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Pre-Clinical Science > Clinical conditions > Flashcards

Clinical conditions Flashcards

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1
Q

What is protein denaturation?

A

Loss of protein structure due to disruption of interactions responsible for secondary and tertiary structure, resulting in loss of function

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2
Q

What are some causes of protein denaturation?

A 
Heat
pH
Organic solvents
Urea
Detergents
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3
Q

Why do denatured proteins lose their function?

A

Have altered active sites so can’t catalyse reactions

Receptors cant bind to signal molecules so cant cause cell signalling

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4
Q

What is the consequences of protein misfolding?

A

Cant perform functions

Accumulate in cells and tissues

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5
Q

What is the name of misfolded proteins?

A

Prion proteins

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6
Q

What is are examples of diseases associated with protein misfolding and how do they occur?

A

Alzheimer’s disease- humans
Spongiform encephalopathy- animals
Prion proteins deposit in the brain which impairs normal functions

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7
Q

What is exocrine pancreatic insufficiency?

A

Not enough exocrine enzymes enzymes are produced so body cant digest or absorb molecules

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8
Q

What are the symptoms of exocrine pancreatic insufficiency?

A

Weight loss

Increased appetite

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9
Q

How is exocrine pancreatic insufficiency diagnosed?

A

Trypsin like immunoreactivity test to test trypsin(digests proteins) levels in the blood, low levels show EPI

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10
Q

How is exocrine pancreatic insufficiency treated?

A

Pancreatic enzyme supplementation
Eating highly digestible low fat diet
Treat cause of chronic pancreatitus

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11
Q

What is pancreatitis?

A

Inflammation of the pancreas, chronic or acute

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12
Q

What are the consequences of pancreatitis?

A

Activate zymogens early so they begin to break down the body tissues and organs rather than food
Can lead to haemorrhage and death if not treated

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13
Q

What are causes of pancreatitis?

A

High fat diet
Iatrogenic- medical treatment involving glucocorticoids
Idiopathic- spontaneous

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14
Q

How is pancreatitis treated in the short and long term?

A 
IV fluid therapy
Anti-emetics
Analgesia and anti-inflammatory drugs
Starving for 24 hours to rest pancreas
Long term management involving diet changes and weight loss
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15
Q

What is hyperammonia?

A

Ammonia not removed in urea cycle so has toxic build up

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16
Q

What are the symptoms of hyperammonia?

A 
Vomiting
Abnormal gait
Head pressing
Seizures
Coma 
Death
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17
Q

How is hyperammonia caused?

A

Portosystemic shunt allows blood to bypass the liver so it isn’t detoxified in urea cycle for ammonia excretion
Lack of enzymes for urea cycle

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18
Q

How is hyperammonia treated?

A

Close portosystemic shunt
Reduce dietary protein
Medication to manage ammonia excretion
Supplement urea cycle enzymes

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19
Q

Define coenzymes?

A

Carriers and donors of functional groups, usually have dietary precursors due to body not being able to synthesise them

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20
Q

What are common coenzyme deficiencies?

A

Thiamine/B1

Cobalamin/vitamin B12

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21
Q

What are the signs of thiamine deficiency?

A

Lethargy
Anorexia
Neurological signs
Seixures

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22
Q

How is thiamine deficiency diagnosed and treated?

A

Given thiamine to see if symptoms improve

Thiamine supplements and dietary changes

23
Q

What is the consequences of cobalamin deficiency?

A 
Un functioning enzymes
Poor body conditions
Inability to gain weight
Weakness
Vomiting
Diarrhoea
24
Q

How is cobalamin deficiency treated?

A

Supplements

25
Q

What is polysaccharide storage myopathy?

A

Genetic equine condition causing incorrect glucose storage

Too much glycogen synthase produces causes long chains with minimal branching, relatively resistant to amylase

26
Q

What structure is glucose normally stored?

A

Glycogen with alpha 1-6 branches for easy release and alpha 1-4 branches to make chain

27
Q

What enzymes are involved in glycogen formation and breakdown?

