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MD2002 > ESA preparation questions > Flashcards

ESA preparation questions Flashcards

1
Q

What is necrosis?
(cell death)

A

Death of cells or tissues due to bioenergetic failure or loss of plasma membrane integrity

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2
Q

Uses of apoptosis

A

-Embriology- to formlumen of tubes
-Response to growth signals: menstruation
-Inflammation: killing neutrophils that have reached their life span.
-Tumour prevention
-Immune system- T cells releasing perforin to activate apoptosis of virally infected cells.
-Autoimmune disease: immune cells killing body’s cells.
-HIV-AIDS: destruction of CD4 cells

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3
Q

Differences between Intrinsic(I) and Extrinsic (E) ways of triggering apoptosis.

A

Extrinsic activated by interaction of external triggers and receptors like cytokines while Intrinsic activated due to DNA, nucleus or mitochondria damage.

Intrinsic ,apoptosome is formed by leaked Cyt c and Apaf-1 which directly activates caspase, while Extrinsic involves triggering the caspase cascade from the primary messenger.

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4
Q

What occurs in a lymphoma

A

Mutation in p53 gene in a B cell causing them to secrete Bcl2 instead of antibodies. Increase concentration of Bcl2 means apoptosis isn’t triggered, so cell can’t die. Accumulation of these cells cause a cancerous mass: lymphoma

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5
Q

Treatments for problems in apoptosis control

A

-Anti-Bcl2 for lymphoma
-Drugs that target IAP in cancer, so caspase can fragment the cell.
-Drugs that target caspase-3 in Alzheimer type dementia

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6
Q

Functions of muscle

A

-Body movement
-Body posture- contraction and relaxing of skeletal muscles
-Support and protection
-Sphincter control
-Movement along GI tract
-Regulation of blood flow- smooth muscle in blood vessels
-Temperature regulation- skeletal(shivering) and smooth m.(hair standing)

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7
Q

Characteristic of muscles

A

-Extensibility: extends
-Excitability: response to stimuli
-Contractility: shortens
-Elasticity: recoil/ resting after stretching

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8
Q

Common features of muscles

A

-They have actin and myosin
-Use aerobic oxidative and anaerobic glycolytic respiration
-Need calcium ions
-Can be stimulated

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9
Q

Explain muscle development

A

-Embryonic mesoderm cells-myoblasts, proliferate.
-Myoblasts fuse together to form myotube
-Myotube matures into muscle fibre

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10
Q

Characteristics of skeletal muscle

A

-100 to 600 nm length
-Multinucleated
-Attached to skeleton by tendons#
-Has striations and sarcomere as contractile units

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11
Q

Characteristic of cardiac muscle

A
  • Cardiomyocytes: 100 nm length
    -Slightly striated
    -25-35% of cell volume is mitochondria
    -Uses aerobic respiration
    -Myogenic
    -Controlled by ANS
    -Branched cells
    -Intercalated disks of gap junctions and desmosomes
    -Uni/binucleated
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12
Q

Characteristic of smooth muscle

A

-100 to 200 nm
-uninucleate and unstriated
-Contraction triggered by ANS, stretch, hormones
-Gap junctions(connects electrically) and Focal adhesions( connects structurally)

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13
Q

Characteristic of gap junctions

A

-Made up of 6 connexons
-Site of low electrical resistance
-Electrically links cardiomyocytes and smooth muscle cells by ion diffusion

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14
Q

Define latent period

A

Time from peak of action potential to onset of contraction of muscle fibre. It is needed for action potential to be delivered deep into muscle fibre.

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15
Q

Examples of Ca 2+ channel blocking drugs.

A

-Nifedipine: blocks DHPR, used to treat hypertension, migraine and atherosclerosis.

-Dantrolene: blocks RYR, used to treat malignant hyperthermia. It is a spasmolytic drug acting as a skeletal muscle relaxant.

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16
Q

Describe Malignant Hyperthermia

A

-Mutation in type 1 RYR that arises in response to general anaesthetics and depolarising muscle relaxants, which is only discovered.
-Symptoms: rigidity, fever, high HR and acidosis.

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17
Q

Describe Skeletal and Cardiac muscle relaxation

A

SERCA- Pumps 2 Ca2+ for every ATP molecule. It gets activated when there is high conc. of Ca 2+

Calsequestrin-stores Ca 2+ at high concentrations and releases at lows. Binds to 43 Ca 2+ per Calsequestrin molecule.

Ca2+/Na+ exchanger(cardiac M.) - For every 1 Calcium out, 3 Sodium in. So Na+/K+ pump to even the ion conc.

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18
Q

Contraction of cardiac muscle

A

Circ-Calcium Induced Calcium Release
-Type 2 RYR used
-25% of calcium use DHPR, 75% use Circ.
For CIRC, Ca 2+ binds to RYR-2 triggering it to open by ligand gating

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19
Q

Explain rigor mortis

A

Muscular stiffness that last from 4h to 50h after death. Explanation:
-After death Ca2+ leak out of SR and triggers actin-myosin cross bridges.

-Because of low ATP or lack ATP the cross bridges can’t be broken meaning the actin and myosin stay bound for long time-muscle stiffness
- Proteolytic enzymes breakdown actin and myosin after 50h.

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20
Q

Characteristics of fast glycolytic vs slow oxidative fibres

A

Slow oxidative: High number mitochondria, high blood supply and high myoglobin.

Fast glycolytic : high number of metabolic stores( creatine phosphate, glycogen) and larger in size

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21
Q

Motor units: definition and description

A

Single motor unit that innervates many muscle fibres.

Small muscles: more nerve fibres for a few muscle fibres.
Large muscles: less nerve fibres for hundreds of muscle fibres.

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22
Q

Characteristics of small and large motor units

A

Motor units are recruited from small to large. The greater the number of motor units recruited, the stronger the force of muscle contraction.

Small motor units: more excitable, conduct action potential slowly-Type I

Large motor units: less excitable, conduct action potential more rapidly. Type II

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23
Q

Characteristics and examples of Multi-unit smooth muscle

A

-Separate fibres with their own nerve endings.
-Independent contraction
Example: ciliary muscles, vas deferens and piloerector muscles.

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24
Q

Unitary/single-unit smooth muscle

A

-Sheets of electrically coupled cells
-Contract in unison
-Connected electrically by gap junctions
-Examples: Git, blood vessels, uterus, bile ducts

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25
Q

Structure of Smooth muscle

A

-Dense bodies: act as Z discs and anchors Actin. Consists of alpha actinin, desmin and vimentin.

-SR: less developed, associated with sarcolemma.

-Caveolae: remnants of T tubule, forms pouch like I foldings in sarcolemma. Contains loads of Ca 2+ channels.

-Gap junctions and focal adhesions

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26
Q

Mechanisms for ECC in smooth muscle

A

Voltage-gated L type Ca 2+ channel- allows CICR thanks to RYR
Receptor operated calcium channel
Store operated calcium channels

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27
Q

Myosin activation

A

Calmodulin+ Ca ion+ MLCK= activated calmodulin-complex

The complex phosphorylates the 2 myosin heads

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28
Q

Relaxation

A

When Ca2+ too low, some of it dissociates from calmodulin dissociating the calmodulin-MLCK complex.

Myosin phosphatase dephosphorylates the phosphorylated myosin heads breaking the cross bridges

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29
Q

Regulators of Smooth muscle contraction

A

-Stretch
-Hormones
-Components in ECF
-Electrical activity from pacemaker cells

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30
Q

Define catabolism

A

Degradation of molecules to release energy

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31
Q

Define anabolism

A

Synthesis of molecules to store energy

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32
Q

Which steps are involved in Investment, cleavage and energy harvest?

A

Investment- Step 1 and 3

Cleavage- Step 4

Energy harvest- Step 7 and 10

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33
Q

What chromosome does each subunit of lactate dehydrogenase come from

A

Subunit M- LDHA- chromosome 11

Subunit H= LDHB- chromosome 12

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34
Q

Describe the subunit composition of the 5 isozymes of lactate dehydrogenase

A

LDH1-4 M ( high in liver and muscle disease)
LDH2- 3M 1H
LDH3- 2M 2H
LDH4- 1M 3H
LDH5- 5H( high in myocardial infarction)

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35
Q

What are the inhibitors of the key enzymes in glycolysis?

A

Key enzymes: hexokinase, PFK and pyruvate kinase

Hexokinase inhibitor- allosteric inhibition by Glucose-6-phosphate

PFK- allosteric inhibition by ATP, activation by AMP

Pyruvate kinase- inhibition by ATP and alanine, activation by F1,6-BP

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36
Q

Contents of mitochondria

A

Outer membrane: permeable to small molecules and ions
Inner membrane: complexes of electron transport chain and ATP synthase.
Matrix: Citric acid enzymes, pyruvate dehydrogenase, fatty acid oxidation enzymes, amino acid oxidation enzymes.

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37
Q

Name the complexes of respiratory chain and their function

A

Complex I NADH-Q reductase: oxidises NADH and reduces Q
Complex II Succinate-Q reductase: oxidises FADH2, reduces Q
Complex III Q-Cyt C oxireductase: oxidises Q, reduces Cyt C
Complex IV Cyt C oxidase: oxidises Cyt C and reduces O2 into H20.

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38
Q

Explain respiratory chain inhibitors

A

CO and cyanide inhibit Complex IV
Pesticides inhibit complex II and III

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39
Q

How much energy generated per 1 mol of glucose?
How much is trapped in ATP bonds

A

-680 kcal/mol glucose
-280 kcal trapped in ATP
Rest released as heat.

