
purkinje fibres (modified monocytes with extensive gap junctions: rapid direction of AP so ventricles contract in synch)

Smooth:
Not striated
Single nucleus; central
Spindle shaped (fusiform)
Cells retain mitotic activity; can form new smooth musc
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59
Q

Define connective tissue

A

Tissues of mesodermal origin containing:
Cells
Ground substance
Extracellular fibres

Support organs
Fill spaces between organs
Form tendons & ligaments

60
Q

Outline the types of connective tissue

A

Loose: e.g. Blood, adipose tissue, areolar tissue, reticular tissue
Dense regular: e.g. Tendons, ligaments, aponeuroses
Regular irregular: e.g. Dermis, periosteum, perichondrium, dura mater

61
Q

Outline the types of cartilage & where they are found

Type of collagen contained in each

A

Hyaline (type 2 collagen): e.g. Articulating surfaces of long bones, anterior ends of ribs, respiratory passageways, foetal skeleton
Elastic (type 2 collagen): e.g. Pinna, eustachian tube, epiglottis
Fibrocartilage (bundles of type 1 collagen): e.g. Intervertebral discs, knee menisci, pubic symphysis, temperomandibular joint

62
Q

Describe portal systemic anastamoses

A

specific type of anastomosis that occurs between the veins of portal circulation and those of systemic circulation.

Areas (& vessels involved):
Oesophageal (oesophageal branches of azygous vein)
Rectal (middle & inferior rectal veins)
Paraumbilical (superficial epigastric vein)
Retroperitoneal (renal, suprarenal, paravertebral, gonadal vein)
Intra hepatic (inferior vena cava)

63
Q

Describe portal hypertension

Causes

Symptoms

A

high blood pressure in the portal vein system, which is composed of the portal vein, and its branches and tributaries.
Consequences of portal hypertension are caused by blood being forced down alternate channels by the increased resistance to flow through the systemic venous system rather than the portal system.

Prehepatic causes: portal vein thrombosis or congenital atresia.
Intrahepatic causes: liver cirrhosis, hepatic fibrosis
Posthepatic obstruction: at any level between liver and right heart, including hepatic vein thrombosis, inferior vena cava thrombosis, inferior vena cava congenital malformation, and constrictive pericarditis.

Ascites
Hepatic encephalopathy.
Increased risk of spontaneous bacterial peritonitis.
Increased risk of hepatorenal syndrome.
Splenomegaly
Portal systemic anastomoses: Esophageal varices, gastric varices, anorectal varices (not to be confused with hemorrhoids), and caput medusae. Esophageal and gastric varices pose an ongoing risk of life-threatening hemorrhage, with hematemesis or melena.

64
Q

Describe how glycogen enters the main glycolysis pathway

A

Glycogenolysis occurs in liver & skeletal muscles
Glycogen broken down by glycogen phosphorylase & debranching emzyme
Produces glucose 1 P
This is acted on by phosphoglucomutase to produce glucose 6 P
This is acted on by glucose 6 phosphatase in the liver to produce glucose

65
Q

What is the result of chronic persistent hyperglycaemia in the plasma?

A

Aldose reductase converts glucose to sorbitol
Depletes NADPH

Non-enzymatic glycosylation = loss of structure & function of plasma protein

66
Q

Outline the formation of a mature insulin molecule

A

Synthesised as inactive single polypeptide chain = preproinsulin
Removal of signal peptide (signal peptidase)
3 disulphide bonds formed = proinsulin
Removal of C peptide (endopeptidase) = mature insulin molecule

67
Q

How are the disaccharides & dextrins digested?

Name 3’enzymes that digest here

A

Digestion occurs in duodenum & jejunum
Releases monosaccharides: glucose, fructose, galactose

Glycosidase enzymes: large glycoprotein compkexes attached to brush border of membranes of epithelial cells

E.g. Lacatse, glycoamylase, sucrase

68
Q

Why would someone with lactose intolerance suffer from cataracts if they have a high lactose diet?

A 
Accumulation of galactose in tissues
Reduction to galactitol
Depletes tissues of NADPH
Free SH grps cant be maintained
Lens proteins in eye cross linked by disulphide bonds = cataracts
69
Q

How can NADPH be used as a first defence mechanism in cells?

