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Biomed > Human phys y2 s1 > Flashcards

Human phys y2 s1 Flashcards

1
Q

What are IPS cells and what are they used for?

A

Induced pluripotent stem cells that can be used to form cell types and test if a drug has adverse effects

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2
Q

Order of heart layers?

A

Pericardium -> epicardium -> myocardium -> endocardium

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3
Q

What is epicardium?

A

Squamous epithelium with a layer of collagen and elastin that forms a loose layer of connective tissue for blood vessel and fat support

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4
Q

What is myocardium?

A

Thick layer of muscle made up of cardiomyocytes joined by intercalated discs and there are bundles of them with a central nuclei found with connective tissue between them
Contains many capillaries

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5
Q

What does the thickness of myocardium depend on?

A

Health and disease

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6
Q

What is endocardium?

A

Layer of flattened endothelial cells supported by fibrous and elastic connective tissue that form the heart chambers’ lining

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7
Q

Which side of the heart is deoxygenated?

A

Right atrium and ventricle (left side)

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8
Q

Is vena cava for oxygenated or deoxygenated?

A

Deoxygenated (brings blood in, pulmonary arteries take it to lungs)

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9
Q

Right AV valve?

A

Tricuspid

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10
Q

How does oxygenated blood enter and leave heart?

A

Enters via pulmonary veins, leaves via aorta and associated arteries

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11
Q

Left AV valve?

A

Bicuspid

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12
Q

What are the two types of cardiomyocytes?

A
  1. Pacemaker/autorhythmic (1%) - in sinoatrial node and generate action potentials spontaneously and depolarise nearby cells via gap junctions in intercalated discs
  2. Contractile cells - the nearby cells that are depolarised and contract
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13
Q

6 steps of the cardiac cycle?

A
  1. Action potential from pacemaker cells reaches contractile cells via gap junctions
  2. Atrial excitation (contraction) occurs as depolarisation spreads through atrial walls
  3. Electrical impulse reaches AV node (in right posterior of interatrial septum) via internodal pathways
  4. AV node causes 0.09 second delay the atria can eject all the blood before ventricular contraction
  5. Bundle of His (conducting-system fibres) guide impulse to interventricular septum – fibres then divide right and left
  6. Branches lead to purkinje fibres - conduct action potential through myocytes of ventricles = ventricular excitation = blood exits valves
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14
Q

What is atrial systole?

A

Atrial myocytes contract and blood is forced into ventricles

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15
Q

What is atrial diastole?

A

Atrial myocytes relax

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16
Q

What is ventricular systole?

A

Ventricular myocytes contract and blood is forced into the aorta and pulmonary artery

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17
Q

What is ventricular diastole?

A

Ventricular myocytes relax

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18
Q

Do pacemaker cells have a set resting potential?

A

No

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19
Q

7 steps of pacemaker cells’ constantly changing resting potential?

A
  1. Membrane potential starts at -60mV
  2. FUNNY channels open when membrane potential is less than -40mV and allow SLOW influx of Na+ to slowly depolarise
  3. FUNNY channels close just below -40mV (threshold)
  4. Ca channels open, Ca2+ enters cell = rapid depolarisation
  5. Peak of depolarisation = K channels open and Ca channels close and K+ leaves the cell
  6. Repolarisation (normal levels return)
  7. Process repeats
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20
Q

9 step process of electrical impulse from pacemaker cells entering contractile cardiomyocytes and what follows?
(-90mV resting, -70mV threshold)

A
  1. Na+ and Ca2+ move through gap junctions from adjacent cells (voltage rises to threshold)
  2. FAST Na+ channels open and Na+ influx occurs to depolarise
  3. -40mV = SLOW Ca2+ channels open = steady Ca2+ influx
  4. Na+ channels close on approach to action potential peak
  5. Voltage gated K+ channels open = early repolarising phase
  6. K+ efflux is balanced by Ca2+ influx to keep membrane potential stable for 200ms (plateau phase) – more calcium is obtained from SR for contraction
  7. Ca2+ channels slowly close and K+ efflux dominates and repolarisation occurs
  8. Ca2+ actively transported to sarcoplasmic reticulum
  9. Process repeats
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21
Q

3 steps of cardiac excitation-contraction coupling that converts an action potential into a contraction?

A
  1. Excitation:
    • Ca2+ influx during plateau phase as dihydropyridine receptors (voltage-gated Ca2+ channels) open in contractile cardiomyocytes – this Ca2+ induces release of Ca2+ through ryanodine receptor channels from the SR
  2. Contraction:
    • Ca2+ ions bind to troponin C which is attached to muscle filaments as part of a regulatory complex – causes conformational changes in troponin complex = actin exposure so it can bind myosin-ATPase = ratcheting movement (contraction)
  3. Relaxation:
    • Ca2+ unbinds at the end of the plateau phase, pumped back into SR for storage, muscle relaxes as troponin complex resumes normal position
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22
Q

What are the parts of an ECG?

A

P wave = atrial contraction

PR interval = conduction through the AV node

QRS complex = ventricular depolarisation and contraction

ST segment = interval between ventricular depolarisation and repolarisation

T wave = repolarisation of ventricles

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23
Q

How does the parasympathetic nervous system affect heart rate?

A

Controls homeostasis and body at rest (responsible for rest and digest) and decreases heart rate and causes bradycardia (<60bpm)

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24
Q

How does the sympathetic nervous system affect heart rate?

A

Controls body’s response to perceived threat and causes fight or flight, increases heart rate and causes tachycardia (>100bpm)

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25
Q

Why does 90% of the oxygenated blood a foetus recieves from the placenta bypass the lungs?

A

Hard work to get blood into lungs as alveoli contain low o2 amniotic fluid that makes them constrict (hypoxic pulmonary vasoconstriction)

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26
Q

What is the umbilical cord for?

A

Links foetus and placenta, has two umbilical arteries: one for oxygenated blood, other for deoxygenated blood and waste

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27
Q

Process of oxygenated blood reaching a foetus’ body?

A

Oxygenated blood from placenta –> umbilical vein –> inferior vena cava –> right atrium –> left atrium (via foramen ovale) –> left ventricle (via mitral valve) –> aorta –> blood to body

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28
Q

Process of deoxygenated blood leaving foetus?

A

Blood enters foetal heart via superior vena cava –> partially mixes with oxygenated blood from placenta –> right ventricle (tricuspid valve) –> mostly bypasses lungs –> ductus arteriosus –> descending placenta aorta

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29
Q

What is the foramen ovale?

A

One-way valve that links right and left foetal atria and opens when the pressure is greater in the right atrium as the lungs are not functional (pressure in pulmonary > systematic circulation)

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30
Q

What is the ductus arteriosus?

A

Links pulmonary artery with aorta, allows deoxygenated blood to enter descending aorta and leave via umblilical arteries

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31
Q

What happens to a baby’s circulations when it is born?

A

The formamen ovale closes and the baby takes its first breath, clearing the alveoli fluid, reducing pulmonary pressure and increasing systemic blood pressure AND the foramen ovale fuses closed to form the septum

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32
Q

How long does the closure of the ductus arteriosus take?

A
  • There is an initial constriction due to increase in arterial pO2, a drop in circulating prostaglandins and a drop in ductus blood pressure which causes smooth muscle cell death due to hypoxia (scar forms)
  • Functional closure is 18-24 hours after birth
  • Full anatomical occlusion is over days or weeks
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33
Q

What is a symptom of a congenital heart defect and how can they be identified?

A

Cyanosis (blue tinge of skin due to low O2)
Ultrasound

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34
Q

Risk factors for congenital heart defects?

A

Genetic conditions, maternal type I diabetes, foetal alcohol syndrom, rubella, flu, some medications, organic solvent exposure

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35
Q
  • What are septal defects?
  • Symptoms?
  • Treatment?
A

A hole between atria or ventricles that causes blood mixing which increases the pressure of the blood entering the lungs = pulmonary hypertension

Symptoms = breathlessness, tiredness when feeding, poor weight gain, heart murmur, chest infections and high blood pressure

Treated via keyhole surgery

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36
Q
  • What is patent ductus arteriosus?
  • Symptoms?
  • Treatment?
A

Ductus arteriosus remains open after birth which keeps aorta and pulmonary artery connected (abnormal blood flow) which causes pulmonary hypertension and strain on the heart and increases risk of lung and heart infection/damage

Symptoms = breathlessness, heart murmur, sweating, rapid heart rate, poor feeding/weight gain

Treated with prostaglandin inhibitors to stimulate closure OR surgical closure

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37
Q
  • What is coarctation of the aorta?
  • Symptoms?
  • Treatment?
A

Part of aorta not forming correctly normally near the ductus arteriosus where the arteries branch to take blood to head and arms (further narrowing can occur at birth when ductus arteriosus closes

Symptoms are dizziness, fainting, breathlessness, sweating, pounding headache, chest pain and nosebleeds due to high blood pressure in upper body

Treatments = removing narrowed section and reconnecting OR inserting catheter into aorta to widen with a balloon OR high blood pressure can be controlled through lifestyle

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38
Q
  • What is pulmonary valve stenosis?
  • Symptoms?
  • Treatment?
A
  • Narrower than normal so less blood reaches lungs from right ventricle so ventricle works harder = right ventricular hypertrophy (wall thickening)

Heart murmur, tiredness, breathlessness, fainting, chest pains, cyanosis

Balloon valvuloplasty = thin tube with balloon inserted in groin which is threaded to narrowed heart valve and balloon inflates to stretch valve open
OR surgery

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39
Q
  • What is mitral valve stenosis?
  • Symptoms?
  • Treatment?
A
  • Mitral valve (between left ventricle and atrium) is narrowed which reduces blood flow and blood collects in left atrium and back flow into lungs occurs = heart weakening

Tiredness, breathlessness, fatigue, irregular heartbeats, heart murmur, dizziness, chest pain, coughing up blood

Balloon valvuloplasty OR open-heart surgery to replace/repair

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40
Q
  • What is transposition of the great arteries?
  • Symptoms?
  • Treatment?
A

Pulmonary and aortic valves and their respective arteries have swapped positions so the pulmonary artery is on the right and the aorta on the left which means oxygenated blood goes to the lungs and low oxygen blood is in circulation

Cyanosis, pounding heart, weak pulse, breathlessness, poor feeding

Surgical switching of vessels in first month of birth OR prostaglandin injection so the ductus arteriosus doesn’t close and blood mixes

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41
Q
  • What is tetralogy of fallot?
  • Symptoms?
  • Treatment?
A

Four problems:
1. Ventricular septal defect
2. Pulmonary stenosis
3. Right ventricular hypertrophy
4. Overriding aorta (enlarged aortic valve, blood received from both ventricles)

Cyanosis (can occur in tet spells when baby cries or feeds), endocarditis (increased risk of heart infection), irregular heart rhythm, dizziness, fainting, seizures, delayed growth

Treatment must be surgery soon after birth whereby pulmonary valve is widened/replaced, passage to pulmonary artery widened, VSD patched and repaired

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42
Q

What are two examples of acquired heart diseases?

A

Atherosclerosis and aneurysms

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43
Q

What is atherosclerosis?

A

Thickening of artery walls with fat and cellular matter that restricts blood flow and eventually causes rupture and even occlusion that prevents blood flow = hypoxia

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44
Q

3 layers of arterial wall?

A
  1. Intima = lines blood vessel lumen, made of endothelial cells and connective tissue
  2. Media = smooth muscle, matrix proteins, provides strength and elasticity and allows expansion
  3. Adventitial layer = outer layer, fibrous connective tissue
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45
Q

6 steps of atherosclerosis development?