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40
Q

Aim of Absorptive state

A

To store nutrients in mobilizable form

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41
Q

Aim of postabsorbtive/fasting state

A

To provide metabolites for respiration and ATP synthesis

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42
Q

Blood glucose values in mmol/L and their interpretation

A

-Less than 3: Severe hypoglacaemia
-Less than 3.9: Hypoglacaemia
-Around 7 or a bit less: Normal
-7 to 10: High blood sugar
-More than 10: Severe hyperglacaemia

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43
Q

Define gluconeogenesis.

What processes are involved in it?

Name the sources for gluconeogenesis

A
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44
Q

-What endocrine hormones stimulate glycogenolysis?
-What enzymes are required and what is their function?

A
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45
Q

If 1g of glycogen produces 250 kcal, how much kcal would 1 g of triglycerides produce and why?

A

1500 kcal
Because the same weight of triglycerides produces 6 times as much energy as glycogen.

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46
Q

What are the destinations of the products of lipolysis

A

Products: glycerol and fatty acid chains
GLYCEROL
-Converted into glyceraldehyde-3 phophate. This can become pyruvate and then acetyl CoA. Goes into Citric Acid Cycle(CAC)

FATTY ACID
Via beta oxidation they become acetyl coA. CAC
In the process, NADH and FADH2 is also produced which can end in the electron transport chain, generating ATP.

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47
Q

What happens when the glucose is low?

Name the ketone bodies

A

At low glucose, oxaloacetate converted into pyruvate. (limiting reactant of CAC)
So acetyl Coa becomes ketone bodies via ketogenesis.

Ketone bodies: acetone, acetoacetate and 3-hydroxybutyrate.

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48
Q

Why does a diabetic patient have a fruity smell on breath?

A

In diabetes, more acetoacetate produced than used up, so build up of ketone bodies in the bloodstream leads to the fruity smell of acetone in breath

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49
Q

What does muscle use as fuel when active or resting?

Why doesn’t muscle glycogen enter the bloodstream?

A

Mostly fatty acids but also glucose and ketone bodies.

Glycogen gets converted into G-6-P and then enters glycolysis. (it has to be in the G-1-P format to be released into bloodstream)

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50
Q

What structures are on the same coronal plane as ASIS

A

Pubic tubercle and pubic crest

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51
Q

Name the types of joints present in the pelvis and the ligaments that support them

A

-Pubic symphysis: secondary cartilaginous. Supported by arcuate ligament and superior ligament.
-Anterior sacro-iliac joint: synovial joint. Supported by anterior sacro-iliac ligaments
-Posterior sacro-iliac joint: fibrous joint.
Supported by posterior sacro-iliac ligaments and interosseous ligaments.

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52
Q

Name the gateways for the pelvic girdle and what bundles pass through them

A

-Greater sciatic foramen: sciatic nerve and gluteal neurovascular bundle

-Lesser sciatic foramen: internal pudendal neurov. bundle

-Obturator foramen: obturator neurov. bundle

-Gap below inguinal ligament: femoral neurov. bundle

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53
Q

Function of the hip joint ligaments

A

-Prevent hyper-extension
-Save energy when standing
-Stabilise hip joint.

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54
Q

Names and functions of the capsular ligaments

A

Iliofemoral :prevents hyper-extension at hip joint
Ischiofemoral: prevents hyper-extension
Pubofemoral: prevents hyper-abduction at hip joint

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55
Q

Characteristics of the knee joint

A

-Articular surfaces have shapes complementary to each other.

-Muscles supporting it run either side of the knee joint to avoid interfering with the movement.
-They have collateral ligaments

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56
Q

What ligaments or tendons reinforce the knee joint from the outside?

A

-Anteriorly: patellar ligament and quad tendon
-Laterally: Iliotibial tract, lateral retinaculum
-Medially: medial retinaculum
-Posteriorly: Oblique popliteal and arcuate popliteal ligaments.

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57
Q

Functions of the menisci

A

-Absorb shock
-Help in locking the knees
-Propiception
-Decreased friction
-Increase congruence of articular surface

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58
Q

Angles in the lower limb

A

Q angle: Angle between the anatomical axis of the femur and the tibia shaft.

Collodiaphysial angle: Angle between short axis of the neck and head of the femur

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59
Q

Collodiaphysial angles and diagnosis

A

Coxa vara: Less than 120 degrees
Normal: 120-135 degrees
Coxa valga: More than 135 degrees.

Wider in children

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60
Q

Name the ligaments in the sole of the foot and their function

A

They both assist in inversion and eversion of the foot.
-Long plantar ligament
-Spring ligament- supports head of talus and most of the body weight

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61
Q

Name all the muscles in the gluteal region and their function

A

-Gluteus maximus- Extends, abducts,adducts, and laterally rotates at hip junction. Locks the knee

-Gluteus medius: abduction and medial rotation

-Gluteus minimus: abduction and medial rotation.

-Lateral rotators: laterally rotate femur to keep foot facing forwards when walking

-Tensor fascia lata: Locks the knee, tenses iliotibial tract, extension at hip joint.

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62
Q

What is special about the gluteus maximus?

A

Gluteus maximus has upper fibers that insert into the iliotibial tract which are in charge of abduction at hip joint, while the lower fibers which attach to the gluteal tuberosity which adducts.

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63
Q

Between which structures is the sciatic nerve located.

Why is it important to know this?

A

Between greater trochanter and the ischial tuberosity. And between biceps femoris and between biceps femoris and adductor magnus.

Intramuscular injections in the butt, to avoid damaging the nerve.

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64
Q

Why is the adductor magnus special?

A

It is partially a hamstring muscle and an adductor muscle

Hamstring part: originates from ischial tuberosity and is supplied by tibial nerve. Involves in extending the thigh and medially rotating thigh at hip joint. Inserts into linea aspera

Adductor part attaches to medial supracondyle and originates from inferior pubic ramus. Supplied by obturator nerve and laterally rotates thigh at hip and adducts.

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65
Q

What nerve and spinal segments are tested in
the knee tendon reflex?

A

Femoral nerve
Segments L3 and L4

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66
Q

Borders of the femoral triangle

A

Superiorly: inguinal ligament
Medially: Adductor longus
Laterally: sartorius
Floor: iliacus and pectineus
Roof: fascia lata

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67
Q

Describe femoral hernias

A

Part of intestine go through the femoral canal causing a visceral protrusion. If left untreated it can undergo necrosis

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68
Q

Boundaries of adductor canal

A

Sartorius, vastus medialis and adductor magnus+longus

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69
Q

Name the layers of plantar muscles and the muscles present in them.

A

Layer 1: Flexor Digitorum Brevis, Abductor hallucis and Abductor digiti minimi.

Layer 2: Quadratus plantae and lumbricals

Layer 3: Adductor digiti minimi, opponens digiti minimi, adductor hallucis
oblique/transverse, Flexor Hallucis brevis

Layer4: Dorsal and plantar interossei

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70
Q

Action of lumbricals in the sole of the foot

A

-Flex metatarsophalangeal joints
-Extend interphalangeal joint
-Adduct digits towards hallux

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71
Q

What ligaments support the medial longitudinal arch?

A

-Plantar aponeurosis
-Tibialis posterior, anterior and FHL tendon.
-Spring ligament
-Deltoid ligament

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72
Q

What ligaments support the lateral longitudinal arch?

A

-Long ligament
-Short ligament
-Fibularis longus and FDL tendon
-Plantar aponeurosis

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73
Q

Factors affecting pes planus presentation

A

-Obesity
-Age
-Rheumatoid arthritis
-Diabetes

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74
Q

Name the muscles that lock the knees

A

-Tensor fascia lata
-Glut maximus
-Vastus medialis

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75
Q

In what direction would you fall, if you fall asleep while standing?

A

You would fall forwards because the line of gravity is anterior to the ankle and knee joint and posterior to hip joint.

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76
Q

Name the 8 phases of Gait

A

-Heel strike
-Loading response
-Midstance
-Terminal stance/heel-off
-Pre-swing/toe-off
-Initial swing
-Mid-swing
-Terminal swing

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77
Q

What happens during heel strike?

A

-Hip flexed
-Knee semiflexed
-Foot dorsiflexed
-Arch maintained for shock absorption and weight distribution

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78
Q

What happens during loading reponse?

A

-Foot on the ground
-Hip semiflexed
-Knee semiflexed
-Tightening of ligaments to bear weight
If ground is uneven, inversion and eversion of foot happens.

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79
Q

What happens during midstance

A

Right hip bears all the weight
-R Hip extended
-R Knee extended
-

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80
Q

What happens during terminal stance/heel-off

A

Heel is off the floor
-R Hip is extended
-R Knee is semiflexed
-R foot and toes are plantarflexed
-Plantar arch heightened by: FDL,FHL, Tibialis A and P, FL
-Momentum created by drawing foot forward

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81
Q

What happens during pre-swing/toe-off

A

-R hip extended
-R knee flexed
-Right ankle plantarflexed by: Gatrocn. and soleus.
-Right toes plantarflexed by FDB,FHB and quadratus plantae.

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82
Q

What happens during initial/mid-swing

A

-R hip flexes
-R knee flexed
-R ankle and toes dorsiflexed
-

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83
Q

What happens during terminal swing?

A

-L hip medially rotated
-R hip flexion and lateral rotation

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84
Q

What happens during weight bearing

A

-One limb bears all the weight while the other is off the ground.
-R leg of the ground
-L hip abduction to maintain pelvis by: glut. medius and min.
-L knee extension
-L plantar arches maintained

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85
Q

What muscular movements help maintain balance when walking?

A

Coordination of dorsiflexion, plantarflexion, eversion and inversion

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86
Q

How does momentum help in gait?