A

A reducing agent
Converts glutathione disulphide (GSSG) back to glutathione (GSH) in cells
Glutathione acts as reducing agent to neutralise ROS in cells

70
Q

What is the purpose of phase 1 & phase 2 drug metabolism

A

Phase 1: add/expose a reactive group on a drug

Phase 2: conjugation - add sulphate, glucuronic acid, glutathione

71
Q

Explain why an overdose of paracetamol can be deadly & give ghe treatment of an overdose

A

Saturates both glucoronic & sulphate pathways of usual phase 2 metabolism
Phase 1 metabolism produces toxic compound NAPQI
NAPQI undergoes phase 2 metabolism, conjugating with glutathione
Removes liver cell’s primary antioxidant, leaving them prone to oxidative stress by ROS: can cause liver damage

N-acetyl cysteine

72
Q

Describe how the healthy worker effect leads to bias

A

Use of workers in studies as a representative of the entire population may lead to bias as workers are generally in good health as they are able to work

73
Q

Why does vitamin C result in weakened structures that contain collagen

A

Is a cofactor needed by enzyme prolyl hydroxylase for hydroxylation of proline residues
Lack of vitamin C = weakened tropocollagen helixes

74
Q

Outline elongation of mRNA translation

A

Met-tRNA occupies P site on ribosome
Empty A site allows binding of other amino-acyl-tRNA (An energy requiring reaction)
Complementary anti-codon for codon on mRNA
Peptide bond forms between 2 amino acids via peptidyl transferase
tRNA at P site now uncharged & leaves
Ribosome undergoes translocation (requires energy)
Moves towards mRNA 3’ end, exposing another empty a site

75
Q

Collagen is a main component of connective tissue.
What are the differences in arrangement of collagen fibres in dense regular & dense irregular connective tissue?
How does the difference in arrangement explain the difference in function of the two?

A

Dense regular: collagen packed tightly in parallel, unidirectionally
Max tensile strength, for unidirectional forces

Dense irregular: interwoven bundles packed multidimentionally
Can withstand multidirectional forces, to prevent tearing

76
Q

What is the role of mast cells?

A

Found near blood vessels
Involved in allergic & hypersensitivity reactions
Contain granules of:
Histamine (increase permeability of blood vessel walls)
Heparin (coagulation)

77
Q

What are the products of POMC cleavage?

A

ACTH
Alpha-MSH
Beta-endorphin

78
Q

What does the Barker Hypothesis state?

A

Experience of the foetus in utero during development determines future health if the individual

79
Q

How are zymogens activated

A

Removal of part of the polypeptide chain (proteolytic cleavage)

80
Q

How is cortisol secretion controlled?

A

Negative feedback by levels of cortisol in the blood
Hypothalamus secretes CRH
Pituitary stimulated & secreted ACTH
ACTH stimulates adrenal glands to produce cortisol

81
Q

Outline the process of endochondral ossification from the embryo to the mature adult

A

Mineralisation if hyaline cartilage:

Embryonic:
collar if periosteal bone forms
Central cartilage in the diaphysis calcifies
Primary ossification centre forms in diaphysis

Postnatal:
Medulla becomes cancellous bone
Cartilage forms epiphyseal growth plates
Secondary ossification centres from in epiphyses

Prepubertal:
Growth of bond by interstitial & appositional growth at the epiphyseal growth plates - ossification of epiphyses

Mature adult:
Ossification if epiphyseal growth plate - stop growth
Hyaline cartilage remains at articulating surfaces
(Periosteum only at non-articulating surfaces)

82
Q

What conditions cause normal long bone development to be impaired & why?

A

Pituitary dwarfism:
Lack of growth hormone affects epiphyseal growth plates

Gigantism:
Excess growth hormone (before calcification of epiphyseal growth plates) = extensive endochondral ossification

Acromegaly:
Excess growth hormone (after calcification of epiphyseal growth plate) = excessive intramembranous ossification = large face/jaw, broad features

Achondroplasia:
Failure if proliferation of column formation of epiphyseal cartilage = impaired long bone growth = short limbs (normal trunk)

Rickets:
Lack of calcium/Vitamin D = poor calcification of bone = sift, malformed (epiphyseal plates distorted by body weight)

Oesteogenesis imperfecta:
Defect in collagen = weak bones prone to fracture = deformed bones

83
Q

Describe if & how each muscle type regenerates

A

Skeletal: regenerates vis satellite cells

Cardiac: cant regenerate

Smooth: can regenerate

84
Q

What is the difference in function between myoepithelial cells & myofibrils?