A
  1. Normal artery has a large open lumen
  2. Fatty streak develops during childhood (reversible) but does not protrude lumen
  3. This can develop into stable plaque that protrudes and restricts blood flow, fibrous cap of smooth muscle and extracellular matrix forms to increase tensile strength
  4. Stable plaques can become unstable (larger lipid pool, thinner fibrous cap)
  5. This can rupture, exposes underlying collagen and lipid core that is highly thrombogenic, thrombus occurs, blood vessel occluded = hypoxia
  6. The plaque can also heal and leave a larger plaque = further narrowing
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46
Q

How does the fibrous plaque form?

A

Smooth muscle cells in intima proliferate and produce extracellular matrix molecules

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47
Q

3 factors that cause fibrous cap weakening/thinning?

A
  1. T cell mediators weakening smooth muscle cells’ ability to synthesise collagen
  2. Activated macrophages produce matrix metalloproteinases to break down collagen
  3. Smooth muscle cell apoptosis and macrophage death causes debris = lipid rich necrotic core that creates unstable plaque
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48
Q

What is coronary heart disease?

A

Blockage of coronary arteries that causes angina (chest pain) and sometimes myocaridal infarction if heart muscle becomes ischaemic

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49
Q

Symptoms of coronary heart disease?

A

Angina (low blood flow to heart), myocardial infarction (if blood flow is occluded), aching, tightness, pain in upper body, sweating

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50
Q

3 ways of diagnosing coronary heart disease?

A
  1. Angiography - catheter inserted in groin, threaded to coronary artery, dye injected, x-ray shows narrowing
  2. Blood tests - heart muscle damage during heart attack releases substances like troponin
  3. ECG changes - during a heart attack it can differentiate between complete occlusion and a milder form called non-STEMI (not occluded)
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51
Q

How is coronary heart disease treated? (4)

A
  • Blood thinning meds like aspirin
  • Surgery
  • Coronary angioplasty and stent replacement (balloon opens artery, stent remains to hold it open, drug eluting stents can increase patency)
  • Coronary artery bypass graft (blood vessel taken from elsewhere in the body and attached above and below artery where it is narrowed or blocked)
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52
Q

When does a stroke occur?

A

When carotid or cerebral arteries are occluded

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53
Q

Stroke symptoms?

A

Face drooping on one side, weakness in one arm, slurred speech, unable to speak, severe headache, difficulty swallowing, blurred vision, dizziness, confusion

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54
Q

3 ways a stroke is diagnosed?

A
  1. Brain scan - dark areas = low O2 (must be done within the hour)
  2. Swallow test = observed swallowing as they may inhale food or drink which can cause pneumonia
  3. Carotid ultrasound = shows narrowing or blockages of carotid arteries (must occur within 48 hrs)
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55
Q

Treatment of a stroke?

A

Short term = thrombolytic drugs to break down blood clots, throbectomy to remove thrombus, carotid endartectomy (neck incision to remove fatty deposits)
Long term = medication combination (anti-platelets, anti-coagulants, anti-hypertensive meds and cholesterol reduction in diet)

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56
Q

What is peripheral artery disease?

A

Atherosclerosis in peripheral arteries that causes ischaemia in limbs

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57
Q

What is ischaemia?

A

Hardening and obstruction of blood vessels causing lack of blood flow to legs and feet

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58
Q

Symptoms of peripheral artery disease?

A

Critical limb ischaemia (hypoxic = ulcers, unhealing wounds and gangrene), intermittent leg cramp during exercise (claudication)

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59
Q

Diagnosis of peripheral artery disease?

A

Stethoscope identifies weak/absent pulse below narrowed artery, whooshing sounds suggest poor wound healing, ankle-brachial index compares blood pressure in ankle and arm, ultrasound or angiography shows blood flow and diagnoses affected arteries

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60
Q

Treatment of peripheral artery disease?

A

Lifestyle changes - exercise, smoking cessation, weight loss, better diet
Surgery e.g. angioplasty, bypass grafting, amputation (for limb ischaemia)

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61
Q

What is an aneurysm?

A

Localised, blood-filled dilation of a blood vessel caused by disease or weakening of the vessel wall that occur in specific locations in the vasculature (most are abdominal aorta or brain)
Vessel wall weakening eventually causes rupture that causes major internal bleeding

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62
Q

3 mains factors causing aortic aneurysms?

A
  1. Inflammation – many inflammatory cells are in aneurysmal tissue, cytokine production by immune cells and cells native to the vessel wall cause inflammatory responses
  2. Proteolysis = excessive reactive oxygen species from things like smoking activate matrix metalloproteinases (MMPs) that break down the extracellular matrix and elastin and collagen to weaken vessel wall
  3. Smooth muscle cell apoptosis = loss of structural integrity in vessels, thinning and weakening too
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63
Q

Symptoms of abdominal aortic aneurysms?

A

Sudden, severe abdominal pain, dizziness, sweaty, pale, clammy skin, fast heartbeat, shortness of breath, fainting (all at the point of rupture)

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64
Q

How is an abdominal aortic aneurysm diagnosed?

A

Abdominal ultrasound

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65
Q

How is an abdominal aortic aneurysm treated?

A
  1. Small (<5.5cm) dilation = 3-6 monthly scans to see if it is growing, lifestyle changes
  2. Large (>5.5cm) dilation = surgical intervention, graft inserted by endovascular surgery (in groin, guided to aneruysm to strengthen vessel and prevent rupture) OR open surgery (graft placed directly)
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66
Q

What is haematocrit?

A

45% of the blood, composed of RBCs

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67
Q

What is buffy coat?

A

1% of blood, made up of platelets and WBCs

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68
Q

Why do RBCs contain no mitochondria?

A

Prevent use of oxygen so more O2 is delivered to tissues

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69
Q

What is haemaglobin?

A

A polypeptide with 2 alpha and beta chains, and a haem group attached to globins, it is red when it is carrying O2 and blue when it is not, combines with O2 to form oxyhaemaglobin reversibly

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70
Q

Why does haemaglobin bind to the following molecules:
- CO2?
- H+?
- CO?
- NO?

A
  • Transport to lungs
  • Buffers ionised carbonic acid in blood
  • Causes carbon monoxide poisoning (occupies O2 binding sites)
  • Acts as a vasodilator - binds to sulfur in haemaglobin to form SNO which is then released into tissues where it dilates arterioles to allow O2 rich blood to pass round and it stabilises blood pressure
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71
Q

How do different blood types arise?

A

Erythrocytes express agglutinogens which determine it, all the blood types express the H gene:
A = A antigen expressed
B = B antigen expressed
AB = Both antigens
O = Neither antigens so H antigen persists

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72
Q

What does the H gene in all blood types do?

A

It encodes fucose transferase and adds a terminal fucose which forms the H antigen if the transferases in A and B are not present

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73
Q

How do A and B antigens differ?

A

They differ in their terminal sugar added by the transferase enzymes
- A express second transferase that adds acetylgalactosamine
- B express transferase that add galactose

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74
Q

Are the conventional blood groups the only ones?

A

No. There are smaller groups such as the Rhesus factor

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75
Q

Difference between A/B+ and - blood?

A

+ means you have the antigen and are Rhesus protein positive, - means you only have the antigen

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76
Q

Are leukocytes nucleated?

A

Yes and they are bi- or multi- in most cases

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77
Q

2 mains types of leukocytes?

A
  1. Polymorphogranulocytes/ myeloid cells (multi-nucleated, nuclei segmented into lobes, have many granules in cytoplasm)
  2. Mononuclear agranulocytes (one large and non-segmented nucleus, no granules)
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78
Q

What are granules?

A

Secretory vesicles that contain cytotoxic molecules (enzymes and antimicrobial peptides) that destroy foreign cells

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79
Q

3 types of granulocytes?

A

Basophils, neutrophils, Eosinophils

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80
Q

Basophils:
- What do they have a strong affinity for?
- What is the nucleus hidden by?
- What is the nucleus like?

A
  • Basic dyes such as methylene blue dye
  • Granules
  • Bi or tri-lobed
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81
Q

Neutrophils:
- Dye preference of granules?
- What is the nucleus like?

A
  • No preference, neutral, remain pale-pink
  • Multi-lobed
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82
Q

Eosinophils:
- Dye preference?
- Nuclei lobing?

A
  • Granules take up eosin stain to be bright red/pink
  • Bi
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83
Q

Difference between acidic and basic dyes?

A
  • Acidic dyes like eosin stain basic components like cytoplasm
  • Basic dyes like methylene blue stain acid components like nucleus
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84
Q

2 types of agranulocytes?

A
  1. Monocytes - large, oval/crescent shaped nucleus, circulate briefly then reside in tissue, mature into macrophages
  2. Lymphocytes - small, large spherical nucleus, are either T or B cells
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85
Q

2 things basophils synthesise and store?

A
  1. Histamine for hypersensitivity responses, causes vasodilation, increases blood flow to injured tissue and blood vessel permeability, allows neutrophils and clotting proteins to get to connective tissue
  2. Heparin = anticoagulant, removes fat particles in blood, inhibits blood clotting, attracts WBCs to area
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86
Q

Neutrophils:
- What do they act as?
- How do they work?
- Why do they degenerate and form pus?

A
  • The first line of defence against bacterial infections
  • Attracted towards bacteria by chemotactic factors released by damaged tissue/antibodies attached to antigens on surface of microorganism and then they engulf bacteria by endocytosis or phagocytosis and destroy them by releasing granule contents
  • Have limited protein synthesis machinery so cannot replenish active enzymes
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87
Q

Eosinophils:
- Roles?
- Why must they be strictly regulated?

A
  • Defend against parasitic infection, role in allergic responses, inflammation by amplifying it through activating synthesis of chemical mediators
  • The cytotoxic molecules can destroy healthy cells
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88
Q

What do monocytes/macrophages do?

A

Spend 3 days in circulation and then mature in tissues into macrophages which do phagocytosis of bacteria and then act as antigen presenting cells that present components of bacteria to lymphocytes to amplify immune response

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89
Q

Lymphocytes:
- Role?
- 2 types?

A
  • Recognise self vs non-self antigens presented by APCs
  1. B-lymphocytes
  2. T-lymphocytes
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90
Q

What do B-lymphocytes do?

A

Produce many antibodies to neutralise a pathogen or they tag it for destruction by cells like macrophages

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91
Q

What do T-lymphocytes do?

A

Can respond as Helper T-cells to produce cytokines to direct immune system
OR Cytotoxic T-cells that release cytotoxic proteins that destroy pathogen or pathogen-infected cells
They also produce memory cells

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92
Q

Main function of platelets?

A

Coagulation and haemostasis

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93
Q

What are platelets?

A

Fragments of megakaryocytes found in bone-marrow bound cells, they are detached anucleate vesicles with cytosolic enzyme systems that enables them to have a secretory function

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94
Q

Why are platelets contractile?

A

They have a high conc of actin and myosin so they can contract and be motile

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95
Q

5 steps of haemostasis (platelets)?

A
  1. Vessel injury exposes collagen and thromboplastin that activates platelets and recruits them for plug formation (primary haemostasis)
  2. Vasoconstrictors released by platelets = smooth muscle contracts
  3. Collagen and thromboplastin activate clotting cascade = thrombin activation
  4. Thrombin catalyses conversion of circulating soluble fibrinogen to insoluble fibrin monomers
  5. Fibrin monomers polymerise, cross-link and accumulate with platelets into a dense and tight aggregate (clot) (secondary haemostasis)
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96
Q

What is plasma?

A

Acellular fluid component of blood containing ions, inorganic and organic molecules (5% of body weight)

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97
Q

4 types of plasma proteins synthesised in the liver?