A

-It helps propel body forward
-Causes dorsiflexion of ankle and toes.

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87
Q

Name the branches of the internal iliac artery

A

-Superior gluteal artery
-Inferior gluteal artery
-Internal pudendal artery
-Obturator artery

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88
Q

Name the branches of the femoral artery

A

-Superficial circumflex iliac artery
-Superficial epigastric artery
-External pudendal artery
-Profunda femoris

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89
Q

Branches of profunda femoris

A

-Lateral circumflex femoral artery
-Medial circumflex femoral artery
-4 perforators.

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90
Q

What arteries form the cruciate anastomoses to the hip joint

A

-Medial/lateral circumflex femoral artery
-Inferior gluteal artery
-1st perforator

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91
Q

What arteries form part of the trochanteric anastomoses?

A

-Superior/inferior gluteal arteries
-Lateral/medial circumflex femoral arteries

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92
Q

Explain the possible treatments for subcapital and intertrochanteric fractures

A

Subcapital fracture- cuts off blood supply to the head of the femur which could lead to necrosis. Hip replacement needed.

-Intertrochanteric fracture: doesn’t fully cut off the blood supply, can be repaired by placing a screw.

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93
Q

Name the branches of the popliteal artery

A

-Superior medial genicular artery
-Superior lateral genicular artery
-Inferior medial genicular artery
-Inferior lateral genicular artery
-Middle genicular artery

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94
Q

What arteries originate from the posterior tibial artery

A

-Common fibular artery
-Nutrient arteries
-Lateral and medial plantar arteries

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95
Q

What structures do superficial inguinal lymph nodes receive lymph from?

A

-anterior Lower abdominal wall
-Perineum
-Skin of iliac crest
-Gluteal region
-superficial Lower limb

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96
Q

What structures do deep inguinal lymph nodes receive lymph from?

A

-Superficial lymph nodes
-External genitalia
-Lower limb

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97
Q

Order in which main lymph nodes drain into each other from small to main

A

-External iliac nodes
-Common iliac
-Lumbar lymph nodes
-Cisterna chyli
-Thoracic duct
-Pirogov’s venous angle
-Vein system(between left subclavian and internal jugular vein)

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98
Q

Branches of the femoral nerve

A

-Saphenous nerve
-Anterior cutaneous femoral nerve

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99
Q

What are the most common cancers?

A

-Breast
-Prostate
-Lung
-Bowel

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100
Q

-Constituents of tumour

-What makes up the stroma?

A

Neoplastic cells surrounded by stroma-supporting cells
Connective tissue, fibroblasts, blood vessels, immune cells

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101
Q

Name the 6 hallmarks of cancer

A

-Self-suficient in growth signals
-Insensitive to stop growing
-Tissue invasion, metastasis
-Limitless replicative potential
-Evasion of apoptosis
-Sustained angiogeneis

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102
Q

Phases of cancer development

A

-Initiation+ promotion
-Growth
-Diagnosis
-Outcome: death, relapse, metastasis, cure

Prediction can only be done between diagnosis and outcome

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103
Q

Characteristics of benign tumour

A

-Well circumscribed
-No necrosis
-No invasion
-No metastasis
-Slow growth

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104
Q

Characteristics of malignant tumour

A

-Poorly circumscribed
-Necrosis
-Tissue Invasion
-Metastasis
-Rapid growth

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105
Q

Clinical effects of a benign tumour

A

-Occupies space: obstruction, epilepsy, abnormalities
-Haemorrhage in pulmonary and GI
-Affects hormone production if present in endocrine glands

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106
Q

Where does prostate, lung, breast and ovary cancer metastasise into?

A

Prostate c.- bone
Lung c.- brain and adrenals
Breast c.- bone, liver, brain and lung
Ovary c.- peritoneal cavity

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107
Q

Name and explain the 6 different shapes of tumours

A

Sessile-grow locally within environment
Pedunculated polyp-on external surface
Fungating- begins to invade tissue
Ulcerative- caused by necrosis
Papillary
Annular- around lumens

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108
Q

Describe the macroscopic features of benign tumours

A

-Well circumscribed
-Intact surface
-Exophytic growth
-Homogenous cut-surface

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109
Q

Describe the macroscopic features of malignant tumours

A

-Poorly circumscribed
-Ulcerated surface
-Endophytic growth
-Heterogenous-cut surface
-Grows into tissue
-Begins to be surrounded by blood vessels

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110
Q

Describe the microscopic features of benign tumours

A

-Normal mitotic figures
-Well differentiated
-Resemble tissue of origin
-Little nuclear pleomorphism

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111
Q

Describe the microscopic features of malignant tumours

A

-Variable resemblance
-Variable differentiation
-Lot of nuclear pleomorphism or anaplastic
-Abnormal mitotic figures

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112
Q

What are the cytological features of malignant tumours

A

-High ratio of nucleus to cytoplasm
-Nuclear hyperchromasia
-Nuclear pleomorphism
-Abnormal chromatin structure
-Abnormal mitotic figures

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113
Q

-Describe differentiation of tumour cells
-Describe grading

A

-Differentiation: resemblance to tissue of origin
-Grading: degree of differentiation

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114
Q

Explain the grading system

A

Grade I: well differentiated
Grade II: moderately differentiated
Grade III: poorly differentiated
Grade IV: nearly anaplastic

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115
Q

Explain the TNM staging

A

T-Tumour size: T1, T2, T3, T4
N- Degree of Lymph node involvement: N0, N1,N2
M- Degree of metastasis: M0, M1- to lungs, M2- to liver and lungs

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116
Q

Explain the Duke’s staging system

A

Used for bowel cancers
A-cancer confined within bowel wall
B-Cancer grows through bowel wall but withoout lymphatic involvement
C-Lymphatic involvement
D- Spreads to other tissues

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117
Q

What nomenclature rule does epithelial and mesenchymal benign tumours follow?

A

Epithelial benign: papilloma or adenoma
Mesenchymal benign: cell of origin+ -oma

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118
Q

How would you call a benign and a malignant tumour in the squamous tissue?

A

Benign- squamous cell papilloma
Malignant- squamous cell carcinoma

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119
Q

How would you name a benign and malignant tumour in the adipose tissue?

A

Benign-lipoma
Malignant-liposarcoma

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120
Q

List the 6 miscellaneous tumours

A

-Myeloma- melanocytes
-Blastoma- embryonic cells
-Teratoma
-Lymphoma
-Cysts
-Carcinoid tumours

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121
Q

Characteristics of teratoma

A

-Contains ectoderm, mesoderm and endoderm
-Germ cell origin
-Ovarian tertoma- benign
-Testicular teratoma- malignant

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122
Q

Types of carcinogens

A
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123
Q

State and explain the stages of chemical carcinogenesis.

A
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124
Q

Describe the latent period of cancer

A
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125
Q

Explain the scrotal cancer and chimney sweeps incident

A
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126
Q

Explain the bladder cancer and dye industry incident

A
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127
Q

Mechanism of action of 2-napthylamine

A
  1. 2-NTA converted into 2-aminophenol(carcinogen) in the liver
  2. 2-aminophenol detoxified into glucoronide
  3. Glucoronide excreted by the kidneys and goes to bladder
  4. Urothelial cells in bladder express beta-glucoronidase which converts glucoronide into 0-aminophenol (carcinogen)
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128
Q

What is asbestosis?
How does it occur?

A
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129
Q

How does smoking increase the risk of cancer?

A
  1. Tobacco contains tar which contains carcinogenic 3,4-benzopyrene.
  2. Benzopyrene converted into benzopyrene diol epoxide by Aryl Hydrocarbon Hydroxylase (AHH)
  3. AHH is upregulated in smokers
  4. More BDE produced which binds to DNA forming damaging products
  5. It also causes guanine mutations in K-Ras and p53 genes.
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130
Q

What is transitional cell carcinoma

A

-Masses of Cancer in the uroethilial cells in the bladder
-It is multifocal- all tumours arise from the same origin

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131
Q

Detoxification of carcinogens

A

-Carcinogens detoxified by Glutathione S Transferase (GSTM-1)
-GSTM-1 is polymorphic so it has a null GSTM-1 allele which doesn’t do anything.
-People with homozygotic null GSTM-1 have increased risk of cancer.

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132
Q

Name carcinogens in diet

A

-Fertilisers in drinking water
-Food additives
-Nitrosamines from bacteria: they can cause liver and GI cancer
-

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133
Q

Explain aflatoxicosis

A

-Poisoning of the liver when ingesting aflatoxins.
-Aflatoxicosis+ Hep B= Liver cancer
-Produced by a fungi in the skin of shells of peanuts
-Causes mutation of p53 gene

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134
Q

Why are large intestine tumours more frequent than small intestine tumours?

A

-Large intestine crypts express lot of BCl2
-Bcl2 prevents apoptosis leading to accumulation of colon cells mutations
-Small intestine crypts don’t express Bcl2 so the risk of cancer is much lower

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135
Q

What conditions does UV light increase the risk of?

A

-Xeroderma pigmentosum
-Freckling of skin’
-Basal cell carcinoma
-Squamous cell carcinoma
-Melanoma

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136
Q

Properties of malignant cells

A

-Disordered proliferation
-Disordered apoptosis
-Angiogenesis
-Disordered differentiation
-Invasion and metastasis

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137
Q

Describe the process of cell malignancy

A

-Dysplasia: cells escape basal layer and start to proliferate
-Carcinoma in situ: Benign tumour that is still localised
-Invasion: Becomes malignant tumour
-Metastasis: Tumour spreads to other tissues

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138
Q

Define oncogenes

What type of mutation is an oncogene mutation?

A

Oncogenes: genes that when mutated can drive neoplastic behaviour and trigger excess proliferation despites negative signals.