A

Myoepithelia:
Assist secretion of some exocrine glands

Myofibrils:
Secrete collagen at sites of wound healing/contract to bring edges together

85
Q

Damage to a piece of DNA has occurred via deamination of a base.
How is this repaired?

A

Base excision repair

Faulty base removed by enzymes & replaced by correct one

86
Q

Why is build up of phenylpyruvate in PKU a problem?

A

Inhibits uptake of pyruvate into mitochondria
Glucose isn’t metabolised as effectively
Can lead to brain damage
(brain highly dependent on glucose metabolism to function)

87
Q

What is the function of hormone sensitive lipase & how is it regulated

A

Controls release of fatty acids from adipose tissue
Phosphorylated = activated by glucagon & adrenaline
Dephosphorylated = inhibited by insulin

88
Q

How is erythropoiesis controlled?

A

Interstitial peri tubular cells of kidney detect low pO2 (hypoxia)
Increase production of erythropoietin
Stimulates production of rbc’s, increasing tissue oxygenation
Kidney detects tissue oxygenation & reduced production of erythropoietin

89
Q

Around what day does compaction occur & what does it produce?

A

Day 4

Trophoblast & inner cell mass (embryoblast)

90
Q

What is the difference between pharmacodynamics & pharmacokinetics

A

Dynamics = what drug does to the body

Kinetics = what body does to the drug

91
Q

Why might someone with type 1 diabetes get blurred vision?

A

Insulin deficiency = high plasma conc of glucose
Uptake of glucose by eyes dependent on surrounding conc of glucose (not insulin)
Therefore lots of glucose taken up by eyes, giving blurred vision

92
Q

What are 2 functions of platelets

A

Prevent blood loss

Adhere to damaged cell walls by aggregating together

93
Q

Name the types of white blood cells & what they do

& shape of nucleus

A

Basophils
Neutrophils: phagocytosis, migrate to site of infection (multilobed)
Monocytes: become macrophages, phagocytosis (kidney shaped)
Eosinophils: phagocytosis, release cytotoxic particles (bilobed)
T lymphocytes: helper/killer - express CD4 receptor (deep staining)
B lymphocytes: humoral immunity, secrete Ig, stimulated by antigens

94
Q

Describe the histology of the thyroid gland

A

Follicular cells contain thyroglobulin colloid
Follicle surrounded by simple cuboidal or columnar epithelia
C cells darkly stained & found in epithelia

95
Q

What parts of the cell does haematoxylin stain purple

What part of the cell does Eiosin stain pink

A

Acidic components (e.g. Nucleus, chromatin)

Basic components (e.g. Cytoplasmic proteins, extracellular fibres)

96
Q

Outline the synthesis of T3 & T4

A

Transport of iodine into epithelia (against conc gradient)
Thyroglobulin (tyrosine rich protein) secreted by exocytosis into lumen
Iodination of tyrosine side groups forms MIT or DIT
DIT + MIT = T3
DIT + DIT = T4

97
Q

Explain the process of DNA sequencing using the Sanger method

A

Radioactively stained ddNTPs added to template strand with DNA polymerase
Depending on which ddNTP used, strand will terminate at diff places
Produces lots of DNA fragments if diff lengths that can be denatured with heat & separated with gel electrophoresis

98
Q

How is Myasthenia Gravis treated?

A

Acetylcholinesterase inhibitors (e.g. Neostigmine)

99
Q

What is non-disjunction between chromosomes

A

Failure of homologous pairs to split in meiosis

can lead to extra chromosome (e.g. Trisomy 21)

100
Q 
Distinguish between these different types of microscopy:
Phase contrast 
Dark field
Fluorescence
Confocal

What are they?
What are the useful for?

A

PC:
Interference of 2 combining light waves
Enhancing image of unstained cells

DF:
Exclude unscattered beam from image
Live/unstained samples

Fl:
Molecule targeted with Fluorescent antibodies
Multiple fluorescent stains for one sample

Con:
Tissue labelled with fluorescent probes
Eliminates out of focus flare/produce 3D image/ living specimens

101
Q

Why is blood considered to be a connective tissue?

A

Has fluid/semi fluid matrix
Contains fibres (soluble, un-clotted blood)
Derived from mesoderm

102
Q

What two properties of heamoglobins enable them to be separated by electrophoresis

A

Net charge

Size

103
Q

What possible molecular explanations are there for the presence of abnormal heamoglobins in the patients blood

A

Production of structurally abnormal Hb molecules due to mutation in globin structural gene

Presence of abnormal ration of subunits due to over or under production of globin subunits

Change in post-translational modification of globin sub-units

104
Q

What is anaemia?