A
  1. Albumin = contributes to osmotic pressure and it exerts osmotic force across capillary wall as they are impermeable to plasma proteins so water is pulled across blood – transports bilirubin, bile salts and penicillin
  2. Globulins - there are many types = 1. Gamma globulins (immunoglobulins) are antibodies 2. Alpha and beta globulins are transport proteins and have a role in blood clotting 3. Some inactive precursor proteins
  3. Fibrinogens
  4. Others that are less abundant
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98
Q

Where do blood cells come from?

A

From bone marrow where haematopoiesis occurs (haematopoietic stem cell –> committed stem cell or progenitor cell)

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99
Q

What stimulates erythrocyte differentiation?

A

Erythropoietin from the kidney

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100
Q

What stimulates platelet production?

A

Multiple cytokines depending on the action of granulocyte and macrophage colony stimulating factor (GM-CSF) and thrombopoietin

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101
Q

How does granulocyte production occur?

A

Cytokines in different development stages – most important = interleukin-3, granulocyte colony stimulating factor and GM-CSF

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102
Q

What stimulates monocyte/macrophage differentiation?

A

GM-CSF then macrophage colony stimulating factor (G-CSF)

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103
Q

What stimulates eosinophil differentiation?

A

GM-CSF and interleukin-5

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104
Q

What stimulates basophil differentiation?

A

Interleukin-3 and 4

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105
Q

Difference between T and B lymphocyte development?

A

B complete most of it in bone marrow
T are generated in thymus from precursor cells that migrate from bone marrow

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106
Q

What do erythrocytic diseases cause?

A

Anaemia (no. of erythrocytes and o2-carrying capacity is not sufficient for body’s physiological needs)

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107
Q

What causes anaemia?

A

Iron deficiency, nutritional deficiencies, acute and chronic inflammation, parasitic infection, inherited/acquired disorders affecting haemoglobin synthesis/RBC production and survival

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108
Q

How does anaemia affect erythrocytes?

A

Affects number, size and colour

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109
Q

What are macrocytic anaemias?

A

Enlarges erythrocytes (defective maturation) to become reticulocytes — causes vitamin deficiencies

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110
Q

What is microcytic anaemia?

A

Shrinks erythrocytes due to abnormal haemoglobin production

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111
Q

What is an example of a microcytic anaemia?

A

Thalassemia

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112
Q

What is normocytic anaemia?

A

Reduced erythrocytes due to normal factors like cancer, viruses, chronic kidney disease, RBC destruction

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113
Q

Examples of normocytic anaemia?

A

Sickle cell anaemia, autoimmune haemolytic anaemia

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114
Q

What is autoimmune haemolytic anaemia?

A

When the body produces auto-antibodies against erythrocyte antigens so immune system targets them — these antibody-opsonised erythrocytes are phagocytosed by macrophages in the spleen which damages the membrane and cases haemolysis = spherical erythrocytes and then the complement system is activated and lysis occurs

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115
Q

Why can autoimmune haemolytic anaemia not be treated with a blood transfusion?

A

The auto-antibodies are directed against high incidence antigens on all erythrocytes

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116
Q

Symptoms of autoimmune haemolytic anaemia?

A

Fatigue, dizziness, dysponea on exertion (due to low O2), jaundice, tea-coloured urine (increased bilirubin in plasma = increased urobilin in urine)

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117
Q

How is autoimmune haemolytic anaemia diagnosed?

A

Direct Coombs test
- Uses anti-human antibodies that bind to human antibodies
- If disease is present there will be an agglutination in the bottom of the tube as the auto-antibodies on the erythrocytes’ surface are tagged

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118
Q

2 treatment options of autoimmune haemolytic anaemia?

A
  1. Immunosuppressive therapy using corticosteroids that suppress immune system (prevents RBC destruction)
  2. Plasmapheresis – filters blood, removes harmful antibodies
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119
Q

What is sickle cell anaemia?

A

RBCs become sickle shaped and do not flow well due to sticky and inflexible nature and they get stuck at branch points and in small blood vessels which can block blood flow, stopping oxygen-rich blood movement = sickle cell crisis and organ damage

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120
Q

What causes sickle cell anaemia?

A

Point mutation in gene encoding beta haemoglobin – changes glutamic acid to valine = haemoglobin changes shape and clumps and causes rigid, non-liquid protein strands to form in RBCs in hypoxic conditions = sickle shape

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121
Q

How does sickle cell cause anaemia?

A

The cells block the spleen filter (also causes spleen damage)

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121
Q

Diagnosis of sickle cell anaemia?

A

Blood test for haemoglobin S (defective)

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121
Q

Symptoms of sickle cell anaemia?

A

Anaemia, fatigue, frequent infection, sickle cell crisis

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122
Q

Treatment of sickle cell anaemia?

A

Blood transfusion, bone marrow transplant

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123
Q

Why is having sickle cell anaemia a benefit in malaria regions?

A

Cells rupture prematurely and cannot host parasite

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124
Q

What is thalassemia?

A

Mutations cause unpaired globin polypeptide chains = aggregates and precipitate = RBC damage and lysis

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125
Q

What causes thalassemia?

A

Mutations or deletions in haemoglobin gene (either alpha or beta) = insufficient haemoglobin production = anaemia

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126
Q

Symptoms of thalassemia?

A

Anaemia, fatigue, palpitations, shortness of breath, bone distortion, hepatosplenomegaly (enlarged liver and spleen)

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127
Q

What causes hepatosplenomegaly?

A

Extramedullary heamatopoiesis to produce more erythrocytes

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128
Q

Diagnosis of thalassemia?

A

Blood or genetic testing

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129
Q

Treatment of thalassemia?

A

Blood transfusion, folic acid supplements (promotes erythropoiesis), bone marrow in severe child cases

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130
Q

What must occur alongside blood transfusion in thalassemia?

A

Iron chelation to remove excess iron build up

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131
Q

What is cyclic neutropenia?

A

A leukocytic disease that is an autosomal blood disorder caused by mutations in the ELANE gene (encodes neutrophil elastase) which causes neutrophil maturation failure

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132
Q

How does cyclic neutropenia work?

A

Normally neutrophil elastase inhibits neutrophil differentiation but when mutated it is excessively inhibitory so there are longer trough periods of decrease to 0 every 3 weeks and then for up to 5 days it rebounds

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133
Q

Symptoms of cyclic neutropenia?

A

Frequent infections, fever, ulcers of mucous membranes in mouth

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134
Q

Diagnosis of cyclic neutropenia?

A

Blood cell count, bone marrow biopsy

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135
Q

Treatment of cyclic neutropenia?

A

Stimulation of neutrophil production e.g. granulocyte colony-stimulating factor treatment or haematopoietic stem cell transplant

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136
Q

What is leukocytosis?

A

Increased number of leukocytes

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137
Q

What are the 5 types of leukocytosis?

A
  1. Neutrophilia = infections and inflammation
  2. Lymphocytosis = viral infections and leukaemia
  3. Monocytosis = certain infections and cancer
  4. Eosinophilia = allaergies and parasites
  5. Basophilia = leukaemia
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138
Q

Diagnosis of leukocytosis?

A

Blood cell counting

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139
Q

6 treatments for leukocytosis?

A
  1. Antibiotics for infection
  2. Anti-inflammatories for inflammation
  3. Antihistamine/inhaler for allergic reaction
  4. Chemotherapy/radiation/stem cell transplant for leukaemia
  5. Medication changes if a drug is causing it
  6. Treatment for causes of stress and anxiety
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140
Q

What is leukaemia?

A

Cancer of WBCs due to DNA damage/mutation during haematopoiesis - starts in blood-forming tissue to over-produce abnormal, immature WBCs

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141
Q

2 types of leukaemia?

A
  1. Acute myeloid leukaemia
  2. Chronic myeloid leukaemia
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142
Q

Characteristics of acute myeloid leukaemia?

A

Abnormal differentiation of myeloid cells, accumulation of immature myeloid precursor cells in bone marrow and peripheral blood which causes differentiated RBCs, platelets and WBC shortage

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143
Q

What does chronic myeloid leukaemia cause?

A

Splenomegaly due to more differentiated myeloid cells in blood

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144
Q

Symptoms of leukaemia?

A

Anaemia, weakness, tiredness, shortness of breath, light-headed, palpitations, frequent infection, fever, malaise, sweating, bleeding and bruising, heavy periods, nosebleeds, bleeding gums

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145
Q

Diagnosis of leukaemia?

A

Full blood count, genetic testing, X-rays, scans, lumbar puncture, bone marrow biopsy

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146
Q

7 steps of HIV?

A
  1. Glycoprotein spikes on HIV virions recognise and bind CD4 reeptors and CCR5 coreceptor on surface
  2. HIV endocytosed
  3. HIV injects viral enzymes (including transcriptase and integrase) and RNA
  4. Reverse transcriptase transcribes single stranded RNA genome of HIV into cDNA
  5. Reverse transcriptase uses host cell’s DNA polymerase to create double stranded viral DNA
  6. Viral integrase integrates viral DNA into host cell genome so it produces viral mRNA and protein
  7. Protein forms viral particles that bud off of T cell and infect other CD4+ T cells
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147
Q

Why does HIV cause loss of immunity?

A

Infects and destroys CD4+ helper T cells that normally produce cytokines to activate immune cells

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148
Q

What does HIV also cause?

A

Chronic inflammation that inhibits haematopoiesis which slows CD4+ cell production

Thymus can become infected which inhibits T-cell maturation

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149
Q

What can HIV lead to?

A

Acquired immune deficiency syndrome (AIDS) as cell mediated immunity can be fully lost eventually

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150
Q

Symptoms of HIV?

A

Short flu-like symptoms in early weeks, then asymptomatic for years but immune damage is occurring

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151
Q

Diagnosis of HIV?

A

Blood, saliva or blood spot tests

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152
Q

Treatment of HIV?

A

Post-exposure prophylaxis if patient was at risk, antiretroviral meds to prevent viral replication

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153
Q

What is haemophilia?

A

An X-linked recessive platelet disorder caused by mutation and deficiency in clotting factors = clotting is defective

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154
Q

Why are clotting factors important?

A

Convert prothrombin to thrombin and fibrinogen to fibrin

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155
Q

What is the difference between haemophilia A and B? (cause)

A

A is factor VIII deficiency, B is factor IX deficiency

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156
Q

Symptoms of haemophilia?

A

Internal/external bleeding after injury, spontaneous bleeding into joints (chronic pain and disability)

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157
Q

Diagnosis of haemophilia?

A

Blood test, amniocentesis prenatally if family history

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158
Q

Treatment of haemophilia?

A

No long term cure but replacement therapy for clotting factors or gene therapy works

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159
Q

What is gene therapy in haemophilia?

A

Functional copy of clotting factor is packaged in a recombinant adeno-associated viral vector that is then taken up into liver cells and expressed

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160
Q

2 layers of glisson’s capsule?

A
  1. Serosa outer (mesothelium, single squamous epithelium)
  2. Fibrous inner (fibroplasts like collagen)
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161
Q

What is the liver blood supply?

A
  1. 25% of cardiac output from hepatic artery
  2. Portal vein – from intestine, left gastric vein (stomach and oesophagus) and superior mesenteric (rectum)
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162
Q

2 types of liver cells?

A
  1. Parenchymal (hepatocytes)
  2. Non-parenchymal
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163
Q

What are types of parenchymal cells?

A

Periportal, intermediate and perivenous

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164
Q

What are types of non-parenchymal?

A

Endothelial, kupffer, lipocytes, biliary epithelial (cholangiocytes)

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165
Q

What is the liver made up of?

