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Posters > Review posters 12/05/2016 > Flashcards

Review posters 12/05/2016 Flashcards

1
Q

AST

A

aspartate amino transferase

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2
Q

It what situations does AST become raised?

A

In acute liver injury. However it also becomes raised in heart and muscle.

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3
Q

ALT

A

Alanine aminotransferase

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4
Q

In what situations is ALT raised?

A

Acute liver cell injury

Specific to the liver

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5
Q

Describe the relationship between ALT and AST

A

If both ALT and AST are raised- liver injury.

If just AST is raised- likely to be heart or muscle

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6
Q

ALP

A

Alkaline Phosphatase

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7
Q

In what situations is ALP raised

A

Generally raised in biliary tree damage and in certain bone cancers

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8
Q

GGT

A

Gamma glutamyl transferase

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9
Q

In what situations is GGT raised?

A

GGT specific to the liver/biliary tree

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10
Q

Describe the relationship between ALP and GGT

A

If both GGT and ALP are raised- liver/biliary tree

If only ALP- somewhere else

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11
Q

Albumin

A

Raised in chronic liver damage

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12
Q

Prothrombin time

A

Time it takes for blood to clot. Clotting factors are produced by hepatocytes and will not be produced in liver damage.
It is the first thing to show in liver injury

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13
Q

In what other situations can PTT be raised

A

Use of blood thinner e.g. aspirin and potassium vitamins.

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14
Q

What percentage of a persons weight is water?

A

60%

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15
Q

The fluid inside the body is made up of:

A

Extracellular fluid and intracellular fluid

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16
Q

Extracellular fluid is made up of:

A

Plasma fluid and interstitial fluid

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17
Q

How can extracellular fluid control MAP

A

If there is a drop in plasma volume, fluid from the interstitium will move across to counteract this.

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18
Q

Which hormones help to regulate plasma volume and hence MAP

A

Anti-Natriuretic Peptide (ANP)
The Renin-angiotensin-aldosterone-system
Anti-diuretic hormone (ADH)

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19
Q

Describe the Renin-Angiotensin-Aldosterone system

A

The kidneys (juxtaglomerular complex) produce renin. The Renin then goes on to activate angiotensinogen (produced by the liver) to form angiotensin I. Angiotensin I is then converted to angiotensin II by ACE. Angiotensin II stimulates the cerebral cortex to produce aldosterone.

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20
Q

What effects does aldosterone have on the body?

A

It causes vasoconstriction, thirst and ADH release to increase blood pressure.

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21
Q

When does renin get released?

A

When the renal pressure is low
When the Na+ concentration is low
Stimulation of renal sympathetic nerves

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22
Q

When is ANP released?

A

Released in response to atrial dilation by atrial muscle cells.

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23
Q

What does ANP cause?

A

Causes excretion of salt and water in the kidneys
Vasodilates
Decreases renin release

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24
Q

When is ADH released?

A

Stimulated by reduced extracellular volume or an increase in extracellular osmolarity

25
Q

Where is ADH synthesised and stored?

A

Synthesised by the hypothalamous, stored in the posterior pitautry

26
Q

What does ADH cause?

A

Kidney tubules to increase the reabsorbtion of water

Vasoconstriction

27
Q

ADME

A

Absorption- Drug getting into the systemic circulation
Distribution- Drug leaving the systemic circulation and entering the tissues
Metabolism- converting the drug to its more polar form
Excretion- excreting the drug from the body

28
Q

Oral availability

A

The fraction of the drug that gets into the systemic circulation after being ingested

29
Q

Systemic availability

A

The fraction of the drug reaching the systemic circulation after absorption

30
Q

First pass metabolism

A

Drugs administered orally can undergo first pass metabolism. This is where they get deactivated by the liver or brush border enzymes before reaching the systemic circulation.

31
Q

Factors affecting drug absorption

A

Solubility- has to be able to dissolve
Chemical stability- some drugs may become inactivated by the stomach acid
Lipid to water partition co-efficient- the more lipid soluble a drug is- increased rate of diffusion
Degree of ionisation

32
Q

What is the degree of ionisation?