Why would is patient suffering from anaemia likely to feel tired?

A

Lower than normal conc of Hb in the blood

Low Hb associated with reduced ability to carry oxygen to tissues
Reduced aerobic metabolism
Inadequate ATP level yo maintain cell function

105
Q

What does a crude mortality rate ratio of 2 indicate for A compared to B

A

A has twice the rate of deaths than B

106
Q

If a crude mortality rate ratio is found to be 2 for A compared to B:

What characteristics of the populations would you like to know before accepting A is more deadly than B?

How would this explain the mortality rate ratio?

A

Age distribution of the populations

Age distribution may be acting ad a confounder
If A has more elderly population than B, & elderly people more likely to die, then A may have a higher mortality rate than B because of its more elderly population

107
Q

What visualisation techniques may be used to investigate rectal bleeding from suspected cancer

A

Endoscopy/ sigmoidoscopy/ colonoscopy with poss biopsy

Barium enema

108
Q

What macroscopic features of rectal cancer leads to bleeding

A

Ulceration

Raised/ stenotic/ fungating/ invading wall

109
Q

State the epithelia of the large intestine & anal canal

A

Large intestine = simple columnar (non-ciliated)

Anal canal = stratified squamous, keratinized

110
Q

From which embryonic tissue does the mucosa of the gut arise?

A

Endoderm

111
Q

What components, other than epithelium, are included in the intestinal mucosa

A

Lamina propria

Smooth muscle / muscularis mucosa

112
Q

Describe TNM staging for cancer

Describe Duke’s staging for bowel cance

A

TNM:
T = tumour. size of the original (primary) tumor & whether invaded nearby tissue,
N =node. nearby (regional) lymph nodes involved,
M =metastasis (spread of cancer from one part of the body to another).

Duke's:
A = confined to bowel wall
B = thru muscle wall, lymph nodes clear
C = lymph node involvement
C1/C2 = highest node clear/involved
113
Q

What enzyme is usually measured in the blood in order to establish diagnosis of acute pancreatitis

A

Serum amylase

114
Q

What are the common precipitating (causes/triggers onset) factors to the development of acute pancreatitis

A

Galls stones
Alcohol
Hypothermia
Various drugs

115
Q

Why might blood glucose be elevated in someone with pancreatitis

A

Destruction of Islets of Langerhans leading to diabetes

116
Q

What are the strengths & weaknesses of a case control study

A 
Strengths:
Quick
Inexpensive
Good for rare diseases
Range of exposures can be studied for one disease
No concerns with loss to follow up

Weaknesses:
More prone to information bias (e.g. Recall bias)
More prone to selection bias (therefore choice of controls crucial)
Nt good for rare exposures
Cant necessarily establish exposure preceded onset of disease
Cant directly measure incidence

117
Q

What happens to carbohydrate eaten in excess lf the body’s immediate requirement for energy?

A

Stored as glycogen in the liver & skeletal muscle

Converted to fatty acids & stored as TAGs in adipose tissue

118
Q

What are the histological features of an adipocyte from white adipose tissue

A

Large lipid droplet (TAG) filling the cell
Nucleus pushed to one side
Small amount of cytoplasm pushed to one side
Small number of mitochondria

119
Q

How are fatty acids transported in the blood?

Why does the conc of FAs in the blood never increase much above 3mM

A

Hydrophobic & can only be transported bound to albumin

Albumin only has limited capacity to bind FAs as binding specific & is a limit to amount of fatty acids that can be in circulation in any one time

120
Q

Describe some limitations of the cognitive models such as the health belief model

A

Social & env influences reduced to cognitions
Don’t account for how beliefs/attitudes may change over time
Dont incl emotional components involved
Assume people define risk on rational manner
People may not act rationally
Act out of habit, & not as result of decision
Outcomes may be perceived/valued differently; what is rational to one person may not be for another

121
Q

Which of the following statements best describes the mechanism of action of the antibiotic chloramphenicol?

A Inhibits bacterial protein synthesis 
 B Inhibits bacterial RNA polymerase 
 C Inhibits DNA polymerase  
 D Inhibits mammalian protein synthesis 
 E Inhibits mammalian RNA polymerase
A

A

122
Q

Which of the following intermediates of collagen biosynthesis will signal peptidase act upon?