A

Liver lobules that have a portal triad on each point of the hexagon shaped lobule

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166
Q

What is a portal triad?

A

Branch of hepatic artery, branch of portal vein and a bile duct

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167
Q

Where does the central vein drain in the liver and how does it differ to the portal triad?

A

Drains at sinusoid
Has lower O2 but more waste products

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168
Q

Where does the blood in the central vein come from?

A

Mixing of blood from hepatic artery and portal vein

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169
Q

What does the central vein link?

A

Porto-venous axix

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170
Q

What is the order of hepatocytes in the direction of portal triad into the central vein/porto-venous axis?

A

Periportal –> intermediate –> perivenous

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171
Q

Which hepatocytes have the highest glucose?
Waste?

A

Periportal
Perivenous

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172
Q

Why are periportal more oxidative than perivenous?

A

More o2 in periportal means there are more enzymes for oxidative reactions

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173
Q

What is metabolic zonation in the liver?

A

Different reactions occur in each hepatocyte type

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174
Q

How are hepatocytes polarised?

A

Apical (upper) and basolateral (bottom near endothelial cells of sinusoid)

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175
Q

How do bile acids leave hepatocytes?

A

Via apical membrane

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176
Q

What is enterohepatic circulation?

A

Bile produced by liver –> enters gall bladder via bile duct –> when gall bladder is full the bile empties into small intestine and emulsifies fats –> reabsorbed into portal vein into liver

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177
Q

4 functions of the liver?

A
  1. Metabolic (glucose production, gluconeogenesis, store glucose in form of glycogen, makes cholesterol)
  2. Protein synthesis (plasma proteins, clotting factors)
  3. Solubilsation and transport (bile synthesis, transferrin)
  4. Protection (detoxification phases i and iii, urea cycle, clearance of bacteria by kupffer cells)
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178
Q

What is gluconeogenesis?

A

Partial glycolysis reversal with non-equilibrium reactions that must be separate and distinct

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179
Q

3 non-reversible gluconeogenesis reactions? (and their forward and reverse enzymes)

A
  1. Glucose –> G6P (f = glucokinase, r = glucose-6-phosphatase)
  2. Fructose-6-phosphate –> fructose-1,6-diphosphate (f = PFK, r = phosphatase)
  3. PEP –> pyruvate (forward), pyruvate –> oxaloacetate –> PEP (reverse)
    Enzymes = pyruvate carboxylase, PEPCK
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180
Q

What is albumin used for?

A

Binding/carrier for hormones and fatty acids AND osmoregulation

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181
Q

What carries:
- Copper?
- Iron?
- Thyroid hormone and vitamin A?

A
  • Ceruloplasmin (up to 6)
  • Transferrin (2 at a time)
  • Transthyretin
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182
Q

How does transferrin (TFN) transport iron?

A

Fe binds to form TFN-Fe which changes conformation which makes it a higher affinity for TFN receptors on cells so TFN-Fe enters internalised endocytic pathway which makes cell more acidic so complex disassociates and Fe is in the cell and TFN via blood and TFN receptor goes back to cell surface

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183
Q

What are endobiotics?

A

Naturally produced substances that require metabolism to regulate their levels or facilitate their excretion (such as bilirubin)

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184
Q

2 phases of bilirubin biotransformation?

A

Phase I = oxidative and reductive reactions by addin o2 to functional groups
Phase II = covalent attachment of endobiotic drugs that are water soluble

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185
Q

What is bilirubin made into?

A

Bilirubin gluconuride (catalysed by UDP-glucuronosyltransferase) by adding water soluble glucuronic acid

186
Q

Why must NH3 be removed?

A

It can cause hepatic encephalopathy

187
Q

How is NH3 removed?

A

Urea cycle:
1. Converted to carbonyl phosphate (by carbonyl phosphate synthetase)

  1. Then into citrulline with ornithine (by ornithine transcarboxylase)
  2. Then aginosuccinate with aspartate
    (by arginosuccinate syntase)
  3. Then arginine with fumarate
    (by arginosuccinate lyase)
  4. Then ornithine
    (by arginine)

RELEASING UREA

188
Q

What is glutathione for?

A

Reducing agent preventing oxidative damage

189
Q

2 categories of liver disease?

A
  1. Reversible or irreversible
  2. Acute or chronic
190
Q

Scale of acute liver disease?

A

Mild (viral hepatitis) or severe fulminant hepatic failure that can require a transplant

191
Q

How does chronic liver disease occur?

A

It is progressive and can be caused by alcoholism that can result in cirrhosis that reduces liver function

192
Q

Characteristics of hepatocytes?

A

Quiescent and can proliferate (not in severe damage)

193
Q

What can treat liver disease?

A

Bio artificial liver that pumps blood through that is then detoxified

194
Q

What is irreversible liver disease?

A

Loss of hepatocyte function that results in difficulty regulating blood glucose

195
Q

What does portal to system shunting in irreversible liver disease cause?

A

Increases liver blood pressure which causes back pressure, increased hepatocyte pressure

196
Q

What do stellate cells on sinusoidal membranes in the liver do?

A

Store vitamin A and can produce ECM (containing fibrin, collagen and proteoglycans) in response to injury

197
Q

How can ECM deposition from stellate cells cause rupture and bleeding out?

A

ECM deposition narrows the sinusoid and causes higher blood pressure which results in backflow into the portal vein which increases venal pressure — veins have thin walls so they bulge and form varices (can rupture)

198
Q

What is Poiseulle’s law?

A

Q = pi x p x r^4 / 8 x n x l
(Q is flow, p is pressure, r is radius, n is a constant, l is length)
!/r^4 is proportional to pressure

199
Q

3 manifestations of liver dysfunction due to loss of hepatocytes?

A
  1. Metabolic = lowered glucose (hypoglycaemia), lipid accumulation in liver (hyperlipidaemia), protein metabolism changed so more NH3 releases and less urea produced
  2. Solubilisation = bile acids not produced effectively = poor fat emulsification = lipids not absorbed = fatty faeces (steatorrhoea)
  3. Detoxification = THIS PROCESS BEING DYSREGULATED CAUSES JAUNDICE
    phase ii involves glucuronidation involves bilirubin (from haemoglobin) being combined with water soluble UDP-glucuronic acid to form bilirubin glucuronide (catalysed by bilirubin UDP-glucuronosyl transferase)
200
Q

What is jaundice?

A

Deficiency of UDP-glucuronosyl transferase meaning bilirubin cannot be broken down

201
Q

What can cause jaundice?

A

Bile duct obstruction by gallstones or cancer

202
Q

What is an adverse effect of ethanol on drugs?

A

Ethanol can cause liver to produce more drug-metabolising enzymes which break down drugs such as warfarin quicker which reduces their effectiveness

203
Q

What does lower synthesis of plasma proteins in liver disease cause?

A

Reduced albumin causes oncotic pressure dysregulation and water cannot enter vessels so fluid build up (ascites) occurs due to increased hydrostatic pressure
Causes reduced coagulation too

204
Q

What can altered NH3 metabolism be treated with?

A

Lactulose (causes osmotic diarrhoea to release it)

205
Q

What is gynaecomastia (symptoms of liver disease)?

A

Altered hormone clearance causes lower androgen clearance (increases blood conc) which increases oestrogen via aromatisation (conversion) in periphery (increased breast tissue and testicular atrophy)

206
Q

What causes hepatic encephalopathy?

A

Terminal liver failure — ammonia has crossed blood brain barrier (irreversible)

207
Q

What is the causes of ascites development?

A

Portal hypertension

208
Q

What does endocrinology treat?

A

Hormonal disorders

209
Q

What does adrenal medulla secrete?

A

Catecholamine hormones like epinephrine and norepinephrine

210
Q

What does adrenal cortex secrete?

A

Steroid hormones

211
Q

3 types of steroid hormones?

A
  1. Glucocorticoids (cortisol and cortisone) that regulate carbs, fat and protein metabolism
  2. Mineralocorticoids (aldosterone) that regulate Na and K balance
  3. Sex steroids (androgens)
212
Q

What is cushing’s?

A

Hypercortisolaemia (raised cortisol)

213
Q

Difference between Cushing’s syndrome and disease?

A

Syndrome is the symptoms resulting from high cortisol

Disease is a subtype of syndrome caused by an ACTH-producing pituitary tumour and chronic exposure to excessive levels of circulating glucocorticoids

214
Q

What surrounds adrenal glands?

A

Fibrous capsule

215
Q

3 layers of adrenal cortex (outer to inner)?

A
  1. Zona Glomerulosa
  2. Zona Fascilulata
  3. Zona Reticularis
216
Q

What does the zona glomerulosa secrete (adrenal)?

A

Mineralocorticoids like aldosterone

217
Q

What do zona fascilulata and zona reticularis (adrenal) secrete?

A

Glucocorticoids like cortisol and corticosterone, sex hormones like androgens/dehydroepiandrosterone

218
Q

What are steroid hormones synthesised from?

A

Cholesterol

219
Q

Are cortisol and corticosterone secreted in a bound or unbound state?

A

Unbound but in the cytoplasm they are bound to corticosteroid binding globulin (CBG, also known as transcortin)

220
Q
A
221
Q

6 hormones secreted by anterior pituitary?

A

Basophilic cells secrete follicle stimulating hormone (FSH), leutinising hormone (LH), adenocorticotropic hormone (ACTH) and thyroid growth hormone (TSH)

Acidophilic cells secrete growth hormone and prolactin

222
Q

What hormones does the posterior pituitary secrete?

A

Oxytocin and vasopressin

223
Q

How is cortisol secretion controlled?

A

Corticotropin releasing hormone (CRH) is produced in the hypothalamus and transported to the anterior pituitary and released to stimulate ACTH release which stimulates cortisol secretion from adrenal cortex – cortisol feedsback and inhibits CRH and ACTH secretion (negative feedback)
ACTH is said to be diurnal

224
Q

What does cortisol do when it binds to the glucocorticoid receptor?

A

Translocates into the nucleus where the complex acts as a transcription factor that regulates target gene expression via glucocorticoid response element (GRE) in promoter region

225
Q

Effect of glucocorticoids on muscle?

A

Catabolic effect that decreases glucose uptake, metabolism and protein synthesis but increases amino acid release

226
Q

Effect of glucocorticoids on fat?

A

Lipolytic effect that stimulates lipolysis and increases free fatty acids and glycerol release

227
Q

Effect of glucocorticoids on liver?

A

Synthetic effect that increases glycogen synthesis, gluconeogenesis and blood glucose

228
Q

Effect of glucocorticoids on immune system?

A
  1. Suppression effect whereby circulating monocytes, lymphocytes, basophils and eosinophils are decreased
  2. Anti-inflammatory effect whereby migration of neutrophils to site of injury is decreased
229
Q

Difference between iatrogenic and non-iatrogenic?

A

Iatrogenic = due to external factor like intake of oral corticosteroids

Non-iatrogenic = disease

230
Q

3 types of Cushing’s?

A
  1. ACTH-dependent Cushing’s
  2. Ectopic ACTH syndrome
  3. ACTH-independent Cushing’s
231
Q

What is ACTH-dependent Cushing’s?

A

ACTH-secreting pituitary adenoma (benign tumour of epithelial origin) that causes increased ACTH
68% of Cushing’s cases and is common 20-40 year olds and more in women

232
Q

What is ectopic ACTH syndome?

A

ACTH secreting tumour in the lung (small cell carcinoma) or bronchial carcinoid tumour
15% if Cushing’s, 40-60 year olds, more in men

233
Q

What is ACTH independent Cushing’s?

