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Posters > Review posters 14/05/2016 > Flashcards

Review posters 14/05/2016 Flashcards

1
Q

Process of glycogen synthesis

A

Glucogenesis

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2
Q

Process of glycogen synthesis from non-carbohydrate pre-cursors

A

Gluconeogenesis

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3
Q

Process of glycogen breakdown

A

glycogenolysis

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4
Q

Where is glycogen stored?

A

The liver and muscles

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5
Q

What is the difference between the two places glycogen is stored?

A

The muscle cell has to use to glycogen that is broken down there, whereas the liver can release it into the bloodstream.

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6
Q

When is glycogen broken down?

A

Between meal times.

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7
Q

How are blood sugar levels maintained?

A

Just after a meal- blood sugar levels are at their highest.
Also inbetween meals- glycogen is released to keep blood sugar levels up.
At times like breakfast when you haven’t eaten in a while- gluconeogenesis comes into play.

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8
Q

What is glucogenin and why do you need it?

A

Glycogen synthase cannot make glycogen without an existing chain being present. Therefore you need glucogenin which acts as a starting point at the centre of glycogen. It has catalytic activity which allows it to add small amounts of glucose onto it.

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9
Q

What is UDP glucose?

A

This is activated glucose. Urine disphosphate with a glucose attached to it. The bond between glucose and phosphate contains high energy- this is used to transfer glucose.

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10
Q

Glycogen synthase can introduce 1-6 branches. True or False

A

False

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11
Q

Which enzyme introduces branches into glycogen?

A

Branching enzyme

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12
Q

What catalyses glucogenolysis?

A

Glycogen phosphorylase

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13
Q

What is glycogen converted too in glucogenolysis?

A

Glycogen is converted too glucose-1-phosphate. This can then be converted into glucose-6-phosphate.

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14
Q

What happens in the liver in glucogenolysis?

A

Glucose-6-phosphate is dephosphorylated to glucose which can then be released into the blood via GLUT2.

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15
Q

What is the fate of glucose-6-phosphate in muscle?

A

It undergoes glycolysis and releases energy.

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16
Q

How is glycogenolysis stimulated and at which part of the cycle?

A

Adrenaline and cortisol stimulate glycogen phosphorylase.

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17
Q

Name the precursors used in gluconeogenesis

A

Lactate, amino acids and glycerol

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18
Q

Describe each of the precursors

A

Lactate- derived from anaerobic respiration
Amino acids- glucogenic amino acids. Derived from muscle protein.
Glycerol- from triglycerides in adipose tissue.

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19
Q

Describe gluconeogenesis

A

Extremely energy consuming making of new glucose.

Essentially the reverse of glycolysis- needs specific enzymes to get round the irreversible reactions.

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20
Q

Classes of amino acids

A

Ketogenic- can’t be used in gluconeogenesis

Glucogenic- can be used in gluconeogenesis

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21
Q

What happens to glucogenic amino acids?

A

They are either converted to pyruvate and then to glucose or enter the TCA cycle and are converted to oxaloacetate then glucose.

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22
Q

Hormonal regulation of gluconeogenesis

A

Glucagon - increases gluconeogenesis
Inhibits glycolysis
Insulin- decreases gluconeogenesis
Stimulates glycolysis

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23
Q

What occurs in the embryonic stage of lung development?

A

Respiratory diverticulum forms

Initial branching to give lung, lobes and segments

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24
Q

What occurs in the Psuedoglandular stage of lung development?

A

Formation of terminal bronchioles

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25
Q

What occurs in the cannicular stage of lung development

A

Terminal sacs (alveoli) form.

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26
Q

What occurs in the alveolar stage?

A

maturation of the alveoli

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27
Q

From which layer does the gut evolve?

A

Primarily endoderm and some visceral mesoderm.

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28
Q

Which layer does the heart arise from?

A

Visceral mesoderm.

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29
Q

What does the truncus arteriosus give rise too?

A

Aorta and pulmonary trunk

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30
Q

What does the bulbus cordis give rise too?

A

The right ventricle and outflow tract

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31
Q

What does the ventricle give rise too?

A

The left ventricle

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32
Q

What does the atrium give rise too?

A

The right and left atrium

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33
Q

What does the sinus venosus give rise too?

A

The right atrium and coronary sinus.

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34
Q

What does the vittelline vein do?

A

Drains yolk sac

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35
Q

What does the umbilical vein do?

A

Drains placenta

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36
Q

What does the cardinal vein do?

A

Precursors for systemic venous system.

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37
Q

Ductus venosus

A

Directs oxygen rich blood from the placenta to the IVC bypassing the liver

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38
Q

Foramen ovale

A

Directs oxygen rich blood from the right atrium to the left atrium so it bypasses the lungs

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39
Q

Ductus arteriosus

A

Directs deoxygenated blood from the pulmonary artery to the descending aorta as it goes to the placenta

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40
Q

Which layer forms the gut?