A

Only unionised forms of drugs will be absorbed. This depends on the pKa. pka=pH when 50% of the drug is ionised and 50% is unionised

33
Q

Name some trends with acids/bases and absorption

A

Weak acids and weak bases get absorbed more readily than strong acids and strong bases.
Weak acids get absorbed in the stomach (the acidic environment with an acidic drug means it will not become ionised) whereas weak bases are more likely to be absorbed in the small intestine

34
Q

Bound drugs can move between body compartments. True or false.

A

False- bound drugs cannot move between body compartments

35
Q

Unionised drugs can move between the interstitial water and fat. True or false.

A

True

36
Q

Both unionised and ionised drugs can move between the interstitial water and plasma water. True or false.

A

True.

37
Q

Which routes of taking in drugs go through the liver.

A

Oral and (sometimes) rectal

38
Q

Which routes bypass the portal system and go straight into the systemic system?

A

Sublingual, intramuscularly, transdermal, inhalation and I.v.
Sometimes rectal also.

39
Q

Pathological findings of Crohns

A

SKIP LESIONS
Crypt abscesses- walled off pocket of space forms an abscess. If this were to become infected it would cause a slight fever. However if it were to rupture it would cause peritonitis
Fistula- transmural inflammation goes through one area of bowel and starts to work its way into another. Could also occur between the bowel and the bladder.

40
Q

Pathological findings of Ulcerative Colitis

A

MUCOSAL/SUBMUCOSAL INFLAMMATION
Crypt abscesses also form in UC.
Psuedopolyps- raised area of inflamed tissue that look like polyps

41
Q

Why do you get inflammation in Crohns and UC?

A

Macrophages and neutrophils attack the intestinal wall

42
Q

Treatment of UC and Crohns

A

Mild/moderate- 5 aminosalicylic acid e.g. Mesalazine
Anti TNF therapy
Severe- corticosteroids e.g. prednisolone

43
Q

Treatment of UC and Crohns during relapses

A

Prophylactic antibiotics are used

44
Q

Symptoms of Crohns

A

Commonly affects the terminal ileum and large colon. RLQ (terminal ileum)- Abdominal pain, diarrhoea, weight loss, fatigue.
Colon- diarrhoea +/- blood, fever

45
Q

Symptoms of ulcerative colitis

A

Colon- crampy left iliac fossa pain

Diarrhoea- often bloody

46
Q

Extra intestinal features of UC

A

Joint pain, erythema nodosum, liver disease

47
Q

Tests for UC and Crohns

A

Raised CRP and WCC. Also increased sedimentation rate.
Anaemia (decreased vitamin B12)
Malabsorption (decreased albumin)

Radiology
Barium enema
Biopsy

48
Q

Coeliac disease

A

Ingestion of gluten causes inflammatory response. Stopping gluten stops this.

49
Q

Immunology of coeliac disease

A

Prolamins are indigestable in the gut and therefore just sit there and cause a CD4+ T cell mediated inflammatory response.

50
Q

Symptoms of coeliacs

A 
Fatigue and tiredness
GI symptoms may be absent or mild
Malabsorption
Raised MCV
Iron deficiency
Possible IgA deficiency
51
Q

Who is most commonly affected by coeliacs

A

Middle aged females.

52
Q

Tests for coeliacs

A

Anti-tissue transglutiminase
Endomysal test
Small bowel biopsy
Anaemia, follate deficiency,iron deficiency

53
Q

Treatment of coeliacs

A

Don’t eat gluten

Vitamins

54
Q

Presentation of ischaemic bowel

A 
ACUTELY UNWELL
Presents as sudden onset abdominal pain
Vomiting
Abdominal distension
Absent bowel sounds
Tender stomach
55
Q

Ischaemic intestine

A

Surgical emergency

Gangrenous bowel needs removal

56
Q

Ischaemic colitis

A

May present with blood in poo, accompanied by diarrhoea

57
Q

Tests for ischaemic colitis

A

AXR- may show thumbprinting
Most likely to occur in splenic flexure
Flexible sigmoidoscopy- first line
Biopsy reveals epithelial cell apoptosis

58
Q

Treatment of ischaemic colitis

A

Surgery

May only need symptomatic relief

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