A

Adrenocortical tumour that secretes excess cortisol (either adenoma or carcinoma)
17% of cases, 35-40 year olds, more in women

234
Q

How is the ACTH/cortisol feedback loop disrupted in Cushing’s?

A

There is a loss of feedback inhibition due to increased ACTH secretion and a loss of cortisol sensitivity

235
Q

Clinical features of Cushing’s disease?

A

Moon face, buffalo hump, thin extremeties, striae, diabetes mellitus, muscle wasting, fat trunk or abdomen, psychiatric effects

236
Q

Why may Cushing’s patients have headaches and problems with peripheral vision?

A

Headaches caused by pituitary tumour stretching dura

Decreased peripheral vision as pituitary gland sits below optic chiasma (any swelling of adenoma will press on this and reduce vision)

237
Q

Why do some Cushing’s patients have diabetes mellitus?

A

Cortisol increases glucose synthesis (increased expression of G6P) in liver, decreases glucose uptake into fat and muscle, increased lipolysis (more fatty acids to be used instead of glucose for energy)

238
Q

Why do Cushing’s patients have muscle wasting?

A

Decreased protein synthesis and increased protein catabolism

239
Q

Why do Cushing’s patients have obesity/fat redistribution?

A

Central adiposity — redistribution of body fat

240
Q

How does high cortisol prevent glucose from entering fat or muscle cells?

A

It inhibits insulin-stimulated GLUT4 translocation

241
Q

How does Cushing’s affect the skin?

A

Striae (stretch marks), skin thinning (due to glucocorticoids inhibiting fibroplast proliferation and decreasing collagen synthesis), easy bruising as subcutaneous fat depots increase which thins the skin and ruptures subdermal tissues

242
Q

Treatment of Cushing’s?

A

Pituitary = transsphenoidal hypophysectomy and replacement therapy for hormones

Adrenal = bilateral adrenalectomy and steroid replacement therapy

243
Q

How does blood enter and leave kidneys?

A

In via renal arteries and out via renal veins that carry it to the inferior vena cava

244
Q

Role of kidneys?

A

Maintains homeostasis of water, electrolytes and pH via filtration and reabsorption (excess removed in urine) and removes toxic waste products

245
Q

What do nephrons do?

A

Filter blood and transport filtrate to medullary pyramids and eventually bladder

246
Q

4 steps of filtration in the kidneys?

A
  1. Blood from renal artery enters aterioles then glomeruli capillaries and it is filtered to remove small molecules, ions and water
  2. Filtrate enters renal tubules (weaves in and out of cortex and medulla) into proximal convoluted tubule (ions + small molecules reabsorbed) then narrow descending loop of Henle and then wide ascending
  3. Into distal convoluted tubule and then collecting duct
  4. Renal tubules link glomerulus to renal pelvis which links kidney to ureter and bladder
247
Q

Histology of kidney cortex?

A

Contains renal corpuscles (glomerulus and bowmans capsule) – causes intense stain, dense and containing round structures — tubules fill most of the space (rings) and most are proximal

248
Q

Histology of kidney medulla?

A

Many ring-like structures (cross sections of loop of henle and collecting ducts — henle has a thinner and thicker loop, collecting ducts widest)

249
Q

3 functions of the kidney?

A
  1. Filtration of blood plasma
  2. Regulation of blood pressure
  3. Regulation of erythropoiesis
250
Q

3 steps of blood plasma filtration?

A
  1. Glomerular filtration
  2. Tubular reabsorption
  3. Tubular secretion
251
Q

How does glomerular filtration work?

A

Blood enters glomerulus through afferent arteriole and water and small hydrophobic molecules leave the capillary through fenestrated endothelial cells that line the capillaries, the blood then leaves through efferent arteriole

252
Q

What is the Bowmans capsule?

A

Single layer of flattened cells surrounding the glomerulus

253
Q

Role of podocytes in glomerular filtration?

A

They are specialised endothelial cells that have extensions that wrap around capillaries to increase SA and increase filtration efficiency
Also creates filtration barrier with fenestrated endothelium

254
Q

2 ways water and solutes are transporter across tubular epithelial cells lining renal tubules into the renal interstitial fluid and then across peritubular capillary membrane?

A
  1. Paracellularly = between tubular cells
  2. Transcellularly = through tubular cells
255
Q

How is transcellular tubular reabsorption path done?

A

Active transport, passive diffusion or osmosis

256
Q

How does transport into peritubular capillary work?

A

Bulk flow and is mediated by hydrostatic and osmotic force

257
Q

What do proximal convoluted tubules have to increase SA and why?

A

They are lined with tall cuboidal cells with microvilli which create brush border for facilitated diffusion of glucose and amino acids

258
Q

Why is plasma membrane of basal surface of proximal convoluted infolded?

A

Increases SA for Na+ pumps

259
Q

How do the descending and ascending limbs of loop of henle differ?

A

Descending = simple squamous with no microvilli or infolding and few mitochondria (no active transport)

Ascending = simple cuboidal, no microvilli, extensive infolding of basal membrane

260
Q

What is the distal convoluted tubule like?

A

Lined with simple cuboidal epithelium and extensive infolding with many mitochondria

261
Q

How is collecting duct suited to its function?

A

Lined with 2 types of simple columnar epithelial cells:

  1. Principle cells (continue reabsorption and express aquaporins)
  2. Intercalated cells (have microvilli, role in regulating acid-base balance of glomerular filtrate
262
Q

What is tubular secretion in the distal convoluted tubule?

A

Absorption into tubules from blood can occur as a secretory process if there is high concentrations of solutes and wastes in the blood in peritubular capillaries

263
Q

Why is [Na+] a deteriminant in blood pressure?

A

Osmosis - high salt intake increases [Na+] = draws water out of blood vessels into surrounding tissues = increased intravascular fluid volume = increased cardiac output = increased peripheral resistance = increased blood pressure

264
Q

How do kidneys regulate blood pressure?

A

Distal convoluted cells in macula dense detect blood [Na+] and fluid flow and regulate via renin-angiotensin system

265
Q

5 steps of kidneys regulating low bp?

A
  1. Low fluid flow/[Na+] detected = juxtaglomerular cells secrete renin
  2. Renin cleaves angiotensinogen to remove 10 amino acids = angiotensin i
  3. Angiotensin i concerted to angiotensin ii by angiotensin converting enzyme
  4. Angiotensin increases bp
  5. Increase in bp detected by juxtaglomerular cells = renin release ceases
266
Q

4 ways angiotensin ii increases blood pressure?

A
  1. Vasoconstriction = increased peripheral resistance –> cardiac output and then bp
  2. Alsodesterone release so Na uptake/reabsorption by nephrons increases to increase blood Na+
  3. Direct promoting of Na+/water reabsorption in distal convoluted tubules to increase blood volume (and bp)
  4. ADH release from pituitary = aquaporin mobilisation = increased blood volume (and bp)
267
Q

How do kidneys regulated erythropoiesis (RBC generation in bone marrow)?

A

Kidney secretes erythropoietin in hypoxic conditions:
– hypoxia-inducible transcription factor 1 binds to enhancer region of erythropoietin gene = increased expression = release into blood where it binds to erythropoietin receptors on erythrocyte prgenitor cells = increased RBC production

268
Q

What does renal failure cause?

A

Build-up of waste products and water in the blood and a lack of homeostasis of ions and small molecules

269
Q

Causes of acute renal failure? (4)

A
  1. Drugs/medication being combined (nephron damage)
  2. Inflammatory diseases like vasculitis or glomerulonephritin (nephron damage)
  3. Tubular necrosis (due to factors like nephrotoxic drugs and ischaemia) = tubular epithelial cell death which slough off = blocked lumen of tubules
  4. Urinary tract obstruction = increased pressure and slowed urine production = increased pressure and swelling = nephron damage
270
Q

Why is acute renal failure usually reversible?

A

Damaged nephrons can be regenerated

271
Q

What is chronic renal failure caused by?

A

Diabetes (glucose damages filtration units), hypertension (high bp causes damage), medication, repeated acute renal failure

272
Q

Why is chronic renal failure irreversible?

A

Irreversible nephron loss = fewer nephrons = increased glomerular filtration pressure and hyperfiltration = fibrosis and scarring = further nephron damage

273
Q

6 manifestations of altered kidney function?

A
  1. Uremia (nitrogen-containing waste product build up)
  2. Increased hormone build-up (decreased metabolic clearance, changed feedback and secretion patterns)
  3. Loss of normal kidney products
  4. Reduced body temperature
  5. Increased Na+, K+ and water in blood
  6. Haematological abnormalities
274
Q

What does increased Na+, K+ and water in the blood cause?

A
  1. Congestive heart failure (osmotic balance disrupted, increased blood volume and bp)
  2. Oedema/ascites (water accumulated in peripheral tissues and abdominal cavity)
  3. Hyponatemia (excessive water consumption lowers [Na+] = fatigue, muscle spasms and vomiting)
  4. Hyperkalemia (increased K+ = fatal abnormal heart arythmias as K+ changes cardiomyocyte cell membrane polarisation so resting potential is closer to threshold which can cause ventricular fibrillation (uncoordinated contraction) and asystole
275
Q

What are haematological abnormalities?

A

Anaemia, increased susceptibility to infections due to leukocyte suppression by uremic toxins, altered clotting parameters = increased bruising, blood loss in surgery, and risk of spontaneous haemorrhage

276
Q

2 ways renal failure is diagnosed?

A

Blood tests:
1. Serum creatine test = creatinine levels show glomerular function and filtration rate as it is a waste product from muscle metabolism/protein digestion/metabolism (could also use albumin to creatine ratio)
2. Blood urea nitrogen test

277
Q

What is the ‘pump’ of the lungs composed of?

A

Chest wall, respiratory muscles to alter thoracic cavity size, brain regions controlling muscles, and the pathways and nerves linking that

278
Q

3 interconnected regions of airflow?

A
  1. Upper airway (nasal passages and pharynx)
  2. Conducting airway (trachea, bronchi, bronchioles, terminal bronchioles — conduct inhaled air into lungs)
  3. Alveolar/respiratory airway (respiratory bronchioles, alveolar ducts, alveolar sacs — where gas exchange occurs)
279
Q

Why does the right lung have 3 lobes (upper, middle and lower) but the left has only 2?

A

Slightly smaller to make room for the heart

280
Q

What are the lungs covered in?

A

Pleura (tissue layer consisting of outer/parietal membrane and inner/visceral membrane – difference is pleural cavity)

281
Q

What is the pleural cavity?

A

Thin layer of fluid that acts as a lubricant to allow lungs to slip smoothly as they expand and contract

282
Q

What does the pleural membrane contain?

A

Layer of mesothelium and a layer of underlying elastic fibrous connective tissue

283
Q

4 parts of cellular architecture of respiratory system of the lungs?

A
  1. Airway mucosa = layer of mucous/surfactant, an epithelial layer and a basement membrane
  2. Lamina propria = loose connective tissue containing capillaries
  3. Layer of smooth muscle cells (in trachea/bronchus/bronchioles)
  4. Fibrocartilaginous layer (in trachea/some bronchioles)
284
Q

What are the trachea and bronchus lined with?

A

Pseudostratified epithelium (looks stratified/layer but its just dense cells)

285
Q

What is the role of ciliated and secretory cells in epithelium in trachea and bronchus?

A

Innate immunity in airway

286
Q

What is the role of basal cells in epithelium in trachea and bronchus?

A

Progenitor cells in injury

287
Q

What is the role of goblet cells in epithelium in trachea and bronchus?

A

Mucous secretion for lubrication and removal of particulate matter/pathogens via coughing

288
Q

What is the role of ciliated epithelial cells in epithelium in trachea and bronchus?

