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Posters > Review posters 03/05/2016 > Flashcards

Review posters 03/05/2016 Flashcards

1
Q

How is the supply of NAD+ recreated?

A

Anaerobic respiration creates NAD+ in the conversion of pyruvate to lactic acid.
Oxidative metabolism of pyruvate.

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2
Q

What is the purpose of the pyruvate dehydrogenase complex?

A

To catalyse the decarboxylation and oxidation of pyruvate to form the 2 carbon acetyl coA. (oxidative decarboxylation)
Is allosterically regulated by phosphorylation.
Actively determines glucose oxidation in well oxygenated tissues.

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3
Q

How does pyruvate enter the mitochondrial matrix?

A

H+ gradient created. Ion channel called the H+/pyruvate symporter allows facilitated diffusion of pyruvate into the mitochondrial matrix.

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4
Q

Which enzyme in the TCA cycle is not from the mitochondrial matrix?

A

Succinate dehydrogenase.

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5
Q

What is the net yield of one turn of the TCA cycle.

A

3 NADH + H+
1 FADH
1 ATP

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6
Q

Pyruvate dehydrogenase deficiency

A

Carried on the X chromosome.
Only occurs in females.
Causes mental retardation, seizures, poor muscle tone. persistent lactic acidosis and resp problems.

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7
Q

Fumarate dehydrogenase deficiency and hereditary leiomyomatoses and renal cell cancer (HLRCC)

A

Result from defect in fumarate dehydrogenase (TCA cycle enzyme).
Causes muiltiple systemic, benign and malignant tumours.

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8
Q

Type 1 hypersensitivity reactions are mediated by which antibodies.

A

IgE

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9
Q

Describe the hygiene hypothesis

A

Early exposure to microbes in the environment means children are less likely to develop allergies. Overly protected, sterile environments mean childrens immune systems are not mature enough to deal with the new antigens.

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10
Q

Describe the pathophysiology of a type I hypersensitivity reaction.

A

On first encounter: Allergen is in the body.
Mast cells bind to the allergens antigen via Fc receptors and destroy it. IgE antibody created by B cells specific to allergen.
On re-encounter: IgE antibody binds to allergen. Mass mast cell degranulation occurs (release of histamine, leukotriene D4 etc) to kill antigen.
Release of histamine causes smooth muscle spasm (bronchoconstriction), vasodilation (mass oedema) and leukocyte extravation.

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11
Q

Give examples of a type I hypersensitivity reaction.

A

Extrinsic asthma
Anaphylaxis
Food allergy
Drug allergy

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12
Q

How do you diagnose a type I hypersensitivity reaction?

A

Skin prick test
RAST test- measure amount of IgE in serum directed against specific antigen.
Anaphylaxis- mast cell tryptase (product of mast cell granules-wide spread degranulation of mast cells)

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13
Q

Treatment of a type I hypersensitivity reaction.

A 
Avoid stimulus. 
Anti-histamines
Adrenaline (for anaphylaxis)- mass vasoconstriciton
Corticosteroids
Sodium cromoglycate.
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14
Q

What is a type II hypersensitivity reaction.

A

Direct cell killing.

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15
Q

Describe the pathophysiology of a type II hypersensitivity reaction.

A

Macrophages and dendritic cells wrongly recognise a cell or antigen presenting cell. B cells then produce antibodies (IgG or IgM) which activates the complement cascade.
When complement is activated, C3 opsonises the cell to make it more attractive for phagocytosis whereas C5b forms the membrane attack complex which results in cell lysis.

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16
Q

Name the three main roles complement has.

A

Opsonisation
Formation of the membrane attack complex.
Increase permeability of blood vessels.

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17
Q

Name an example of a type II hypersensitivity reaction.

A

Blood transfusions
Goodpastures syndrome- affects basement membrane of cells in the lung.
Guillian Barre syndrome-antibodies bind to peripheral nerve glycoprotien.

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18
Q

Immediate haemolytic transfusion reaction.

A

Can occur if as little as 1ml of blood is transfused.
Pyrexia and rigors.
Tachycardia
Hypotension

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19
Q

Treatment of type II hypersensitivity reactions.

A

Avoidance of stimulus.
Plasmapheresis- removal of pathogenic antigen- blood removed by a cell seperator
Immunosuppressive therapy- plasmapheresis needs this to be effective (rebound antibody production would limit the effects).

20
Q

Describe a type III hypersensitivity reaction.