Dominant mutation: one copy of mutated oncogene can lead to excess proliferation

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139
Q

Triggers of proto-oncogene activation into oncogenes and examples

A

-Mutations in coding sequence. It can cause the gene to be in ON position all the time, creating hyperactive proteins. E.g: Ras oncogene in bowel cancer

-Gene amplification. Many copies of gene due to chromosoma; abnormality Example HER-2 gene in breast cancer

-Chromosomal abnormalities. Overproduction of protein due to problems in regulatory DNA sequence. Fusion of genes can lead to hyperactive fusion protein. E.g Philadelphia chromosome and the bcr-abl fusion gene.

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140
Q

Describe the types of oncogene and an example of each.

A

+Growth factor: Increase in GF. sis in fibrosarcoma

+Growth factor receptor: Increase in GFR.- HER2 in breast cancer.

+ Signal transducer: interferes with intercellular signalling.-ras in bowel cancer.

+ Transcription factors: stimulates the cell cycle dependent transcription.-myc cause Burkitt’s lymphoma

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141
Q

Define tumour supressor genes
What types of mutation affects them?

A

Tumour suppressor genes: genes that inhibit tumour formation by excessive abnormal proliferation.

Recessive mutation: 2 copies needed to produce loss of function to create negative signals to stop proliferation

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142
Q

Explain Knudson’s 2-hit hypothesis

A
  1. Inherited retinoblastoma
    -Person inherits absence of 1 RB1 gene
    -Later on, mutation in the RB1 gene leads to loss
    -Causes bilateral retinoblastoma: both eyes affected.
  2. Sporadic retinoblastoma
    -Person has both RB1 genes
    -Due to a mutation, both genes are lost
    -Causes unilateral retinoblastoma: only one eye affected.
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143
Q

Mechanism of action of RB

A

In non-proliferating cells, RB binds to the E2F gene, inhibiting expression to advance into S phase.

If mutation occurs in RB, uncontrolled cell division will occur.

144
Q

Explain the relation between colon cancer and the apc gene

A

-apc gene keeps level of transcription required for proliferation low
-Mutation in apc, means uncontrolled proliferation leading to 80% of colon cancers.

145
Q

Name the 2 types of tumour suppressor genes

A

Gatekeeper and caretaker

146
Q

Describe the characteristics of gatekeeper ts genes

A
147
Q

Describe the characteristics of caretaker ts genes

A

-They maintain integrity of genome by DNA repair

-Involved in nucleotide excision, mismatch repair, DNA double strand break repair

148
Q

What does p53 respond to?

A

-UV radiation
-Ionizing radiation
-hypoxia
-oncogene signalling
-blockage of transcription
-Lack of nucleotides

149
Q

p53 gene stimulates transcription factors. What do these TF do?

A

-Block of angiogenesis
-DNA repair
-Trigger apoptosis
-Cell cycle arrest

150
Q

How does angiogenesis occur in cancer ?

A

-Cancer cells secrete VEGF
-VEGF activates cascade of reaction in endothelial cells
-Secretion of proteins that stimulate new endothelial cells

151
Q

Characteristics of a tumour vascular network

A

-Unstable
-Abnormal function
-Abnormal structure
-Inappropiate location
-Very permeable

152
Q

Steps of invasion+metastasis

A
  1. Cells grow in epithelium forming benign tumour
  2. Tumour cells detach from each other and from the basement membrane
  3. They secrete proteolytic enzymes that break down basement membrane and enter bloodstream
  4. Tumour cell adheres to wall of blood vessel in liver
  5. They enter liver forming micrometastasis
  6. Full metastasis in liver
153
Q

Name examples of diseases caused by mutations in caretaker genes

A

-Xeroderma pigmentosum: failure in recognising DNA damage so no mismatch repair done by caretaker genes.

-Hereditary non-polyposis colon cancer: problem with DNA mismatch

-Inherited breast and ovarian cancer: BRACA 1 gene

154
Q

Name the symptoms of anaemia

A
155
Q

Name the signs of anaemia

A

-Tachychardia
-oedema
-Pale skin
-tachypnea

156
Q

Body adaptation to anaemia

A
157
Q

How can we classify anaemia

A
158
Q

Classification by MCV and examples

A

Microcytic(60-80)
Normocytic(80-100)
Macrocytic (100-120)
Hypochromic: low colouration

159
Q

Characteristics and causes of Iron def. anaemia

A

CHARACTERISTICS:
-low ferritin
-low transferrin,
-normal blood count

CAUSES:
-Low Fe in diet
-Malabsorption
-Blood loss
-Gi bleeding
-Inc. Fe need: pregnancy, growth

160
Q

Clinical signs of iron def. anaemia

A

-Pale skin
-Pica
-Hair loss
-Tachycardia
-Abd pain
-Glossitis

161
Q

Treatment for iron deficiency

A

ORAL: ferrous sulphate/fumarate/gluconate-inc. Hb by 1-g/L/wk
INTRAMUSCULAR: Too painful
IV-ferric carboxymaltose (2 doses) for 15-30 min. Iron dextran for 4-6hr
-Side effect: hypersensitivity, flu-like

162
Q

Characteristics of B12 def.

A

-High LDH
-High bilirubin
-Pancytopenia
-Peripheral neuropathy

163
Q

Causes of B12 def.

A

-Pregnancy
-Vegan
-Pernicious anaemia
-Side effect of metmorfin and oral contraceptives

164
Q

Treatment for B12 Def.

A

-Hydroxocobalamin 1mg: 5dose alternate days, then 3ds/mth
-Cyanocobalamin-given to vegans

165
Q

Causes of folate deficiency

A

-Poor intake
-Increase use: pregnancy, growth,haemolysis
-Malabsorption
-Side effects of antiepileptics

166
Q

Treatment of folate deficiency

A

-Folic acid 5mg/day
-Take before pregnancy so baby don’t have neural tube defects

167
Q

Explain anaemia of blood loss

A

-After blood loss, Hb is normal, but after fluid replacement, Hb low
-For 500mL lost, 10-15g/L of Hb lost
-High reticulocyte count to replace lost RBC
-Treatment: -Blood transfusion might be needed

168
Q

Explain anaemia of chonic disease( reasons, causes, treatment)

A

-Linked to chr. inflamm. disease
-Poor Fe transfer to RBCs because of high hepcidin/cytokines
-Increased inflamm. markers like CRP
-TREATMENT: treat chronic condition first

169
Q

Explain anaemia of renal failure

A

-Low creatinine leads to less Hb bc of less erythropoietin
CAUSES:
-low erythropoietin
-Inflammatory response
-Blood loss during dialysis

TREATMENT: subcutaneous erythropoietin

170
Q

Define haemolysis

A

-Increased RBC destruction
-Caused by issues with RBC enzyme, membrane and globin chains

171
Q

Causes of haemolysis

A

+Congenital spherocytosis: autosomal dominant, defect in spectrum, Causes spherical cells with low life span

+Autoimmune haemolysis: abs attack RBC antigens. Phagocytosis by spleen macrophages.
-Treatment: steroids, rituximab, splenoctomy

+Prosthetic heart valve

+DIC: causes RBC breakdown by fibrin

+RBC enzyme deficiency: def. in G6PD or pyruvate kinase

172
Q

Explain anaemia of abnormal Hb

A

Haemoglobinopathy: sickle cell disease
-causes Chronic anaemia, bone/liver/lung/brain crisis
TREATMENT: hydroxycarbamide, stem cell transplant, supportive care

173
Q

Explain thalassaemia

A

-Cause: imbalance of globin chain production
Beta thalassaemia: decrease in HbF postbirth leads to progressive anaemia

-TREATMENT: transfusion, Stem Cell transplant

174
Q

Explain thalassaemia

A

-Cause: imbalance of globin chain production
Beta thalassaemia: decrease in HbF postbirth leads to progressive anaemia

-TREATMENT: transfusion, Stem Cell transplant, antenatal screening

175
Q

Explain anaemia of marrow infiltration

A

-Haematological malignancies: sample marrow to confirm diagnosis. Other cancers can metastasise into bone
-TREATMENT: chemo and immunotherapy

176
Q

Marrow failures

A

-Myelodysplastic disorders
-Aplastic anaemia

177
Q

Explain myelodysplastic disorders and the treatment

A

-Low Hb + Low RBC can progress to acute leukaemia
-Treatment: Chemo, supportive care, Stem cell transplant

178
Q

Explain aplastic anaemia

A

-E.g Pancytopenia: low blood cells in blood.
-Consequence of chemo
Treatment: supportive care, stem cell transplant. anti-thymocyte globulin.

179
Q

Describe lymphoma

A

-B cell cancer, causing production of monoclonal abs
-Presentation: chance finding, renal failure, bone fracture/pain, hypercalcaemia

180
Q

What conditions does obesity increase the risk of?

A

-Cardiovascular disease
-Cancer
-Low grade systemic inflammation
-Metabolic syndrome
-Osteoarthritis
-Type 2 diabetes

181
Q

Name and explain the appetite regulators

A

-Brain: hypothalamus and pituitary gland
-Hormone: adrenaline, cortisol, insulin, glucagon, thyrosine
-Neural signs: vagal nerve and stretch receptors in stomach that detect distention of the GI
-Nutrient sensor: high glucose, amino acids, fats inhibit appetite

182
Q

What is leptin?