A

Removal of inhaled particles

289
Q

What is the role of secretory epithelial cells in epithelium in trachea and bronchus?

A

Secrete surfactant proteins, defensins, peptides, proteases, reactive oxygen species, reactive nitrogen species = anti-microbials

290
Q

What is the role of epithelial cells in epithelium in trachea and bronchus?

A

Secrete chemokines and cytokines in infections

291
Q

What provides strength and protection to trachea and bronchus?

A

Layer of cartilage

292
Q

What cells do bronchioles contain?

A
  1. Non-ciliated epithelial cells like club/clara cells
  2. Ciliated cells
293
Q

Role of club cells?

A

Secrete defence markers and act as progenitor cells post-injury

294
Q

Why are alveoli surrounded by pulmonary capillaries?

A

Gas exchange

295
Q

2 types of epithelial cells in alveoli?

A

Type 1 = thin, squamous, large cytoplasmic extensions, make up thin-walled layer of lining

Type 2 = thicker, cuboidal, contain granules, produce and store surfactant (stored in lamella inclusion bodies)

296
Q

What is the arrangement of alveoli like?

A

Loose,open with many air pockets, close contact with pulmonary capillaries (only separated by their respective endothelium), connected by alveolar walls (contain network of connective tissue fibres called interstitium)

297
Q

5 functions of respiratory system?

A
  1. Inhalation and exhalation (pulmonary ventilation)
  2. External respiration (gas exchange lungs and air)
  3. Internal respiration (gas exchange blood and cells)
  4. Phonation (air vibrating around vocal cords to create sound)
  5. Olfaction (chemical sensation for smelling)
298
Q

Differences between mechanisms of inhalation and exhalation?

A

Inhalation = diaphragm moves down, intercostal muscles pull up, volume of chest increases, air in

Exhalation = diaphragm relaxes and moves up, intercostal muscles relax and move down, reduced chest cavity, air forced out

299
Q

How is inhalation and exhalation measured?

A

Spirometry = graphic record of different volumes being combined to give total lung capacity

300
Q

Mechanism of gaining oxygen rich blood?

A

O2 poor blood enters lungs via pulmonary artery and divides into capillary network to alveoli — CO2 enters alveolar space through type 1 epithelial cells and o2 leaves into blood and this goes to heart for circulation via pulmonary vein

301
Q

What is surfactant for?

A

Pathogen defence and reducing surface tension (allows alveolus expansion = increased SA)

302
Q

What does surfactant contain?

A
  1. Surfactant proteins
  2. Phospholipids like DPPC to reduce surface tension
303
Q

4 surfactant proteins?

A
  1. SP-A = activates macrophages, can induce uterine contractions
  2. SP-B = organised into tubular network to reduce surface tension
  3. SP-C = enhances phospholipid function to reduce surface tension
  4. SP-D = role in pathogen defence
304
Q

How does surfactant increase SA by reducing surface tension?

A

Surface tension allows liquids to acquire a small SA as the molecules of water at the surface are solely attracted sideways and downwards —- inner alveoli surface contains alveolar fluid (water) and the molecules are attracted to one another so reducing it = increased SA

305
Q

4 other functions of surfactant?

A
  1. Reduces collapse of under-inflated alveoli (atelcatasis)
  2. Provides more even distribution of ventilation amongst alveoli
  3. Improves lung compliance
  4. Infection protection
306
Q

Why do premature babies usually exhibit cyanosis and rapid/shallow breathing?

How is it treated?

A

Lack surfactant so gas exchange is less efficient and blood o2 is lower

Mechanical ventilation and antenatal corticosteroid administration to induce surfactant production by type 2 cells

307
Q

What is Chronic Obstructive Pulmonary Disease (COPD) an umbrella term for?

A

Chronic bronchitis, emphysema, asthma (all cause progressive lung damage)

308
Q

What can COPD cause?

A

Reduced conducting airway diameter (fixed airway obstruction) that leads to increased resistance during ventilation and reduced air flow to the lungs

309
Q

What can cause fixed airway obstruction?

A

Increased secretions and inflammation, bronchial smooth muscle contraction, loss of supporting structures and airway collapse

310
Q

Symptoms of COPD?

A

Chronic cough, wheezing, frequent chest infection, breathlessness, fatigue, muscle wasting

311
Q

Main cause of chronic bronchitis and emphysema?

A

Smoking

312
Q

What is chronic bronchitis?

A

Airway obstruction caused by mucous thickening and hypersecretion of mucous – also causes crackling and wheezing

313
Q

What does co2 build-up normally cause?

A

Hyperventilation to remove it (not in chronic bronchitis patients as they have a resistance to co2)

314
Q

6 pathogenesis of chronic bronchitis?

A
  1. Inhalation of noxious particles = mucousal infllamation = increased wall thickness = narrow lumen
  2. Blockage/narrowing of bronchioles = prevented efficient gas exchange = hypoxia and hypercapnia (co2 build-up)
  3. Hypercapnia = respiratory acidosis (excess co2 reacts with water = carbonic acid\0
  4. Alveolar hypoxia
  5. Right sided heart failure
  6. Fluid retention
315
Q

What does alveolar hypoxia cause?

A

Polycythaemia (increased RBC production), cyanosis, hypoxic pulmonary vasoconstriction (due to lack of o2), pulmonary hypertension, right-sided heart failure, fluid retention

316
Q

How does chronic bronchitis cause right-sided heart failure?

A

O2 poor, co2 rich blood return to right atrium and exits via left and right pulmonary arteries
Constriction of pulmonary blood vessels = hypertension = back flow to right side of heart = sustained backflow = increased workload = hypertrophy

317
Q

How does chronic bronchitis cause fluid retention?

A

Pulmonary hypertension reduced blood flow to left side of heart = lower left ventricular output = reduced cardiac output and blood volume = aldosterone release = water retention = peripheral oedema

318
Q

Difference between visible manifestation of chronic bronchitis vs emphysema?

A

Chronic bronchitis = visible cyanosis and peripheral oedema

Emphysema = pink-tinged skin and barrel chest

319
Q

What does emphysema cause?

A

Dyspnoea (difficulty breathing) and tachypnoea (rapid breathing)

320
Q

Why do emphysema patients have accessory muscles in neck and upper chest?

A

Air trapping = diaphragm and intercostal muscles cannot support breathing alone

321
Q

Why do emphysema patients hyperventilate?

A

In response to increased alveolar co2 levels

322
Q

Why do emphysema patients have progressive alveoli destruction and what does this mean for them?

A

Oxidants inhibit protease inhibitors which activates protease and elastase

Loss of elastin fibres prevents alveolar recoil and causes airway collapse, hypercapnia and hyperventilation

323
Q

Why does emphysema cause lower gas exchange?

A

Connective tissue between alveoli degrades = larger air sacs = lower SA

324
Q

What does improper alveoli recoiling cause?

A

Air trapping = chronically inflated lungs = reduced expiratory reserve volume and vital capacity (but residual volume is higher)

325
Q

What does loss of elasticity and increase in airspace cause?

A

Physiological dead space

326
Q

Role of PNS?

A

Connects CNS to limbs and organs

327
Q

2 components of PNS?

A
  1. Somatic nervous system
  2. Visceral motor system
328
Q

What does somatic nervous system do?

A

Delivers voluntary control of body movements via skeletal muscles

329
Q

What does visceral motor system do?

A

Controlled by autonomic nervous system (involuntary control of smooth muscle and glands)

330
Q

What is an effector?
(what is it in visceral and somatic?)

A

Muscles that contract in response to nerve innervation
Visceral = smooth muscle
Somatic = striated skeletal muscle

331
Q

3 steps of skeletal muscle innervation?

A
  1. Brainstem and spinal cord have local circuit neurons that synapse at the axon with upper motor neurons
  2. Upper motor neurons make synaptic connections with the relevant lower motor neurons
  3. Lower motor neurons transmit information to skeletal muscles (alpha motor neurons directly innervate striated skeletal muscle fibres and can innervate many at once (multiple synapses formed = end plates)
332
Q

What is a motor unit?

A

A neuron and all the muscle fibres it innervates

333
Q

How is ACh synthesised and transported to synsapse?

A

Synthesised at nerve terminals of alpha motor neurons (have many mitochondria for this) from acetyl CoA and choline (catalysed by choline acetyl transferase) and then transported and stored in synaptic vesicles

334
Q

What do postsynaptic membranes usually have a lot of?

A

Folds and indentations to increase the SA

335
Q

What are found on ridges of folds and indentations’ clefts of postsynaptic membrane of a neuromuscular junction and how are they activated?

A

Nicotinic acetylcholine receptors that are activated by Na+ influx into muscle fibre which causes depolarisation (end plate potential) = muscle action potential reached = contraction

336
Q

What happens to excess ACh?

A

Hydrolysed to acetyl choline esterase and choline is recycled

337
Q

What are nicotinic acetylcholine receptors (nAChR)?

A

Ligand gated ion channels with 5 subunits that form a cylinder and 2 ACh binding sites (at alpha-gamma and alpha-delta interfaces)

338
Q

What happens when ACh binds to both nAChR binding sites?

A

Conformational change via twisting mechanism = ion channel opening = Na+ entry into muscle cell = end-plate potential = nAChR closure = ACh unbinds and is degraded

339
Q

How is contraction of muscle triggered?

A

Once end-plate potential reaches -50mV the Na+ channels on muscle cell membrane open = action potential propagated along muscle membrane down the t tubule causing contraction

340
Q

What is myasthenia gravis?

A

An autoimmune disease that causes transient or persistent weakness/abnormal fatigue of skeletal muscles or be limited to ocular muscles (droopy eyelids)

341
Q

What does myasthenia gravis effect?

A

Postsynaptic membrane (loss of folds/indentations = fewer nAChRs) and there are autoantibodies against nAChR or MuSK

342
Q

How can myasthenia gravis be exhibited?

A

Action potential stimulation – will show decreasing amplitude as they cannot sustain a muscle contraction

343
Q

3 possible mechanisms for immunopathogenesis of myasthenia gravis?

A
  1. Inhibition of nAChR
  2. Antigenic modulation
  3. Complement mechanisms
344
Q

How could inhibition of nAChR cause myasthenia gravis?

A

Blocks ACh binding site or ion channel will prevent end-plate potential, action potential and muscle contraction generation
— antibodies bind to loop called main immunogenic region (MIR) in alpha subunit (not on ACh binding site)

345
Q

How could antigenic modulation cause myasthenia gravis?

A

Antibodies can cross-link 2 antigen molecules = cellular signals for accelerated endocytosis and degradation
Autobodies can cross-link 2 nAChRs = internalisation and degradation

346
Q

How could complement mechanisms cause myasthenia gravis?

A

Autoimmune response caused membrane attack complex (MAC) to destroy post-synaptic membrane which causes loss of junctional folds = a loss of action potential

—– occurs as antigen-antibody complex is bound by C1q that recruits C1 complex which cleaves C2 and C4 = C4bC2a (C3 convertase) —- a cascade occurs = MAC production = pores in cell membrane = lysis and destruction

347
Q

What do patients without antibodies against nAChR have?

A

Autoantibodies against other neuromuscular junction proteins associated with nAChRs like MuSK (muscle specific kinase) and low density of lipoprotein receptor related protein 4 (Lrp4) and agrin

348
Q

Why are MuSK, Lrp4 and agrin important for nAChR organisation into clusters at synapse (4 steps)?

A
  1. Agrin is secreted by motor nerve terminal and binds to Lrp4
  2. MuSK dimerises and autophosphorylates itself
  3. Associated proteins of MuSK pathway (e.g. nAChR beta subunit) are also phosphorylated
  4. Rapsyn is recruited to phosphorylate nAChRs to stabilise postsynaptic clusters of nAChRs
349
Q

What do MuSK autoantibodies do?

