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2.2 Clinical Chemistry > Practical Exam > Flashcards

Practical Exam Flashcards

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1
Q

What are the causes of hypoproteinaemia?
(5)

A

Salt retention syndromes - increased water retention and apparent decrease in concentration

Liver disease - decreased production of proteins

Renal disease - increased loss in urine

Burns - increased loss of proteins in exudate

Malabsorption - decreased production through lack of essential amino acids

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2
Q

What are the causes of hyperproteinaemia
(3)

A

Dehydration - reduced water volume results in an apparent increase in protein concentration

Immune response -> increased production of all Ig due to an infection/inflammation

Multiple myeloma -> increased production of a single clone of Ig due to a neoplastic increase in plasma cells

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3
Q

List some diseases that may cause an increase in total protein
(8)

A

Chronic infection e.g. TB
Liver dysfunction
Dehydration (chronic diarrhea, diabetic acidosis)
Respiratory distress
Haemolysis
Cryoglobulinaemia
Alcoholism
Leukaemia

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4
Q

List some diseases that cause a decrease in total protein
(8)

A

Malnutrition and malabsorption
Liver disease
Diarrhea
Severe burns
Loss through urine in severe kidney disease
Low albumin
Low globulins
Pregnancy

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5
Q

What are the causes of decreased albumin
(9)

A

Decreased synthesis
- analbuminaemia
-hypoalbuminaemia

Increased catabolism

Increased loss
- Nephrotic syndrome
- Exudate loss in burns
- Haemorrhage
- Gut loss

Redistribution
- Haemodilution
- increased capillary permeability
- Decreased lymph clearance

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6
Q

List three abnormalities of albumin synthesis

A

Bisalbuminaemia -> genetic variant of albumin - no clinical consequences

Analbuminaemia -> low synthesis -> slight consequences e.g mild oedmea

Hyperalbuminaemia -> high albumin found only artefactually i.e. prolonged venous stasis, loss of protein free fluid - dehydration

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7
Q

Why measure albumin?

A

To find out if hyperproteinaemia is due to dehydration, hypergammaglobulinaemia, or high albumin

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8
Q

What are the diagnostic differences between dehydration and hypergammaglobulinaemia

A

Dehydration = high total protein and high albumin
Hypergammaglobulinaemia = high total protein and normal/low albumin

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9
Q

What does high total proteins, albumin and globulins indicate?

A

Dehydration

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10
Q

What does high total proteins, normal/low albumin and high globulins indicate

A

Immune response

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11
Q

What does very high total proteins, normal/low albumin and very high globulins indicate?

A

Multiple myeloma

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12
Q

What does low total proteins, albumin and globulins indicate
(5)

A

Liver disease (globulins might be normal)
Renal disease
Salt retention syndrome
Intestinal malabsorption
Burns

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13
Q

What does low total protein, normal albumin and low globulin indicate

A

Immune deficiency

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14
Q

Write a note on some of the important pieces of information on diabetes
(3)

A

GLUT4 = insulin responsive glucose transporter -> found in skeletal muscle, cardiac muscle, adipose tissue

Preproinsulin, proinsulin, insulin + C peptide

Insulin signalling promotes externalisation of preformed GLUT) -> receptor formed inside the cell but in diabetes no insulin produced so the receptor never gets the signal to be expressed on cell surface -> therefore glucose can not be transported into the cell

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15
Q

Write a note on some of the important pieces of information on diabetes
(3)

A

GLUT4 = insulin responsive glucose transporter -> found in skeletal muscle, cardiac muscle, adipose tissue

Preproinsulin, proinsulin, insulin + C peptide

Insulin signalling promotes externalisation of preformed GLUT) -> receptor formed inside the cell but in diabetes no insulin produced so the receptor never gets the signal to be expressed on cell surface -> therefore glucose can not be transported into the cell

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16
Q

Write a note on some of the important pieces of information on diabetes
(3)

A

GLUT4 = insulin responsive glucose transporter -> found in skeletal muscle, cardiac muscle, adipose tissue