A

Hormone produced by pituitary gland that inhibits hunger and appetite by binding to neuropeptide Y

183
Q

Describe “glucose sparing”

A

When brain is prioritise for the use of the glucose when glucose conc. is lower, while the rest tissues use other sources of energy

184
Q

List the hyperglacaemic hormones

A

-Glucagon
-Adrenaline
-Cortisol
-Growth hormone
-Thyroid hormones

185
Q

Effects of Growth hormone

A

-increase Amino acid uptake
-Glucose catabolism
-Gluconeogenesis
-Lipolysis
-Fat mobilization

186
Q

Effects of cortisol

A

-Lipolysis
-Fat mobilization
-Gluconeogenesis
-Protein breakdown

187
Q

Effects of testosterone

A

-Stimulates protein synthesis

188
Q

Effects of thyroxine

A

-Glucose uptake
-Protein synthesis
-Fat mobilization
-Lipolysis
-Glucose catabolism

189
Q

Describe the events that happen during the 1st day of prolonged fasting

A

-All body glycogen stores used in 1 day
-Glucose sparing, muscles use fatty acid while brain use glucose
-Triglycerides limited ability to become glucose

190
Q

Describe the events that happen after +3 days of prolonged fasting

A

-Build up ketone bodies
-Brain uses ketone bodies
-Amino acid preserved for gluconeogenesis later

Maintaining protein is VITAL for survival when fasting

191
Q

State the name and function of the 4 cell types in the islets of Langerhans

A

-Alpha cell: glucagon
-Beta cell: Insulin
-Gamma cell: somatostatin
-Pp cell: pancreatic polypeptide

192
Q

Effects on insulin in the body

A

Increase blood glucose by:
-trigger stranslocation of GLUT 2 transporter
-Inc. glucose facilitated diffusion
-Protein synthesis
-Lipogenesis
-Glycogenesis

193
Q

What triggers insulin release?

A

-Parasympathetic NS
-High blood glucose
-Glucose-dependent insulinotropic peptide(GDIP)

194
Q

Effects of glucagon in the body

A

-Glycogenolysis
-Gluconeogenesis
-Lipolysis

195
Q

Effects of adrenaline in the body

A

-Glycogenolysis
-Stimulate glucagon, inhibit insulin
-Trigger use of fatty acid by muscle

196
Q

Characteristics of diabetes mellitus

A

-Chronic metabolic disease caused by insuficient insulin or effects
-Causes chronic hyperglycaemia
-Increases the risk of: Cv disease, neuropathy, vascular damage

197
Q

Describe Type 1 diabetes, causes and treatment

A

-Caused by autoimmune response to beta cells in pancreas. No insulin produced.
-Can be genetic or environmental causes
-TREATMENT: insulin injections

10% of diabetes cases are Type 1

198
Q

Describe Type 2 diabetes, causes and treatment

A
  • tissue insenstivity to insulin
    -CAUSE: Linked to lifestyle and diet and genetics
    -TREATMENT: diet, exercise, metmorfin

90% of diabetes cases are Type 2

199
Q

-Health consequences of diabetes

A

-Glucose in urine
-Dehydration: low H2O reabs. becauSe of excess glucose.- Polyuria and polydipsia
-Tissue injury
-Peripheral neuropathy
-Autonomic nerve disruption-bladder control. CV reflex

200
Q

Consequences of the tissue injury of diabetes

A

-Vascular damage
-Ischaemia
-MI
-Stroke
-Renal failure
-Blindness

201
Q

Metabolic consequences of diabetes

A

-Inc. ketone bodies conc.
-Metabolic acidosis: high ketone bodies, low pH and dehydration-lead to diabetic coma and death
-Increased use of fats: leads to low glycolysis but high gluconeogenesis.

202
Q

Define atherosclerosis

A

Disease in which blood vessel clogged due to an atheroma

203
Q

Define atheroma

A

Fibro-fatty plaque that consists of a intimal fibrous cap that surrounds a lipid-rich core.

204
Q

Factors leading to decrease in death rate of MI/stroke due to atherosclerosis.

A

-Prevention of atherosclerosis
-Prevention of recurrence
-More efficient treatment

205
Q

Risk factors of atherosclerosis

A

-Age
-Sex
-Smoking
-Diabetes: due to vascular damage
-Hypercholesteraemia
-Hypertension

206
Q

Pathogenesis of atherosclerosis

A

-Chronic endothelial injury
-Role of macrophages
-Smooth muscle proliferation
-Role of cholesterol/lipids
-Thrombus fomration
-Fibro-lipid plaque

207
Q

Causes of Chronic Endothelial Injury

A

-Haemodynamic disturbances
-Hypercholesteraemia
-Hypertension
-Smoking
-Toxins
-Viral infection
-Immune reaction

208
Q

Name the adhesion molecules secreted by endothelial cells

A

-VCAM-1
-ICAM-1
-P-selectin
-E-selectin

They increase monocyte adhesion and migarion into tunica intima

209
Q

Components of atheroma

A

-FIBROUS CAP: smooth muscle, macrophages, foam cells, collagen, new blood vessels

-NECROTIC CENTRE: cell debris, cholesterol crystals, calcium, foam cells

210
Q

List the places where atheroma can appear from most common to least common

A

-Abdominal aorta
-Coronary artery
-Popliteal artery
-Descending thoracic aorta
-Carotid artery
-Circle of Willis artery

211
Q

List the complicated lesions that can result from atherosclerosis

A

-Haemorrhage
-Rupture
-Calcification
-Thrombosis
-Aneurysm

212
Q

Explain the primary prevention against atherosclerosis

A

They prevent incidence of atherosclerosis. Includes:
-Stop smoking
-Control hypotension
-Weight loss and red. cal intake
-Reduction in LDL

213
Q

Explain the secondary prevention against atherosclerosis

A

They prevent complications after having atherosclerosis
-Anti-platelet drugs
-Decrease in lipid levels

214
Q

Steps of atheroma formation

A

1.Endothelial dysfunction: Allow leukocyte and monocyte adhesion+ migation into tunics intima

2.Macrophages in tunica intima ingest oxidated LDL becoming foam cells. Foam cells die, and crystallised chol. forms.
-Proteins produced trigger smooth muscle migration from t. media to intima.
-Fatty streak: accumulation of dead foam cells

  1. Collagen & matrix deposits+ sm. caused fatty streak to become fibro-fatty atheroma
    -Atheroma contains lipid debris, collagen and lymphocytes
215
Q

What do drugs target?

A

-Ion channels
-Receptors
-Carrier molecules
-Enzymes

216
Q

State the Law of Mass of Action

A

The rate of a chemical reaction is proportional to the product of the concentration of reactants.

217
Q

Explain how you would do the experiment to prove the Law of Mass of action and calculate constant key

A
  1. Add drug to a solution of receptors
  2. Filter out the bound receptors from the unbound.
  3. Incubate the solution.
  4. Calculate [unbound r.] and [bound r.]

[Drug]+[receptors]=[occupied receptor

218
Q

What is Kd and what does it represent?

A

Concentration of drug required to occupy 50% of the receptors.
-Measure of affinity

219
Q

Define affinity and its formula

A

-Affinity: measure of concentration range over which drug binds to its receptOR. Also measures how strong the bind between drug and receptor is.

pD2=-log 10 ( Kd)
pD2 is the -log10 of the [drug] required to occupy 50% of the receptors.

220
Q

Define the efficacy of a drug

A

-Efficacy: Ability of a drug to generate/initiate response once bound

-When the max. response of a tissue can be obtained when less than 100% of receptors are occupied

221
Q

Define the Receptor Theory and state its formula

A

There is a relationship between magnitude response and concentration of drug.

Response=[occupied receptors]/[total number of receptors]

222
Q

State the formula for Stimulus and Response

A

Stimulus=[occupied receptors]/[total number of receptors]
Response= frequency x stimulus

223
Q

What is the difference between powerful and efficacious drugs?

A

-Powerful drug produce high stimulus upon occupation. Responses summate till they reach maximum.

-Efficacious drug produces max. response when occupying few receptors.

224
Q

What is the effect of partial agonists on full agonists and why is that so?

A

Partial agonist reduce the effects of full antagonist. Because both bind to the same active site so they compete to bind to the receptor.

Partial agonist are less efficacious than full agonists.

225
Q

Describe competitive antagonism

A

Inhibitory compound reversably binds to the same active site than the agonist.

226
Q

What is the effect of competitive antagonism on the dose response curve and why?

A

-Curve shifts to the right, but max. response still reached.

-Because more drug required to create a response as antagonists are now bound to the receptors.
-V max is still reached but at a slower rate

227
Q

What is Ka?

A

Concentration of antagonist that makes it necessary for twice as much agonist to be added, to create the same response than when the antagonist is absent.

228
Q

State Schild’s equation

A

r= ratio by which [D] must be added to overcome [A].

r=([A]/ka)+1

A=antagonist

229
Q

What is pA2 and what does it indicate?

A

pA2= -log10(Ka)
Affinity of antagonist to receptor

230
Q

Characteristics of irreversible competitive antagonism

A

-They dissociate really slowly or not at all
-They bind to active site
-Decreases V max.

231
Q

Action of allosteric modulators

A

-Non-competitive inhibitor
-They bind to the allosteric site
-Conformational change to receptors

232
Q

Describe inverse agonists

A

They can reduce the activity of an active receptor
-They produce a response opposite to the normal one

233
Q

List 4 drug receptor interactions and their examples

A

-Direct control on ion channels: nACh receptors
-Direct control of effector enzymes via phosphorylation: insulin receptor
-Indirect activation via G protein/metabotropic receptors: mACh receptors
-Direct control on DNA transcription- oestrogen receptor

234
Q

What is homeopathy?

A

-Believe that the more you dilute an homeopathic medicine the more potent it is.

235
Q

State the chemical equation for competitive antagonism.