A

Block assembly of agrin-Lrp4-MuSK complex = MuSK autophosphorylation prevented = nAChR phosphorylation = rapsyn recruited = cytoskeleton tethering

350
Q

What does interruption to MuSK kinase signalling cause?

A

Disassembly of postsynaptic AChR clusters = inefficient muscle stimulation

351
Q

6 myasthenia gravis treatments?

A
  1. Routine maintenance = acetylcholinesterase inhibitors to boost ACh levels and low dose corticosteroids to inhibit immune cells
  2. Acute crises = plasmapheresis to remove lgG or intravenous immunoglobulin to stop complement cascade by binding to C1q
  3. Thymectomy (removal of thymus to stop T cell production) in severe cases
  4. B cell proliferation inhibitor = monoclonal antibody blocks it and reduces autoantibody production
  5. Complement cascade inhibitor = monoclonal antibody that binds C5 and reduces MAC
  6. Neonatal Fc receptor inhibitor = reduces circulating autoantibodies by reducing circulating lgG
352
Q

Where are nuclei located in skeletal muscle cell?

A

Under sarcolemma (multinucleate)

353
Q

What is the z line?

A

Where 2 actin strands connect

354
Q

What is the A band?

A

Thick myosin ii filaments

355
Q

What is the I band?

A

Thin actin filaments and titin connectors attached to z disc

356
Q

How does contraction occur?

A

Actin filaments are pulled towards the centre as the end of the bipolar myosin filament moves towards the positive ends of actin

357
Q

How does rapid contraction occur?

A

Synchronised shortening of multiple sarcomeres

358
Q

7 steps of Ca2+ release from the sarcoplasmic reticulum triggering myosin movement?

A
  1. CNS innervates alpha motor neurones
  2. Alpha motor neurones innervate skeletal muscles
  3. Exocytosis of ACh into synaptic cleft
  4. ACh binds nAChRs = conformation change = pore opens = influx of Na+ = local depolarisation (end-plate potential)
  5. Depolarisation reaches -50mV = voltage-dependent Na+ channels on muscle membrane open = action potential propagates along muscle membrane and down the T tubules
  6. Action potential triggers Ca2+ release from the sarcoplasmic reticulum (surrounds all myofibrils)
  7. Calcium release synchronously causes muscle contraction
359
Q

What are muscular dystrophy diseases?

A

Diseases causing early onset progressive muscle weakness that all have a genetic cause (like a gene coding for muscle proteins or transcription factors) that determines type

360
Q

What is Duchenne’s muscular dystrophy (DMD)?

A

X-linked recessive, abscence or reduction of dystrophin, causes muscle weakness and wasting with onset of 2-5 years old and life expectancy of 30 — results in delayed motor developmental milestones, learning difficulties

361
Q

What is Becker’s muscular dystrophy (BMD)?

A

X-linked recessive, shorter dystrophin, milder than dmd but similar, onset >7, cardiomyopathy usually causes death and cardiac disease common in males and females, females also get cardiac arrythmias, cardiomyopathy and heart failure

362
Q

What is cardiomyopathy?

A

Stiffening and thickening of the heart muscle

363
Q

What is dystrophin and why do disorders affect males more?

A

A gene on the X chromosome that codes for a rod-like cytoskeletal protein on the inner muscle membrane that connects muscle fibre’s cytoskeleton to the extracellular matrix via laminin

Males only have one X chromosome (no inactivation occurs like in females)

364
Q

What does N-terminus of dystrophin do?

A

Anchors F-actin via actin binding domains to connect to intermediate filaments

365
Q

What does C-terminus on dystrophin bind to?

A

3 binding partners:
1. Beta-dystroglycans = transmembrane protein linking extracellular alpha-dystroglycan to further link laminin and extracellular matrix

  1. Sarcoglycans (transmembrane)
  2. Dystrobrevin,syntrphin and nNOS (intracellular)
366
Q

What does C-terminus and dystrobrevin, syntrophin and nNOS do?

A
  • The complex protects muscle from physical forces by transmitting contraction/relaxation force to tendons and connective tissue
  • nNOS produces nitric oxide to cause vasodilation so muscles get o2
  • Contains spectrin-like repeats = rigidity
  • Proline-rich regions for bends
  • Acts as a linker to connect muscle fibre to the cytoskeleton, extracellular matrix, tendons and ligaments
367
Q

What are the genetic mutations like in DMD?

A

65% deletion, 25% point mutation, 10% partial duplications

368
Q

What do frameshifting deletions/ duplications and nonsense point mutations in DMD cause?

A

Premature stop codons = unstable truncated transcripts with low expression

369
Q

What are the 2 mutational hotspots in DMD?

A
  1. Exons 45 to 55 to remove central portion of rod domain
  2. Exons 3 to 19 to remove some or all of actin binding domain 1 and a portion of the rod
370
Q

What does loss of dystrophin cause?

A

Loss of associated proteins = muscle membrane fragility

Also causes nNOS mislocation = ineffective vasodilation = ischaemic damage to muscle

371
Q

How is dystrophin mutated in BMD?

A

Dystrophin is partially functional as the reading frame, csytein-rich domain and C-terminal are all preserved as dystrophin undergoes small, internal truncations

If actin binding domain 2 is missing then dystrophin is less stable and effective

372
Q

What is DMD muscle pathology?

A

Normal satellite cells respond to damage by proliferating and differentiating but in DMD they cannot keep up and progressive telomere shortening occurs which causes muscle wasting — these damaged muscle cells disintegrate and are proteolysed and replaced by connective tissue and fibroblasts

373
Q

5 DMD treatments?

A
  1. Corticosteroids (standard treatment)
  2. Gene replacement therapy of defective gene
  3. Exon skipping therapy using anti-sense oligonucleotides to restore open reading frame with frame shifting deletions (makes it BMD)
  4. Gene editing with CRISPR/Cas9 to repair/excise mutations via target modification
  5. Stem cell therapy to introduce functional dystrophin gene for muscle repair
374
Q

What is gene replacement therapy in DMD?
Challenges?

A
  • Replacement of defective dystrophin
  • Most viral vectors do not infect skeletal muscle (adeno-associated viruses do though), gene is huge and these viruses cannot fit it, low effect in trials
375
Q

What does exon skipping therapy do in DMD?
Challenge?

A

Antisense oligonucleotide binds to defective region so translation machinery skips it and this can excise and exon to join other exons together (BMD symptoms)

Personalised, costly, time-consuming

376
Q

Mechanism of gene editing with CRISPR/Cas9 in DMD?

A

Induces exon skipping to restore dystrophin expression and is delivered via adeno-associated viruses

377
Q

Mechanism of stem cell therapies treating DMD?
Challenges?

A

Use of satellite cells, bone-marrow derived cells, mesenchymal stem cells, induced pluripotent stem cells

Limited capacity to expand numbers in vitro/iPSCs risk uncontrolled growth, delivery is a challenge, many muscles to restore

378
Q

Why is personalised medicine in DMD so challenging?

A

There are thousands of dystrophin mutations so every person needs a completely individual strategy

Restoring the reading frame would not compensate for functional loss of deletions of critical dystrophin domains

379
Q

What broad medicine is being made for DMD?

A

AON-induced skipping for most common frameshift mutation sites

380
Q

What does the sensory nervous system do?

A

Relays information from internal and external environment back to CNS via sensory nerves

381
Q

2 types sensorimotor neuron?

A
  1. Spinal cord motor neurons (can be somatic or autonomic) and efferent neurons send signals from CNS to muscles
  2. Dorsal root ganglion sensory neurons — afferent neurons carry sensory information from receptors to skin and other organs to CNS
382
Q

What causes neuropathy?

A

Axon damage (slows down axonal signalling)

383
Q

2 types of schwann cells?

A
  1. Myelinating = envelops axon and wraps around membranes many times
  2. Non-myelinating = envelops axon in a single layer of membrane to give nutrients and support
384
Q

What is a fascicle?

A

A bundle of peripheral axons

385
Q

What is epineurium?

A

Packs fascicles and blood vessels together and blood vessels provide oxygen and nutrients and remove waste products

386
Q

What is endoneurium?

A

Connective tissue wrapped around each nerve fibre

387
Q

What is perineurium?

A

Loose, arealar connective tissue surrounding fasicles

388
Q

What is epineurium?

A

Tough, fibrous connective tissue sheath around nerve and its blood vessels

389
Q

What causes peripheral neuropathies?

A

Damage to peripheral nerves (extremities first), diabetes, alcoholism, uremia, drug related, infection

Result is damage to myelin sheath (repairable) or axon (limited repair)

390
Q

Symptoms of peripheral neuropathies?

A

Sensory loss, altered pain sensation, muscle weakness, poor balance, autonomic dysfunction

391
Q

Diagnosis of peripheral neuropathies?

A

Nerve conduction studies and electromyography taken at distal and proximal site — loss of myelin shows slower speed of conduction (time for distal stimulation to produce action potential increases)

392
Q

What is demyelinating neuropathy?

A

Prolonged distal motor latency and slowed nerve conduction

393
Q

What is axonal neuropathy?

A

Decreased amplitude in distal and proximal action potential, distal motor latency and conduction velocity are unaffected

394
Q

What is diabetic peripheral neuropathy?

A

Hyperglycaemia compromises Schwann cell and axonal function and damages supporting blood vessels — sensory nerve damage reduces quality of life

395
Q

How does hyperglycaemia cause peripheral neuropathy?

A

Excess glucose increases glycolysis which perturbs normal homeostasis and causes high energy demands for sustaining action potentials

Osmotic and redox stress damages nerves — hyperglycaemia causes hexokinsase to become saturated and G6P is converted to sorbitol via the polyol pathway (this cannot pass through cell membrane = accumulation = osmotic stress), sorbitol is also converted to fructose = protein glycation = use of NAD+ = redox stress

396
Q

Difference between small and moderate demyelinations?

A

Small = myelin ruffling, loosens (due to loss of adhesion molecules)

Moderate = large spaces between myelin layers = axon exposure = damage

397
Q

What are inherited peripheral neuropathies?

A

Group of heterogenous conditions due to mutations affecting schwann cell function, axonal proteins, neuronal function (mutations in any of these groups causes peripheral neuropathy)

Normally due to gene dosage effect - duplication unbalances myelin formation

398
Q

Symptoms of inherited peripheral neuropathies?

A

Balance issues, clumsiness, muscle weakness, foot abnormalities, more ankle injury, lower leg weakness

399
Q

What is Guillain-Barre syndrome?

A

Autoimmune peripheral neuropathy (acute) that follows respiratory infection or gastroenteritis that causes axonal degradation and/or demyelination of peripheral nerves due to macrophage

400
Q

Treatment of Guillain-Barre syndrome?

A

Plasma exchange to remove circulating antibodies, intravenous lgG (binds C1q = reduced complement activation)

401
Q

Why are some autoimmune peripheral neuropathy cases caused by molecular mimicry?

A
  1. Infection by Campylobacter jejuni which expresses lipoloigosaccharide on its surface which is similar to ganglioside (GM1) on nerve cell membrane
  2. Antibodies are produced against C jejuni which also target GM1
  3. Complement cascade is activated and MAC causes membrane damage
402
Q

Examples of infectious peripheral neuropathy?

A

Leprosy (mycobacterium leprae), HIV, herpes zoster (cold sores), lyme disease, diptheria

403
Q

How does leprosy cause damage?