A

Glycogen synthase- alpha 1-4
Glycogen branching enzyme- alpha 1-6
Amylase- breaks bonds

28
Q

What are the effects of polysaccharide storage myopathy?

A

Over production of glycogen but little available glucose
Lack of energy
Muscle stiffness
Muscle breakdown for use as fuel

29
Q

How can polysaccharide storage myopathy managed?

A

Low-starch and high fat diet to provide fuel

30
Q

What is phosphofructokinase deficiency?

A

Deficiency of phosphofructokinase enzyme which is crucial for formation of fructose-1,6-biphosphate in preparatory phase of glycolysis, with out it glycolysis cant take place

31
Q

What are the symptoms of phosphofructokinase deficiency?

A

Muscle fatigue
Weakness
Pain
Stiffness

32
Q

What are the causes of phosphofructokinase?

A

Genetic but recessive present in spaniels

33
Q

What is the treatment for phosphofructokinase?

A

Change in diet to high protien, high fat and low carbohydrates
Reduce exercise

34
Q

What do yeast and bacteria use to store polysaccharides?

A

Dextrans

35
Q

What are the issues associated with dextran’s in the body?

A

Form plaque and allow bacteria to stick to teeth

Cause gum and tooth damage

36
Q

What are lectins?

A

Proteins that bind to carbohydrate on cell membranes and allow extraversion of leukocytes, present on some bacterial and viral pathogens

37
Q

What is the lectin found in influenza virus and what is its effect?

A

Haemagglutinin
Binds to cell surface carbohydrates to allow viral membrane to fuse with cells membrane so viral genome can enter cell and replicate

38
Q

How can lectins be helpful for treatments?

A

Get targeted to inhibit attachment to cells

39
Q

What are lipomas?

A

Benign masses due to abnormal adipose cell growth

40
Q

What are signs of lipomas?

A 
Mobile mass in skin
Slow growth of mass
Pain free
Squishy
Fine needle aspiration contains cells with large lipid vacuoles
41
Q

What are the treatments for lipomas?

A

Removed when cause mobility issues or look unsightly

Eat low fat diet to possible prevent

42
Q

What is ketoacidosis caused by?

A

Intense gluconeogenesis causes acetyl CoA to form into ketone bodies, prolonged for a long time

43
Q

What are the issues of ketoacidosis?

A

Lower plasma pH, kidneys produce acidic urine
Increased urination rate
Dehydration

44
Q

What is the role of vitamin K?

A

Cofactor for adding carboxylic acid to activate or inactivate clotting factors

45
Q

What are symptoms of vitamin K deficiency?

A 
Bruising
Red spots on MMs
Prolonged bleeding
Spontaneous haematoma
Haemorrhage
46
Q

What causes vitamin K deficinecy?

A

Vitamin K absorption defects in in gut
Recycling defects
Recycling blockers

47
Q

What is the role of COX enzymes?

A

Prostaglandin synthesis

48
Q

What are the issues associated with COX blocking drugs?

A

Block pain but can prevent gastric secretions causing stomach irritations, ulcers and gastric bleeding

49
Q

What are the benefits of COX blocking drugs?

A

Pain and inflammation relief

Reduces risk of heart attacks and strokes from preventing formation of thromboxane platelets

50
Q

What are fatty acid metabolism disorders?

A

Body cant produce or use enzyme needed to oxidise fatty acids, energy from fatty acids not available

51
Q

What are the different types of fatty acid disorders?

A

Defects in oxidation- fatty acids cant form so cant enter mitochondria for oxidation
Defects in carnitine shuttle- acyl CoA cant enter mitochondria for oxidation

52
Q

What are the effects of fatty acid metabolism disorder?

A

Fatty acid build up in liver as sent from adipose but cant be broken down
Excess glucose use for energy causing hypoglycaemia, weakness, fatigue and seizures

53
Q

How is fatty acid metabolism disorder treated?

A

High fibre, low fat diet

Frequent meals to avoid use of fat stores

Pre-Clinical Science (5 decks)

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