A

The endoderm forms the mucosa, ducts and glands

The viceral mesoderm forms the lamina propria, muscle layers and submucosa.

41
Q

Dorsal mesentary

A

Greater omentum

42
Q

Ventral mesentary

A

Lesser omentum

43
Q

What layers form the liver?

A

Endoderm- liver cells and biliary tree

Septum transversum- Kupffer cells and connective tissue

44
Q

What layer forms the spleen?

A

Mesoderm

45
Q

What occurs in the stomach during lipid absorption?

A

Gastric lipase is released. Heat and churning from the stomach allows mixing. At first- hydrolysis is slow. As it precedes, fatty acids act as surfactants breaking down lipid molecules and aiding emulsification.
Emulsified fats are ejected into the duodenum.

46
Q

What occurs in the duodenum during lipid absorption?

A

Pancreas releases pancreatic lipase. Bile salts help to emulsify fats.
Bicarbonate in the pancreatic juice neutralises the stomach acid.

47
Q

Role of bile salts

A

Released in response to CCK
Increase the surface area of the lipids- however block small lipids from pancreatic lipase. Colipase therefore has to stop this by bonding to both.

48
Q

How are short chain free fatty acids absorbed?

A

Passive diffusion into enterocytes and then into the villus capillaries

49
Q

How are long chain free fatty acids absorbed?

A

They are absorbed and then resynthesised to form triglycerides and put into chylomicrons.

50
Q

What are chylomicrons?

A

Exocytose from enterocytes and are carried in lymph vessels up to the subclavian vein via the thoracic duct.

51
Q

How is cholesterol absorbed?

A

Transport by endocytosis via NPC1L1

52
Q

How is vitamin B12 absorbed?

A

Binds with intrinsic factor. Absorbed in terminal ileum by endocytosis.

53
Q

How are fat soluble vitamins absorbed?

A

Vitamin A, D, E, K

Passively transported to enterocytes- incorporated into chylomicrons

54
Q

How are water soluble vitamins absorbed?

A

Vitamin B, C, H

Active transport

55
Q

How is iron absorbed?

A

Ferrous (Fe2+) is absorbable
Ferric (fe3+) is not.
Transported via Haem carrier protien 1, divalent metal transporter 1 and feropartin.

56
Q

How is calcium absorbed?

A

Passively paracellularly
Active intracellularly
Regulated by D3 and parathyroid hormone.

57
Q

True aneurysm

A

All three parts of the vessel wall are left intact

58
Q

False aneurysm

A

Aneurysm has breached through the vessel wall

59
Q

Pathogenesis of abdominal aortic aneurysm

A

Decreased elastic fibres and collagen in the vessel wall. Also muscle cell loss. This leads to aortic dilatation.

60
Q

Symptoms of abdominal aortic aneurysm

A

Acute severe pain in epigastric region radiating through to the back when ruptured
If intact- generally no symptoms

61
Q

Treatment of AAA

A

Surgical resection/repair if greater than 5.5cm in diameter. If less than 5.5cm, 6 monthly ultrasound and CT monitoring

62
Q

Investigations into AAA

A

Duplex ultrasound

CT

63
Q

Shapes that AAA’s can form.

A

Saccular- yolk sac
Fusiform
Mycotic- after infection

64
Q

What is angina?

A

Crushing/tightness feeling in the chest on exercise. Associated shortness of breath. Relieved by GTN spray

65
Q

When can angina come on?

A

With exercise, after meals, in the cold, anger/excitement

66
Q

Managing stable angina

A

GTN spray- patient should sit down and take 2 puffs and symptoms should stop.
Aspirin/clopidogrel to prevent further clot aggregation
Beta blocker or calcium channel blockers to decrease preload to the heart.

67
Q

Lifestyle advice in angina

A

Exercise 150 minutes of moderate exercise or 75 minutes of vigorous exercise a week.
Eat healthily- cut out red meat, reduce salt. Eat meditarranean diet.
Smoking cessation
Alcohol decrease

68
Q

If no change occurs after lifestyle modification, you would:

A

Either put them on a dihydropyridine and a beta blocker or a long acting nitrate e.g. isosorbide nitrate.

69
Q

Symptoms of unstable angina

A

Chest pain/crushing/tightness at rest. Not relieved by GTN spray.

70
Q

How would you treat unstable angina

A

MONAC

medical emergency

71
Q

Describe the process of plaque rupture

A

Plaque ruptures and exposes subendothelial collagen and von Willeband factors. The circulating platelets in the blood recognise these and start to form a monolayer (fatty streak). They become activated by thromboxane A2 and ADP causing them to clump together. This causes an inflammatory reaction and more cells occlude the vessel. Blood clots may form and complete occlusion occurs.