A

[D]+[R]+[A]= [DR]+[AR]

D=drug R= receptor A=Antagonist

236
Q

Structure of lipoproteins

A

-Central core containing TriGlycerides and cholesterol ester
-Hydrophobic coat: apoproteins, phospholipids, apolipoproteins, cholesterol

237
Q

Types of lipoproteins

A

-VLDL
-LDL
-IDL
-HDL
-chylomicrons

238
Q

Levels of cholesterol in mmol/L and their meaning

A

Less than 5: normal
5-6.4: mildly high
6.4-7.8: moderately high
Greater than 7: very high

239
Q

List the drugs that lower cholesterol levels

A

-Statins
-Ezetimbe
-PCSK9 inhibitors
-Bempedoic acid
-Bile sequestrants
-Fibrates
-Colestyramines

240
Q

Explain effects of Statin

Include action, examples, side effects

A

Inhibits HMG coA reductase
-Inhibits cholesterol synthesis
-Use for prevention of MI, stroke, arterial disease, people with familial hypercholesteraemia and for patients with low serum chl

EXAMPLE: atorvastatin, simvastatin
SIDE EFFECTS: GI disturbance, rash, insomnia, myositis

241
Q

Explain effects of Ezetimbe

Include action, examples, side effects

A

Decreases Chl uptake
-Inhibits sterol carrier proteins in brush border of duodenal enterocytes.

242
Q

Explain effects of PSCK 9 inhibitors

Include action, examples, side effects

A

Inhibits Chl degradation
-Inhibits enzyme that degrades LDL receptors in liver cells
EXAMPLE: alinocumab, evolcumab
SIDE EFFECTS: flu-like, muscle pain

243
Q

Explain effects of Bempedoic acid

Include action, examples, side effects

A

Decreases Chl synthesis
-Inhibits ATP citrate lyase
-Used when pt allergic to statins
SIDE EFFECTS: anaemia, gout, hyperuricaemia

244
Q

Explain effects of fibrates

Include action, examples, side effects

A

Activate lipoprotein lipase
-Decreases [VLDL] [TG+chl]
-Increases [HDL]
-Inc. LDL removal

USES: for patients with diabetes+ dyslipidaemia, high LDL, TF or low HDL

245
Q

Explain effects of Bile sequestrants

Include action, examples, side effects

A

They sequester bile
-Decrease cholesterol stores in liver as more chl needed for more bile acids
-Not used much- not very effective

246
Q

Explain effects of colestyramines

Include action, examples, side effects

A

Binds to bile
-Inc. metabolism of Chl into bile acids
-Inc. LDL receptors in liver
-Inc. LDL uptake
-SIDE EFFECTS: GI-related symptoms

247
Q

Factors affecting drug absorption

A

-Barriers to absorption
-Lipophility of drug
-drug ionisation
-Route of administration

248
Q

Factors affecting distribution

A

-Drug ionisation
-Lipid solubility of drug
-Capillary permeability
-pH of compartment
-cardiac output and stroke volume
-plasma protein binding

249
Q

Plasma proteins

A

-Albumin
-Alpha-1 glycoprotein
-globulin
-lipoprotein

250
Q

Interaction of warfarin and aspirin

A

-Normally 98% of warfarin remains bind to albumin and the rest unbound
-Aspirin displaces warfarin in albumin increasing conc. of unbound drug
-Warfarin has very narrow Therapeutic I o this can be dangerous

251
Q

Factors affecting distribution between fluid compartments

A

-Drug binding to the compartments
-Fat: water ratio
-permeability across barriers
-pH partition

252
Q

Characteristics and effects of bethanechol

A

-Quaternary ammonium
-Highly charged: isn’t absorbed in GI
-Treats GI hypotonia

253
Q

Characteristics and effects of pilocarpine

A

-Tertiary amine
-Less charged
-Used in small concentrations in the eye
-Treats glaucoma

254
Q

Why is it important to make sure someone is pregnant before giving them medication

A

Foeal circulation ahs different pH than maternal’s. Thi means that weak acid/bases that don’t get ionised in mum, can get ionised in Foetus.
-Causes toxic effects for baby

255
Q

Factors involved in platelet adhesion

A

-Glycoprotein Ib and von Willebrand’s factor: allows platelets to bind to blood vessel wall
-Glycoprotein IIb/IIIa: allows binding between platelets
-Fibrinogen
-Factors that attrcat other platelets.

256
Q

Types of blood donations and components

A

-Platelets from transfusion:
-Cryoprecipitate: contains vWfactor,fibrinogen and factor VIII
-Fresh frozen plasma: normal [coag. factors]
-Specific coag, factors: to treat haemophilia

257
Q

Explain Tranexamic acid

A

-Inhibits plasminogen activation
-Used after deliver, post operation, trauma and GI bleeding
-Oral/IV

258
Q

Explain effects of aspirin on coagulation

A

-Inhibits COX-1, inhibiting production of Thromboxane A2 adhesion factor.
-Helps in stroke and MI prevention, transient ischaemic attach and ischaemic stroke.
SIDE EFFECTS: dyspepsia and increased bleeding

259
Q

Explain effects of warfarin on coagulation

A

Inhibits vit K reductase
-Inhibits coagulation cascade so fibrinogen can’t be activated.

-Can be monitored with Prothrombin Time
-Cheap, easy to use, reversible with vit K
-Useful with poor renal function

260
Q

Explain effects of DOACs on coagulation

A

-They can be Factor Xa inhibitor (edoxaban, apixaban) or direct thrombin inhibitors (dabigatran).
-ADV: no food interactions, no need for monitoring, decrease bleeding risk, short half life

261
Q

Explain effects of heparin on coagulation

A

-Activates anti-thrombin: decrease[Xa] and [thrombin]
-Given Subcutan. , Iv or LMWH
-Monitored with APTT(IV) and dalteparin( LMWH) to adjust dose
-Subc and IV used for treat and prevent DVT and PE
-AntI Xa- measure of anticoagulation levels
-SIDE EFFECTS: osteoporosis, increase bleeding, pain at site of injection and heparin induced thrombocytopenia

262
Q

Uses of DOACs and warfarin

A

-To treat DVT and PE-DOACs
-To prevent stroke-warfarin best
-To treat atrial fibrillation- warfarin
-Used after prosthetic valve-warfarin
-To prevent DVT after hip and knee surgery-DOACs only

Be aware of absolute/relative risk reduction, nalance risk and benefits. CHA2DS2-VASc

263
Q

Explain effects of thrombolytic drugs on coagulation

A

Trigger activation of plasminogen
-Destroy thrombus
-tPA: streptokinase and altepase
-USE: to prevent TIA, Ischaemic stroke, MI, use when patient has thrombus on vital organs like brain, liver, heart

264
Q

Function of NSAIDS

A
265
Q

Explain the mechanism of action of aspirin

A

-Inactivates COX-1 by adding acetyl groupto serine forming a covalent bond
-Irreversible, time-dependent inhibition

266
Q

Mechanism of action of ibuprofen

A

-Inhibits COX enzyme by competitive inhibitor of arachidonic acid

267
Q

State and explain the 2 types of COX gene

A

COX 1-its constituitive, always there, maintains GI mucosa
COX 2-Its inducible. Involved in cancer management

268
Q

Name types of prostaglandins and their function

A

PGI2:vasodilator, hyperalgesic, inhibit platelet aggregation
PGF2alpha: bronchoconstrictor
PGE2:vasodilator, hyperalgesic
PGD2:vasodilator, inhibit platelet aggregation

269
Q

Effect of prostaglandins in inflammation

A

PGE2, PGD2 and PGI2 involved in inflammation
-They are vasodilators
-Increase effects of histamine and bradykinin in bv permeability and pain sensory nerves

270
Q

Explain the anti-pyretic effect for NSAIDs

A

-In response to bacterial endotoxins, interleukin 1 is released, which trigger PG in hypothalamus.
-The PG increase the thermo set point, causing fever
-NSAIDs block the PG stopping it from causing fever

271
Q

Explain the analgesic effect of NSAIDs

A

-Histamine, bradykinin and PG activate the nerve endings of nociceptors nerves allowing us to feel pain.

-NSAIDs block the PG, reducing pain

272
Q

What are the effects of histamine and bradykinin

A

-Inflammation
-Increase venule permeability: they losen tight junctions between endothelial cells
-Activate the nerve endings of nocioceptive neurones which can lead to pain

273
Q

Explain characteristics of salicyclates

A

-Pro-drug is acetylsalicylic acid: they can directly acetylate COX enzymes.
-Active compound is salicylic acid thaks to esterase
-Onset of action= 30 min
-Peak plasma concentration

274
Q

Side effects of salicyclates

A

GI bleeding
Systemic: tinnitus, hypersensitivity, nausea, vomiting,
Metabolic :acid/base balance disrupted
-Blood coag. and platelet actions disrupted
CNS: respiratory depression, coma
Renal insufficiency

275
Q

Describe characteristics of propionic acid and fenamates

A

PROPIONIC ACID
No pro-drug. Examples: naproxen and ibuprofen
-Half life of 4-6h

FENAMATES
Example: Mefenamic acid

276
Q

Describe characteristics of ancetaminophen (paracetamol)

A

-Good anti-pyretic and analgesic but poor anti-inflamm.
-Weak COX inhibitor
Peak plasma conc. 30 min-60 min
-Half life: 2-4h
Side effects: hepatotoxicity if overdose
Example: Paracetamol

277
Q

Describe characteristics of selective COX-2 inhibitors

A

COXIBS- used for osteoarthritis and rheumatoid Arth. Used when normal analgesics don’t work
-Bad GIT and heart side effects.