A

Formation of immune complexes.

21
Q

What are immune complexes

A

Antibody and antigen bound together.

22
Q

Describe the pathophysiology of type III hypersensitivity reactions.

A

Antibody binds to antigen. Form immune complexes. These get deposited in small vessels and clog up osmotically active sites. This activates complement and macrophages and neutrophils arrive.

23
Q

Examples of a type III hypersensitivity reaction.

A

Extrinsic allergic alveolitis (farmers lung)- inhaled spores
Bird fanciers lung- avian serum proteins
Acute hypersensitivity pneumonitis- immune complexes deposited in the walls of alveoli and bronchioles.
Systemic lupus erythematosus- Antibodies produces against cell nuclei contents.

24
Q

Treatment of type III hypersensitivity reactions.

A

Avoidance of stimuli.
Immunosuppression
Corticosteroids

25
Q

Describe a type III hypersensitivity systemic response.

A

Fever
Renal impairment
Vasculinic skin rash
Arthralgia

26
Q

Acute cholecystitis

A

Obstruction of gall bladder emptying due impaction of gall stone.
Causes back up of bile in the gall bladder- causing it to enlarge

27
Q

Biliary colic

A

Term describing the pain felt when a gall stone temporarily obstructs the cystic duct. Pain is usually constant in the epigastrium region. Aggravated/ relieved by eating-especially foods with high fat content.
Nausea and vomiting
Pain may radiate over right shoulder
Could stop spontaneously or need opiate analgesia.

28
Q

Describe the symptoms of acute cholecystitis.

A

Epigastric pain (usually presents as biliary colic).
Pain then becomes more localised in the RUQ.
Rigors and fever.

29
Q

Common bile duct stones

A

stones present in the common bile duct.
Causes- jaundice, fever, biliary colic
Symptoms- tenderness in RUQ

30
Q

Investigations into common bile duct stones.

A

FBC- increased neutrophils
Increased serum bilirubin
Increased ALP
Increased CRP

31
Q

Investigations into acute cholecystitis

A 
Blood tests showing
Raised CRP
Raised ALP
Slightly elevated serum bilirubin
Ultrasound showing presence of gallstones
MRCP or ERCP
32
Q

Management of acute cholecystitis

A 
Nil by mouth
IV fluids
Opiate analgesia
IV antibiotics
Wait for it to settle then perform cholecystectomy
33
Q

Cholangiocarcinoma

A

Second most common cancer of the biliary tree.
Can be intra or extra hepatic
Usually presents with jaundice
Associated with primary sclerosing cholangins, chronic infection

34
Q

Investigations into cholangiocarcinoma

A

Ultrasound
CT
MRCP

35
Q

Treatment of cholangiocarcinoma

A

Resection or chemoradiation

36
Q

Benign polyps of the gallbladder

A

Adenomas

37
Q

malignant cancers of the gallbladder

A

Adenocarcinoma- not related to gallstones.
However related to calcification which is the terminal step in acute cholecystitis
Polyps of the gallbladder greater than 10mm in diameter also may cause malignancy.

38
Q

Pleural effusion

A

Fluid in the pleural cavity

39
Q

Causes of pleural effusion

A

Lymphatic drainage insufficient
Inflammation
Increased pressure in the lungs

40
Q

Symptoms of pleural effusion

A

Chest pain- pleuritic. Fluid compresses the lungs.
Dry cough- lungs think fluid is inside them so cause you to cough- however the fluid is actually external.
Shortness of breath

41
Q

treatment and investigations

A

thoracocentesis- needle aspirates fluid. Fluid then tested to see if it is transudative or exudative

42
Q

What is the difference between transudate and exudate fluid.

A

Transudate- caused by hydrostatic pressure changes.
Due to decreased protein in the blood vessel.
In the fluid there would be
less than 30g/l of protein

Exudate fluid is due to inflammatory causes. During inflammation the blood vessels become wider and the endothelial gaps become bigger therefore protein can move out of the vessel.
In the fluid
Greater than 30g/L of protein

43
Q

Treatment of pleural effusion

A

Treat underlying cause in transudative e.g. control blood pressure.
In exudative drain fluid.

44
Q

Empyema

A

Pus in the pleural space.

45
Q

Pathology of empyema

A

Effusion occurs.
Infection of the fluid
Pus collecgts
Chest cavity and lungs ‘stick together’ causing breathing difficulties.

46
Q

Treatment of empyema

A

Drained or removed during surgery.

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