72
Q

What is a myocardial infarction?

A

Cardiac myocytes undergo prolonged ischaemia due to atherosclerotic plaque rupture occluding the coronary arteries. If this ischaemia goes on for too long- the heart muscle will start to die off.

73
Q

Anterior MI

A

V1-V6

74
Q

Inferior MI

A

II, III, AvF

75
Q

Lateral MI

A

I, AvL

76
Q

Posterior MI

A

V1, V2 reciporical

77
Q

Anterolateral

A

I, AvL and V4, V5, V6

78
Q

Anteroseptal

A

V1-V3

79
Q

Acute management of MI

A 
M- morphine and an anti-emetic
O-oxygen 15L/min
N- nitrates GTN spray
A- aspirin- 300mg
C-clopidogrel -300mg at start and 300mg later

In NSTEMI also add low molecular weight heparin

80
Q

Management after MI

A

Beta blocker
Ace Inhibitor
Dual antiplatelet therapy- aspirin and clopidogrel
Statin

81
Q

When should a person undergo thrombolysis.

A

When it is not possible to PCI a patient within 120 minutes

82
Q

What treatment is for a NSTEMI

A

Can do PCI, CABG or thrombolysis.

83
Q

Lifestyle changes of MI

A

Smoking cessation
Decreased cholesterol
Increased exercise

84
Q

Describe the development of an atherosclerotic plaque.

A

Irritants in the blood such as LDL cholesterol, hypertension and smoking toxins cause endothelial cell damage. The LDL cholesterol then infiltrates the subendothelial space and becomes oxidised. This is called the fatty streak. Macrophages are recruited to the area and start to digest the LDL cholesterol. However they gorge themselves and die as foam cells. The macrophages released cytokines which causes an inflammatory response. Also smooth muscle cells start to notice the aggregation and migrate into the plaque and form a fibrous cap. They also deposit calcium hardening it.

85
Q

How can you distinguish between left and right heart failure?

A

Left heart failure causes pulmonary oedema. Right heart failure causes peripheral oedema.

86
Q

Define heart failure

A

The heart cannot meet the demands of the body.

87
Q

Left sided heart failure

A

The muscle cannot contract with as much force and therefore not all the blood is emptied. This increases the pressure in the left ventricle. The pressure then backs up to the left atrium and eventually to the lungs causing pulmonary hypertension. This may cause pulmonary oedema.

88
Q

Right sided heart failure

A

Heart muscle in the right ventricle cant contract as well therefore blood is left in the ventricle. This increases the pressure in the ventricles and the pressure in the atria therefore increases, backing it up to the body (specifically the ankles).

89
Q

Causes of heart failure

A

Cardiomyopathy- disease of the heart muscle causing it to not contract as well
Decreased force of contraction due to death of cardiac myocytes
Valvular disease- regurgitation means blood flows backwards- the heart has to work harder requiring more oxygen.
Coronary heart disease- ischaemia of the muscle

90
Q

Classes of heart failure

A

Class 1- no symptoms at rest or on exercise
Class 2- no symptoms at rest- symptoms on vigorous exercise (mild limitation)
Class 3- no symptoms at rest- symptoms on mild exercise
Class 4- symptoms at rest and exercise

91
Q

Investigations into heart failure

A

ECG- exercise and non
Echo- stress and non
Blood tests
Chest X-ray

92
Q

Treatment of heart failure

A

Aimed at relieving symptoms and preventing worsening of disease
Lifestyle-
Cessation of smoking
Decrease alcohol intake
Dietary modification - salt restriction, portion control, low sodium diet
Drugs- diuretics e.g. furosemide
Beta blockers
Ace inhibitors
Spiranolactone (pottasium sparing diuretic)

93
Q

Acute management of AF

A

If haemodynamically unstable, has paroxysmal or persistent AF- electrical cardioversion
Otherwise cardiovert using IV amiodarone with beta blockers or calcium channel blockers to control rate.
LOW MOLECULAR WEIGHT HEPARIN

94
Q

Class I antiarrhythmic

A

N- Na+ channel blocker. Rhythm control- prolong refractory period
Lignocaine, disopyramide, flecainide

95
Q

Class II antiarrhythmic

A

B- beta blockers. Rate control. Work on SA and AV node

E.g. metoprolol

96
Q

Class III antiarrhythmic

A

K+ channel blockers. Rhythm control- prolong refractory period
e.g. amiodarone

97
Q

Class IV antiarrhythmic

A

C- Calcium channel blockers. Rate control- work on SA and AV nodes
e.g. verapamil, amlodipine

98
Q

Treatment of chronic AF

A

Beta blockers or calcium channel blockers
Rhythm control if symptomatic
Warfarin anticoagulant

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