278
Q

Clinical uses of NSAIDs

A

Analgesia: for post operative, bony metastasis, headache, dysmenhorrea and backache

Short Term: paracetamol, ibuprofen, aspirin
Long Term: diclofenac and naproxen

279
Q

Phases drug metabolisms

A

PHASE I: Oxidation, reduction and hydrolysis- to relieve reactive group or add one.
Functionalisation-modification of properties

PHASE II: Synthetic conjugation reactions- detoxifies reactive compounds to make them more hydrophilic

280
Q

Characteristics of cytochrome P450 enzymes

A

-Monooxygenases present mostly in gut or liver
-There are 57 genes code for CYP450
Function: Biosynthesis of fatty acids, bile acids and steroids
Metabolism of endogenous and exogenous compounds

281
Q

Explain the metabolism of paracetamol

A

-Paracetamol broken down into sulphate, glucoronide and X metabolite
-X metabolite broken down by CYP450 into toxic metabolite.
-In the presence of glutathione, toxic metabolite combines with glutathione to become conjugated and exxcreted
-In the absence of glutathione it binds to hepatic proteins which is really toxic.

282
Q

Interaction of warfarin and phenorbital

A

-Warfarin broken down by CYP450
-Phenorbital increases the expression of CYP450
-Increase breakdown of warfarin, decreasing its effect

283
Q

Interaction of grapefruit juice and statin

A

Simvastatin broken down by CYP3A4
Grapefruit juice inhibits CYP3A4
Simvastatin conc. in blood increases

284
Q

Factors affecting pharmacokinetic parameter

A

-Age
-Sex
-Pregnancy
-Body weight
-Diet
-Genetic variability
-Disease
-Other medications
-Ethnicity

285
Q

Describe the process of nuclear envelop breakdown

A

-Cdk phosphorylates lamin protein in inner nuclear membrane causing it to breakdown in metaphase.

-During telphase, lamins and nuclear pore proteins are dephosphorylated so nuclear envelop forms again.

286
Q

Explain the importance of cohesin

A

-Cohesin keeps sister chromatids together
-Cohesin must be broken down in anaphase:
+separase enzyme inhibited by securin
+securin broken down by ubiquitin+proteasome
+Separase degrades cohesins allowing chromatid separation in anaphase

287
Q

Define aneuploidy

A

Condition in which person has abnormal number of chromosomes in haploid set because of problems with chr attaching to the right pole in metaphase

TREATMENT: Taxol. Targets , phase causing cell arrest and death(anti-mitotic)

288
Q

Cohesion in meiosis

A

-Cohesion of homologous chr. occurs thanks to Rec8(has cohesin)
-In anaphase I rec 8 is degraded by separase everywhere except centromere
-In anaphase II rec 8 in centromere also degraded to allow sister chromatids to separate.

Problems with this leads to non-disjunction of chromosomes

288
Q

Cohesion in meiosis

A

-Cohesion of homologous chr. occurs thanks to Rec8(has cohesin)
-In anaphase I rec 8 is degraded by separase everywhere except centromere
-In anaphase II rec 8 in centromere also degraded to allow sister chromatids to separate.

Problems with this leads to non-disjunction of chromosomes

289
Q

Explain the effects of non-disjunction in meiosis I and II

A

MEIOSIS I Leads to uniparental heterodisomy. We end up with a viable nucleus with both chromosomes from both parents of the parent’s chromosome

MEIOSIS II-Leads to uniparental homodisomy. We end up with a viable nucleus with both chromosomes from th

290
Q

Define allelic heterogeneity

A

Different mutations in same gene can cause same disease

291
Q

Define locus heterogeneity

A

Same disease caused by mutations in one of several genes
Example: HHT. HHT1: Endolgin gene mutation. Affects mouth
HHT2: ALK1 gene mutation. Affects tongue

292
Q

Complications in Mendelian inheritance

A

-Non-penetrance: failure of a genotype to manifest
-Variable expression: Different family members show different features of a disorder
Both seen more in dominant conditions

293
Q

Explain the causes of Ischaemic Heart Disease

A

-LDL receptor mutation: causes hypercholesteraemia. Aitosomal dominant
-Apolipoprotein E: kinked to hypercholesteraemia

294
Q

Explain PD-L1 and the action of Checkpoint Inhibitory Therapy on it

A

-PD-L1 Is a protein that turns off T cell and inhibits immune response.
-Cancers upregulate PD-L1 to avoid immune cells attack
-Monoclonal Abs block the PD-L1

295
Q

Neutrophils chemotaxis with IL-8

A

-Rolling adhesion
-Tight binding to endothelium
-Diapedesis: transmigration
-Migration: to site of infection

296
Q

Explain the effects of TNF-alpha

A

-Secreted by macrophages in infection
-Trigger phagocyte migration, increase plateled adhesion to blood vessel wall
-Triggers phagocytosis and containment of infection
-Stimulates adaptive immune system.

297
Q

Describe T-cell self-proliferation

A

-Inactive T cells express low-affinity IL-2 receptor
-When active they express high affinity IL-2 receptor and IL-2
-The IL-2 secreted binds to the receptor inducing proliferation

298
Q

Characteristics of dendritic cells

A

-Professional APCs so activates T and B cells

-Sample external environment continuosly and become activated when pathogen found.

-They hold on to antigens for a long time to allow B cells to produce Abs with increasingly high affinity to the antigens.

-They express Pattern Recognition Receptors to know whether cell is abnormal or normal.

299
Q

Barriers to infection

A

MECHANICAL: tight junctions, air and fluid flow, movement of mucus by cillia

CHEMICAL: Fatty acids in skin, lysozymes, low stomach pH , defensins and cryptidins.

MICROBIOLOGICAL: Competition with flora in skin . The flora produce olicins.

300
Q

What receptors do phagocytes need to do phagocytosis of infective agents?

A

-Mannose r.
-Glucan r.
-CD14 R: for Lipopolysaccharides
-CD11b/CD18
-Scavenger receptor

301
Q

Distribution of antibodies

A

-IgG and IgM: main in plasma.
-Dimeric IgA: secretion in all body
-IgE near epithelial surface
-IgG+monomeric IgA= main of ECF
-Foetus receives IgG
-Brain is free from Antibodies

302
Q

Function of antibodies

A

-Block virus receptors
-Promote phagocytosis: they coat pathogen
-Mast Cell degranulation thanks to IgE
-Antibody-dependent cell-mediated cytotoxicity: NK binds to Fc of antibody bound to pathogen triggering killing of pathogen.

303
Q

Drugs involving antibodies

A

-Infliximab: Anti-TNF. Treats Rheumatoid A, psoriasis, inflammatory bowel disease
-Herceptin: Anti-HER2. Treats breast cancer.
-Glovac: anti-tyrosine kinase. Treats chronic myeloid leukaemia

304
Q

Characteristics of nicotinic AChR

A

-Ionotropic
-They have specific functions
-Has a narrower range of results.
-Muscle has 2 alpha, 1 beta and 1 gamma subunit
-Ganglia has 2 alpha and 3 beta subunits.
LOCATION: NMJ, PSNS ganglia, SNS ganglia and CNS

305
Q

Characteristics of muscarinic AChR

A

-Metabotropic
-Broad range of functions
-Has a large range of results
-Has 7 transmembrane subunits
-LOCATION: PSNS target organs, sweat glands(SNS)
, CNS and vascular smooth muscle.

306
Q

Reflexes in Special Senses

A

-Rotatory nystagmus: Eye movements driven by moving visual images
-Post-rotatory nystagmus: Eye movements driven by moving fluid in the semi-circular canal of the inner ear
-Baroreceptor reflex: Blood presure regulation
-Interpretation of movements within images in the retina: To make postural readjustments

307
Q

Characteristics of rhytmic motor pattern movement

A

-Voluntary+ reflex
-Termination and initiation is voluntary the rest is automatic
-Once initiated it is repetitive and reflexive.
E.G: chewing, walking

308
Q

What are Renshaw cells? Describe characteristics

A

interneurones that act as feedback inhibition of alpha motorneurones.
-Supress weakly firing motor neurones, encouraging the stronger ones
-Produce economical movement
-They are inhibited by strychnine poisoning leading to convulsions.

309
Q

Explain the uses for medicine regulation

A
310
Q

Functions of the MHRA

A

-Remove drugs from market
-Give licenses and organise clinical trials
-Approve meds in the UK
-Monitors safety of meds

311
Q

Mention the UK medical legislation

A

-Medicine Act 1968: provide legal framework in control of meds.
-Misuse of Drugs 1971: Bans activities around some drugs.
-Misuse of Drugs regulation 2001: Allow possession and supply of drugs for legal reasons.
-Human Medicine Regulations: Pharmacovigilance

312
Q

Name the classing system in the Misuse of Drugs Act of 1971 and examples of drugs.

A

-Class A: cocaine, heroin, magic mushrooms
-Class B: cannabis, methrodone
-Class C: anabolic steroids, benzapyridine

313
Q

Types of chemotherapy

A

-Alkylating agents
-Antimetabolites
-Cytotoxic antibiotics
-Plant derivatives

314
Q

Types of alkylating agents and examples

A

-Nitrogen mustards-cyclophosphomide
Leads to production of phophotamides
-Ethylamines-thiotepa

-Alkylsulphonate- busulphan

+Lipid soluble, can cross BBB. Treats brain cancer; Affects bone marrow but not GI or lymphatics.

-Hyadrines and triazines- temozolomide

-Nitrosureas: calmustrine and lomustrine
+Lipid soluble, can cross BBB. Treats brain and meningal cancers.
-Platinim based compounds-cisplatin
+binds to DNA with NH3 forming cross-links.

314
Q

Types of antimetabolites and examples

A

-Antifolate-Methotrexate
+folate analogue with low lipid solubility
+Blocks DHFR
+polyglutamated: last weeks.