Preproinsulin, proinsulin, insulin + C peptide

Insulin signalling promotes externalisation of preformed GLUT) -> receptor formed inside the cell but in diabetes no insulin produced so the receptor never gets the signal to be expressed on cell surface -> therefore glucose can not be transported into the cell

17
Q

What is produced by the endocrine and exocrine parts of the pancrease

A

Endocrine = alpha cells = glucagon, beta cells = insulin of islets of Langerhans

Exocrine = digestive enzymes to duodenum through ducts

18
Q

What hormones can raise blood glucose

A

Glucagon
Cortisol
Epinephrine
Growth hormone

19
Q

What can be seen in increased blood glucose

A

Increased insulin
Decreased glucagon
Increased glycogenesis
Increased fatty acid synthesis
Decreased glycogenolysis
Decreased gluconeogenesis

20
Q

What can be seen in starvation
(5)

A

Insulin down
Glucagon up
Glycogen depletion
Triglyceride catabolism and ketone formation
Protein breakdown and gluconeogenesis

21
Q

List some causes of atypica/non immune diabetes
(6)

A

Genetic defects of beta-cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas -> endocrinopathies
Drug/chemical induced
Infections

22
Q

List some causes of atypica/non immune diabetes
(6)

A

Genetic defects of beta-cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas -> endocrinopathies
Drug/chemical induced
Infections

23
Q

List some causes of atypica/non immune diabetes
(6)

A

Genetic defects of beta-cell function
Genetic defects in insulin action
Diseases of the exocrine pancreas -> endocrinopathies
Drug/chemical induced
Infections

24
Q

What are the main causes of renal failure

A

Pre- renal e.g. decreased ECFV or MI

Renal e.g. acute tubular necrosis

Postrenal e.g. ureteral obstruction (stones)

25
Q

What are the main causes of renal failure

A

Pre- renal e.g. decreased ECFV or MI

Renal e.g. acute tubular necrosis

Postrenal e.g. ureteral obstruction (stones)

26
Q

What is renal failure

A

A deterioration in renal function leading to a complex of symptoms and signs

27
Q

Why is bilirubin measured
(2)

A

Determining jaundice

Distinguishing conjugated from unconjugated hyperbilirubinaemia -> if unconjugated is high then there is a problem with conjugation in the liver -> high conjugated bilirubin indicated cholestasis

28
Q

Why is ALP measured

A

To diagnose cholestasis

29
Q

Why is ALP measured

A

To diagnose cholestasis

30
Q

Why is AST measured

A

Diagnosing hepatocellular damage
AST>ALT in alcoholic disease, cirrhosis

31
Q

Why is ALT measured

A

Diagnosing hepatocellular disease

32
Q

Why is albumin measured in a liver profile

A

As an indication of how chronic, severe the condition

33
Q

Why is prothrombin time measured in a liver profile

A

Indication of severity -> lack of coagulation factors

34
Q

Write a note on dyslipidemia
(4)

A

A consequence of abnormal liporoprotein metabolism - high lipid levels

Elevated total cholesterol, elevated LDL, elevated triglycerides, decreased HDL

Primary - Caused by gene mutations -> problems with production or clearance of lipids

Secondary - caused by sedentary life and poor diet

35
Q

What are the affects of hypercholesterolemia

A

Major risk factor for coronary heart disease
- cholesterol deposited along walls of blood vessels -> LDL is a key player
- impedes blood flow -> tissues starved of oxygen start to die -> angina/heart attack

36
Q

What increases your chances of coronary heart disease

A

Smoking
High blood pressure
High blood cholesterol
Physical inactivity

37
Q

Write a note on primary hyperlipidaemias

A

e.g. chylomicron syndrome
inability to clear chylomicrons from circulation -> CMs are high in TAGs which leads to profound hypertriglyceridaemia

-> leads to xanthomata -> lipids bursting out

-> treated with low fat diet

2.2 Clinical Chemistry (28 decks)

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