 A Collagen fibre  
 B Collagen fibril 
 C Preprocollagen 
 D Procollagen 
 E Tropocollagen
A

C

123
Q

A mutation is found to have occurred in the last intron-exon boundary of a gene. What is likely to be the first process to be affected by this mutation?

 A Polyadenylation 
 B RNA capping 
 C Splicing 
 D Transcription initiation 
 E Transcription termination
A

C

124
Q

Which of the following are cells of the innate and adaptive immune system, respectively, responsible for the destruction of virally infected cells?

A B lymphocytes and eosinophils

B Cytotoxic T lymphocytes and neutrophils

C Helper T lymphocytes and eosinophils

D Natural killer cells and cytotoxic T lymphocytes

E Macrophages and helper T lymphocytes

A

D

125
Q

When a study is double-blinded, the potential for which types of bias is reduced?

A. Healthy worker effect and selection bias
B. Placebo effect and observer bias
C. Placebo effect and measurement bias
D. Selection bias and observer bias
E. Observer bias and differential misclassification

A

B

126
Q

What is pK

What is the equation for pK

A

Extent to which acid dissociates (strength of an acid)

pK = -log [Ka]

127
Q

What is the Henderson Hasselbach equation

What is it useful for

A

pH = pKa + log ([A][HA])

A = conjugate base HA = acid

Estimating buffer solution
Equilibrium of pH in acid-base reactions
(pI of some proteins)

128
Q

Describe the key features of amino acid metabolism

A

Constant turnover of proteins (making/breaking) makes free aa’s
Can be used to make other proteins

Rich diet = excess aa’s
Liver disposes of excess aa’s

Prob: amine group potentially toxic (transamination or deamination)
Enzymes remove NH2 grp leaving C skeleton, with 2 poss pathways:
Ketogenic aa’s (e.g. Leucine, lysine):
used to make ketone bodies from acetyl CoA
Glucogenic aa’s (e.g. Glutamate, glutamine):
can make glucose (glucoenogenesis)
Some aa’s are both ketogenic & glucogenic:
(e.g. Isoleucine, penylalanine, tyrosine)

129
Q

Describe transamination

A

Transfer of amino group to a keto-acid

Uses alpha ketoglutarate or oxaloacetate (TCA intermediates)
Converts range of aa’s to glutamate or aspartate: useful products
(Can feed into urea cycle)

aa + alpha-ketoglutarate -> glutamate + keto acid
aa + oxaloacetate > aspartate + keto acid

Process is reversible

130
Q

Describe deamination

A

Disposal of amine group (NH2)

Removed from amino acid to form ammonia (NH3)
Converted to ammonium ion (NH4+)

These are very toxic (esp to neurones) & must be removed/converted to non-toxic products:
Glutamate -> aspartate -> urea cycle -> urea (water soluble)
(Ammonia + aspartate -> urea)
(Urea cycle can be up/down regulated)
Glutamate -> glutamine (good store / transport for ammonia)

131
Q

Describe the process of ammonia detoxification

A

Initially NH3 used to synthesise glutamine

Then NH3 (released from glutamine) either excreted directly or converted to urea

132
Q

Describe the synthesis of glutamine

A

Made from Glutamate + ammonia in cells (requires ATP)

Used to Synthesise N compounds (e.g. Purines, pyrimidines)

Excess released from cells, transported in blood to liver & kidney, where broken down to release ammonia (glutaminase)
Kidney: ammonia excreted directly in urine
Liver: ammonia used to make urea

133
Q

Describe visceral vs parietal pain

A

Peritoneal cavity made of visceral & parietal peritoneum
But these dev from diff embryological pathways:

Viscera (e.g surrounding intraperitoneal structures) don’t have somatic nerve supply
When viscera stretched/irritated chemically etc, pain will be referred according to whether that structured belonged to foregut (epigastric) midgut (periumbilical), or hindgut (suprapubic)
Follow splanchnic nerves that exit at dermatome of these central areas
Visceral peritoneum therefore refers pain along the midline

Parietal peritoneum lines the body wall: has more dedicated somatic innervation and therefore is more localised

134
Q

Describe the boundaries of the inguinal canal

A

Floor = inguinal ligament (lacunar ligament medially)
Roof = internal oblique / transverse abdominus (musc arches & aponeurosis)
Posterior wall = transversalis fascia (innermost layer; includes conjoint tendon medially)
Anterior wall = aponeurosis of external oblique

135
Q

What pouched/recesses exist in the peritoneal cavity

Whats their clinical significance

A

Pouch of Morrison/hepatorenal recess/subphrenic recess:
Separates liver & right kidney (behind duodenum)