A

Initially demyelinates and then causes axonal damage to sensory, motor and autonomic parts of PNS

  1. Sensory loss = anaesthesis, anaglesia, inability to distinguish hot/cold
  2. Motor deficit = muscle weakness, paralysis and atrophy
  3. Autonomic nerve fibre damage = impaired sweating, dry skin
404
Q

What can leprosy cause?

A

Damage to peripheral nerves in eyes, face, hands and feet (majorly) causing ulcers, bone destruction, finger and toe shortening

405
Q

How does M.leprae cause nerve damage?

A

Enters nerves via epineurium blood vessels and binds to specific schwann cell sites and becomes ingested = axonal atrophy and segmental demyelination = impaired conduction

It also binds to alpha-dystroglycan complex = activation of PI3K signalling = actin cytoskeleton reorganisation = phagocytosis and internalisation of M.Leprae = cell damage

406
Q

What types of cells is the pancreas made up of?

A

Endocrine and exocrine

407
Q

2 types of exocrine pancreas cells?

A
  1. Acinar (produces pancreatic enzymes)
  2. Ductal (transports pancreatic juice to duodenum)
408
Q

5 types of endocrine pancreatic cells and their respective secreted substance?

A
  1. Alpha (glucagon)
  2. Beta (insulin)
  3. Delta (somatostatin)
  4. PP (pancreatic polypeptide)
  5. Epsilon (ghrelin)
409
Q

What is digestive/pancreatic juice?

A

Ductal cell secretion composed of water, bicarbonate, chloride, sodoim, and potassium to neutralise acid contents of stomach when they enter the intestine

410
Q

What do acinar cells secrete?

A

Proteins like digestive enzymes, proenzymes and trypsin inhibitor

411
Q

Process of protein breakdown?

A

Protein –> peptide (trypsin and chymotrypsin) –> smaller peptide (“”) –> amino acids (carboxypeptidase)

412
Q

How do proteases from the pancreas not digest the pancreas?

A

Produced in inactive form (proenzymes or zymogens), packed into granules and trypsin inhibitor is present

413
Q

How is trypsinogen (trypsin zymogen) activated?

A
  1. Acinar cells produce trypsinogen and release it into duodenum
  2. Enterocytes of intestine secrete enterokinase
  3. Enterokinase converts trypsinogen to trypsin
  4. Trypsin activates all other pancreatic enzymes
414
Q

What hormones stimulate pancreatic juice secretion?

A
  1. Secretin (alkaline aqueous component)
  2. Cholecystokinin (CCK) (enzyme component)

Both are released by enteroendocrine cells in intestinal mucosa

415
Q

4 steps of pancreatic juice secretion?

A
  1. Acidic chyme stimulates secretin release from enteroendocrine cells
  2. Chyme is rich in lipids, fatty acids and proteins = CCK release
  3. CCK and secretin travel to pancreas
  4. CCK stimulates release of enzymes from zymogen granules, secretin causes bicarbonate and water release
416
Q

2 ways CCK stimulates enzyme release?

A
  1. Indirect = vagal nerve activation = pancreas signalled and acinar cells stimulated to release enzymes
  2. Direct = CCK acts on acinar cells via calcium mediated mechanism to allow exocytosis of zymogen granules
417
Q

What is acute pancreatitis?

A

Gallstone blocks pancreatic duct and pancreas becomes inflames

418
Q

What are gall stones?

A

Bile deposits that have precipitated

419
Q

How does cystic fibrosis cause pancreas dysfunction?

A

Can make mucous plug that blocks ducts

Patients should ingest enzymes that cannot leave pancreas

420
Q

What can cause acute pancreatitis?

A

Biliary disease, alcohol, poisons, blunt abdominal trauma, drugs, infection

421
Q

Symptoms of acute pancreatitis?

A

Epigastric pain, nausea, vomiting, ileus (hypomobility of small intestine = constipation), feverdue to leukocyte infiltration into pancreas causing interleukin-1 release

422
Q

How does ligating (tying shut) pancreatic duct affect zymogen granules and lysosomes?

A

Causes lysomal enzymes and digestive enzymes from zymogen granules to become localised which suggests intra-acinar activation of zymogens by lysomal hydrolases = trypsin activation

423
Q

3 main causes of acute pancreatitis?

A

Duct obstruction, acinar cell injury, defective intracellular transport (all can be caused by alcohol) = acinar cell injury which activates enzymes causing acute pancreatitis

424
Q

How much can acute pancreatitis vary?

A

Can be mild swelling, infiltration of neutrophils and oedema and supparation may cause necrosis and abcesses

Can be severe with major necrosis and liquefaction of the pancreas with brown serous fluid in abdomen (fat globules, blood and enzymes)

425
Q

What can severe acute pancreatitis cause?

A

Hypoglycaemia as islets of langerhans are damaged

426
Q

What causes chronic pancreatitis and what characterises it?

A

Recurrent acute pancreatitis (mostly due to alcoholism)

Pseudocysts, fibrosis and intraductal calculi (calcium carbonate stones)

427
Q

2 hypotheses of chronic pancreatitis pathogenesis?

A
  1. Acinar protein hypersecretion
  2. Necrosis-fibrosis sequence
428
Q

What are the signs of acinar protein hypersecretion?

A
  1. Increase in acinar cell size
  2. Increased area of endoplasmic reticulum
  3. Decreased number of zymogen granules and colocalisation with lysosomes (causing trypsinogen activation)
429
Q

What is lithostathine?

A

Peptide secreted into pancreatic juice that normally inhibits protein plug and calcium carbonate crystal formation

Secretion is inhibited by alcohol

430
Q

Cascade of acinar protein hypersecretion hypothesis?

A

Hypersecretion causes cathepsin b to be released from lysosomes and trypsin is released which cause lithostathine to be converted to lithostathine h2 which is an insoluble peptide that forms fibrils which form the matrix of protein plugs = combined with calcium carbonate in protein rich pancreatic juice = calculi

431
Q

What does a protein plug chronic pancreatitis cause?

A

Blocking of pancreatic juice leaving = autodigestion of acini, calculi formation, acinar cell atrophy and ectasia (dilation)

432
Q

What is the necrosis-fibrosis sequence?

A

Lithogenic pancreatitis due to recurrent acute pancreatitis causing scarring and fibrosis:
Acute pancreatitis causes necrosis and inflammation = periductular fibrosis = partial duct obstruction = stasis in ductules = protein plug and calculi = obstruction of ducts by calculi = necrosis of acini and fibrosis

433
Q

What is the oesophagus for?

A

Connects pharynx to stomach and is a conduit for food and liquids, has 2 sphincters and does peristalsis

434
Q

2 types of muscle in oesophagus?

A
  1. Striated (voluntary) – innervated by nucleus ambiguous
  2. Smooth (involuntary) — innervated by dorsal motor nucleus
435
Q

2 sphincters of stomach?

A
  1. Lower oesophageal sphincter (top end)
  2. Pyloric sphincter (bottom)
436
Q

Components of gastric juice and what cell/s of the gastric mucosa produce them?

A
  1. Mucin by surface mucous cell and mucous neck cells
  2. Hydrochloric acid and intrinsic factor by parietal cells
  3. Pepsinogen and lipase by chief cells
  4. Gastrin by G cell
437
Q

3 phases of gastric secretion?

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
438
Q

What occurs in the cephalic phase?

A

Taste or smell of food triggers vagus nerves to trigger HCl, pepsinogen and gastrin production

439
Q

What occurs in gastric phase?

A

Stomach stretches to prepare for food (distension) and gastrin enters blood stream, pepsinogen converted to pepsin and stomach muscles start to churn

440
Q

What happens in intestinal phase?

A

Small intestine regulates the release of chyme from the stomach — CCK and secretin slow emptying and reduce acid production and digestive enzymes production is triggered

441
Q

How does HCl get into the blood?

A

CO2 and H2o combine to form h2co3 which form hco3- and h+ —> h+ enters blood and combines with cl-

PROTON PUMP

442
Q

3 regions of small intestine?

A

Duodenum, jejunum, ileum

443
Q

5 types of small intestine cells?

A
  1. Paneth cell = pathogen defence
  2. Tuft cell = “”
  3. Absorptive enterocytes = nutrient absorption
  4. Enteroendocrine cell = secrete digestive hormones and enzymes
  5. Goblet cells = mucin
444
Q

How does small intestine digest and absorb carbohydrates?

A

Amylase converts it to its respective monosaccharides –> enter absorptive enterocyte by sodium-glucose transporter protein (glucose, galactose) or GLUT-5 (fructose) –> enter circulation by GLUT 2

445
Q

How does small intestine digest and absorb protein?

A

Convert them to amino acids using pepsin in the stomach or pancreatic peptidases in duodenum –> amino acids enter absorptive enterocyte or tri-/di-peptides enter by PepT-1 transporter –> enter circulation by amino acid transporters

446
Q

How does small intestine digest and absorb lipids?

A

Lipids emulsify to be droplets –> become micelles in presence of bile salts –> diffuse into absorptive enterocytes –> packaged into chylomicrons in ER which enter vesicles –> exocytosis into circulation

447
Q

Anatomy of large intestine?

A

Cecum –> colon –> rectum –> anus

448
Q

Role of large intestine?

A

Finish absorption of nutrients and h2o, synthesise some vitamins, form faeces and dispose

449
Q

4 cell types in large intestine and what they do?

A
  1. Absorptive enterocytes = complete absorption
  2. Microvacuolated columnar cell = complete absorption
  3. Enteroendocrine cell = hormones
  4. Goblet cell = mucin
450
Q

4 symptoms of GI diseases?

A
  1. Abdominal or chest pain
  2. Altered food ingestion due to: nausea, vomiting, dysphagia (difficulty swallowing), odynophagia (painful swallowing), anorexia
  3. ALtered bowel movements
  4. GI tract bleeding
451
Q

What is oesophageal achalasia?

A

Motor disorder that leads to functional obstruction – LOS fails to relax with swallowing = dysphagia, regurgitation

452
Q

How does LOS normally work?

A

Using manometry (pressure along oesophagus) – peristaltic wave of pressure after swallow –> drop in pressure once it reaches LOS –> sphincter relaxes –> food enters stomach

453
Q

What is achalasia?

A

Loss of inhibitory neurons so they get the peristaltic wave but sphincter cannot relax as it is not inhibited

If both types of neuron are lost there is not peristaltic wave

454
Q

What is gastritis?

A

Condition where lining of stomach becomes inflamed after it has been damaged by excess acid or pepsin

455
Q

What can cause gastritis?

A

H.pylori bacterial infection, excessive cocaine or alcohol, aspirin, ibruprofen, stressful event, autoimmune reaction

456
Q

What are gastric ulcers?

A

Open sores on the stomach lining

457
Q

Causes of gastric ulcers?

A

H.pylori bacterial infection, lifestyle, aspirin, ibruprofen, stessful event

458
Q

What is Crohn’s disease?

A

Inflammatory bowel disease

459
Q

Causes of crohn’s?

A

Genetic, infection, smoking, diet, defective immune response

460
Q

Symptoms of crhn’s?

A

Diarrhoea, pain, impaired growth, malabsorption, weight loss, inflammation without infection

461
Q

What is diverticulosis or diverticulitis?

A

Acquired deformity whereby mucosa and submucosa herniate through underlying muscularis in large intestine

462
Q

Causes of diverticulosis and diverticultiitis?

A

Age, highly refined diet, low fibre

463
Q

Symptoms of diverticulosis and diverticulitis?

A

Stomach pain, fever and chills, swelling, gas, loose bowels, constipation, low appetite, sickness

464
Q

What can diverticulitis cause?

A

Diverticula to clog with faeces = inflammation = infection

465
Q
A

Biomed (9 decks)

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