-Antipurine-mercaptopurine and fluodarabine.
+mercaptopurine forms fraudulent nucleotides.
+Fluodarabine inhibits DNA polymerase

-Antipyrimidine-cytarabine, fluorouracil and gemcitabine
+ Fluorouracil forms fraudulent nucelotide
+Cytarabine: cytosine analogue. Inhibits DNA polymerae

314
Q

Types of cytotoxic antibiotics and examples

A

-Anthracycline. Inhibits DNA and RNA syntheis sand stops replication.

-Dactinomycin: Interferes with movement of RNA polymerase.

-Bleomycin: Metal-chelating glycopeptides that fragment DNA.
-Binds to diving and non-diving cells and affects G2 phase in cell division
-Mitomycin: bifunctional alkylating agent. Cross links DNA and degrades with free radicals.

315
Q

Types of plant deratives and examples

A

-Spindle poisons: stop spindle fibre formation

-Vinca alkaloids: Bind to tubulin and stop microtubule formation.
+ Vincristine and vinblastine

-Taxanes: Freeze microtubules
+Docetaxel

-Campthetin: Inhibit tropoisomerase I
+iriotecan

-Eteposide: Inhibit mitochondrial function + tropoisomerase II

316
Q

List the side effects of chemo

A

-Tumour Lysis syndrome
-GI symptoms: loss of appetite, constipation, vomiting, diarrhoea
-Bone marrow -myelosuppression
-Mucositis
-Fatigue
-Weight loss/gain
-infertility
-Malignancy
-altered renal function
-Peripheral neuropathy

317
Q

Explain Tumour Lysis Syndrome

A

Acute metabolic emergency caused by rapid cell death
-SYMPTOMS: high urea, phosphate, potassium and calcium ions.
-Leads to renal failure, cardiac arrest, death

318
Q

Explain mucositis and its prevention

A

SYMPTOMS: ulceration, dry mouth, pain and taste alteration.
PREVENTION: assess mouth, anti-bacterial/viral meds, good dental hygiene.

319
Q

What is the effect of chemo on bone marrow

A

-Increases myelosuppression,
-Dec. blood cells and platelets.
-Can be given filgrastim- decreases duration of myelosuppression.

320
Q

What is septic arthritis

A

Infection in synovial fluid and joint tissue causing hot swollen joints.

321
Q

Presentation of septic arthritis

A

-1 to 2 wks of red painful joint
-Fever, sweats, rigors
-Common areas in knee hip, and lumbrosacral spine.
-Fungal, viral and mycobacterial infections delay presentation

322
Q

Predisposing conditions

A

-Rheumatoid arthritis or osteoarthritis
-Joint prosthesis
-IV drug use
-Excess alcohol
-Diabetes
-Intra-articular corticosteroid injection
-Skin ulcers

323
Q

Causative organisms

A

-Staph. aureus
-Strept. pyogenes
-Mycob tuberculosis
-Salmonella
-Brucella: unpasteurised dairy
-Neisseria gonorrhae: STD
-Kingella: infections in children
-Pasturella: animal bites
-Staph. epidermidis: linked to prosthetic material

324
Q

Pathogenesis of septic arthritis

A

Infection is introduced into joint by:
-Direct inoculation
-Trauma
-Iatrogenically
-Haematogenous spread: spreading through bloodstream.

325
Q

Methods to diagnose septic arthritis

A

-Aspiration of liquid from joints
-Peripheral blood cultures
-X Ray joint
-MRI

326
Q

Management of acute septic arthritis is by staph. aureus.

What things would you have to consider

A

-IV fluocloxacillin 2wks
-Oral fluocloxacillin 2-4 wks

-Consider washout, renal+ cardiac function, penicillin allergy, antibiotic advice, if patient had surgery.

327
Q

Treatment for patient in secondary care

A

-Stop antibiotic therapy doesn’t resolve disease and re-culture
-Modify antibiotic treatment
-Might be SIRS
-Further imaging with MRI to know if it is osteomyelitis

328
Q

Describe Reactive Arthritis

A

Caused by HLA-B27 associated with reactive arthritis
SYMPTOMS:
-Conjunctivitis
-Urethritis
-Arthritis
TREATMENT: full dose of NSAID with gastric protection and treatment for precipitating factors.

329
Q

Skin presentation of reactive arthritis

A

-Nail changes
-Oral lesions
-Ulcerative vulvitis
-Keratoderma blennorrhagium
-Circinate balanitis

330
Q

Organisms involved in reactive arthritis

A

-C. difficile
-Salmonella
-Neisseria gonorrhoea
-E.coli
-Chlamydia pneumoniae

331
Q

Describe osteomyelitis

A

-Inflammation of bone and bone marrow due to pyogenic bacteria, (fungi or mycobacteria).

-Bones infected by: local spread(hematogenous), open fracture and foreign bodies

332
Q

Predisposition to osteomyelitis

A

Sickle cell disease= salmonella
Travel, drink milk= brucella
Prosthesis= S. epidermidis
Children under 5=H. influenzae
UTI= E.coli

333
Q

Organisms that cause osteomyelitis

A

-Staph. aureus
-Staph. pyogenes
-Myco. tuberculosis
-Gram negative bacteria

334
Q

Symptoms of osteomyelitis

A

-Painful swollen site
-Reduced movement
-Fever
-Paraplegia
MARKERS
-Fever, WBC, ESR, C-reactive protein.

335
Q

What investigations to diagnose osteomyelitis and what would ?

A

-3 Blood cultures
-Sample pus
-X Ray: no signs in early infection

-MRI : marrow edema present. Used in vertebral osteomyelitis

-CT : periosteal elevation, cortical thinning, scalloping, focal orthopenia( low bone marrow density)
-Presence of sequestrum (old dead bone) and involucrum( new bone around sequestrum)

336
Q

Treatment of osteomyelitis

A

-Chronic O. by s. aureusL oral flucloxacin and penicilin
-MRSA osteomyelitis
-Gram negative bacteria: cipofloxacin, ethambutamol, rifampicin

337
Q

Describe prosthetic joint infection

A

-Infection caused by joint replacement, during operation.
SYMPTOMS: joint pain, fever, swelling and wound drainage.

338
Q

Investigations to diagnose prosthetic joint infection

A

-Blood culture
-Joint aspirate
-Surgery for inspection

339
Q

In what scenarios must the prosthesis be removed?

A

-If patient has poor soft tissue
-Hard to treat infection
-Delayed reimplantation

340
Q

In what scenarios must the limb be amputated?

A

-Resistant necrotizing fascitis
-Severe bone loss
-Failure of soft tissue coverage
-No medical therapy available
-Amputation is the most beneficial options
-Failed attempt of joint replacement.

341
Q

Examples of different potencies

A

Totipotent: embryonic stem cells
Pluripotent: Inner cells of blastocyst
Multipotent: blood stem cells

342
Q

What is commitment?
What 2 stages are involved in it?

A

Each decision that restricts cell fate
Stage 1: Specification- cell can differentiate on its own but can be respecified if exposed to the right chemicals. Reversible

Stage 2: Determination-cell differentiates on its own even when exposed to other stimuli. Irreversible

343
Q

What types of signals can make a cell become specified?

Define cell fate

A

-Extrinsic signals: molecule in environment gives cell spacial info.

-Intrinsic signals: cells own signals indicate what type cell can differentiate into?

-Cell fate: what cell will become in the course of its development

344
Q

Explain the bivalent chromatin in cells

A

Mechanistic basis of fate decisions that only occur at developmental regulator genes.
In embryonic stem cells genes are ON and OFF in a poised position.

345
Q

Process of creating IPS cells

A
  1. Isolate skin cells/fibroblasts
  2. Treat cells with reprogramming factor
  3. Wait until pluripotent cells obtained
  4. Change culture conditions to stimulate further
346
Q

Define HOX genes

A

Group of genes that act as transcription factors that are involved in the development of a body plan.
-They determine body axis and position of limbs.
-Its expression depends on SHH protein, FGF and WNT7

347
Q

Explain the timeline of limb development

A

-Upper limb buds appear in day 24 in somites C5 to T1
-Lower limb buds appear in day 28 in somites L1 to S2
-In week 7 upper limb lateral rotation
-In week 8 lower limb medial rotation

348
Q

Name the 3 axis in development

A

+Proximo-distal axis
+ Antero-posterior/Cranio-caudal axis
+ Dorso-ventral axis

349
Q

Explain the proximo-distal axis-

A

-Ectoderm of the limb bud thickens up and becomes AER.
-AER secretes FGF4 and FGF8, inducing tissues to remain undifferentiated and proliferate.
-As mesenchymal cells move away from AER they differentiate into cartilage and muscle.

350
Q

Explain the cranio-caudal axis

A

It is regulated by ZPA
-ZPA ensures thumb grow in the cranial side of the limb bud.-Spatial position info
-ZPA expresses SHH protein
-ZPA moves distally with AER

351
Q

Explain the dorso-ventral axis

A

-BMP in ectoderm stimulate EN1
-WN7 makes cells to be dorsal while EN1 makes them ventral.
-EN1 inhibits WN7

352
Q

State and explain the types of limb defects

A

-Amelia: complete absence of limb
-Meromelia: partial absence of limbs
-Phocomelia: absence of long bones
-Micromelia: abnormally short “limbs”

Caused by failure of progressive zone to do mitosis in wk4 &5

353
Q

State and explain the type of digit defects

A

Brachydactylyl- short digits
Syndactylyl- fused digits
Polydactylyl: etra digits.
Cleft foot- lobster-like digits.

MD2002 (10 decks)

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