Pouch of Douglas/rectouterine pouch (females):
Between rectum & posterior wall of uterus

Vesico-uterine pouch (uterovesical pouch of Meiring) (females):
Between Uterus, bladder, part of intestinal surface (shallower)

Rectovesicle pouch (males):
Reflects onto posterior wall of bladder

Paracolic gutters:
Between ascending/descending colon & abdominal wall on either side

Are potential spaces that can collect fluid/infection which can then travel around peritoneal cavity
(Often when lying down)

136
Q

In embryological terms, whats the falciform ligament a remnant of

A

The Falciform ligament is a remnant of the Ventral mesogastrium of the foregut

The Liver develops in this mesentery dividing it up into the  
Falciform ligament (Anterior wall- Liver) 
Lesser Omentum (Liver-Stomach
137
Q 
Describe what the following tests show:
ALT
ALP
AST
Albumin
Bilirubin
A

Alanine transaminase (ALT) is specific to hepatocytes and so if they are damaged it is released into plasma.

ALP tends to rise in biliary obstruction and bone disease.

AST is raised in liver damage but is also present in reasonable quantities in cardiac and skeletal muscle and so is not
that specific to the liver.

The healthy liver produces albumin so hepatocyte damage will not result in more albumin

Raised conjugated Bilirubin levels is seen more in Biliary obstruction that occurs after conjugation has occurred
(common bile duct blockage etc).

138
Q

What differences are there in the abdominal wall above & below the arcuate line (line of Douglas)

A

The Rectus muscles are surrounded by the aponeurosis of the other abdominal wall muscles;

  • both anterior and posterior to them above the arcuate line
  • only anterior below it below the arcuate line
139
Q

Explain the origin of the pmf at the inner mitochondrial membrane

A

Three of the enzyme complexes in the electron transport chain also
act as proton translocating complexes (pumps).
These complexes use energy from the electron transport chain to
pump protons from the inside to the outside of the membrane.
The membrane is impermeable to protons and therefore an
electrochemical gradient is established across the membrane.

140
Q

How is ATP produced at the inner mitochondrial membrane

A

Energy from the proton motive force is used to drive the production
of ATP by ATP synthase enzyme.

141
Q

Explain why the pancreas may become diseased in someone with CF

A

The CFTR ion channel is absent.
As a result, chloride ion transport out of the exocrine tissue is
substantially compromised.
Consequently, water does not leave the epithelium in sufficient
quantities to adequately hydrate the secretions.
The secretions therefore contain too little water and become
thickened/viscous, with resultant blocking of the ducts.

142
Q

Name some general mechanisms that can be used to regulate enzyme activity

A 
Proteolytic cleavage
Vary substrate concentration.  
Allosteric effectors.  
Product inhibition.  
Phosphorylation/dephosphorylation.  
Binding to a regulatory protein.  
Sequester enzyme/substrate in an organelle.  
Proteolytic degradation (via ubiquitination).  
Change rate of transcription.  
Change rate of translation.
143
Q

How is trypsin formed from trypsinogen?
Why is trypsin initially produced as trypsinogen?
How is any premature activation of trypsin in the pancreas
dealt with?

A

Enterokinase breaks a peptide bond between the N-terminal 6
amino acids to form mature trypsin.

Formation of an active form of trypsin in the pancreatic cells
would result in proteolytic digestion of the cell.

Specific trypsin inhibitors produced by the body that bind to the
active site and block enzyme activity.

144
Q

How is the General Fertility Rate calculated?

State ONE ADVANTAGE that General Fertility Rate has with
respect to the Crude Birth Rate?

State ONE DISADVANTAGE that General Fertility Rate has
with respect to the Crude Birth Rate.

A

General Fertility Rate = (Number of live births [in a year]) /
(Number of 15-44 year old women).

The General Fertility Rate denominator is relevant to giving
birth, i.e. fertile women.

The General Fertility Rate requires the number of 15-44 year old
women to be known which is difficult to ascertain in some
parts of the world.

145
Q

What substrates can be converted to glucose in the liver

A 
Galactose.  
Glycerol.  
Fructose.  
Pyruvate.  
Lactate.  
Glucogenic amino acids.
146
Q

What is the function of the mucociliary escalator

A

Waft/move mucus up airway via cilia to throat, in order to be swallowed
Works as a barrier to infection

Mock exam Qs (2 decks)

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