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
Where is ADH synthesised and stored?
Synthesised by the hypothalamous, stored in the posterior pitautry
26
What does ADH cause?
Kidney tubules to increase the reabsorbtion of water | Vasoconstriction
27
ADME
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
Oral availability
The fraction of the drug that gets into the systemic circulation after being ingested
29
Systemic availability
The fraction of the drug reaching the systemic circulation after absorption
30
First pass metabolism
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
Factors affecting drug absorption
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
What is the degree of ionisation?
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
Name some trends with acids/bases and absorption
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
Bound drugs can move between body compartments. True or false.
False- bound drugs cannot move between body compartments
35
Unionised drugs can move between the interstitial water and fat. True or false.
True
36
Both unionised and ionised drugs can move between the interstitial water and plasma water. True or false.
True.
37
Which routes of taking in drugs go through the liver.
Oral and (sometimes) rectal
38
Which routes bypass the portal system and go straight into the systemic system?
Sublingual, intramuscularly, transdermal, inhalation and I.v. Sometimes rectal also.
39
Pathological findings of Crohns
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
Pathological findings of Ulcerative Colitis
MUCOSAL/SUBMUCOSAL INFLAMMATION Crypt abscesses also form in UC. Psuedopolyps- raised area of inflamed tissue that look like polyps
41
Why do you get inflammation in Crohns and UC?
Macrophages and neutrophils attack the intestinal wall
42
Treatment of UC and Crohns
Mild/moderate- 5 aminosalicylic acid e.g. Mesalazine Anti TNF therapy Severe- corticosteroids e.g. prednisolone
43
Treatment of UC and Crohns during relapses
Prophylactic antibiotics are used
44
Symptoms of Crohns
Commonly affects the terminal ileum and large colon. RLQ (terminal ileum)- Abdominal pain, diarrhoea, weight loss, fatigue. Colon- diarrhoea +/- blood, fever
45
Symptoms of ulcerative colitis
Colon- crampy left iliac fossa pain | Diarrhoea- often bloody
46
Extra intestinal features of UC
Joint pain, erythema nodosum, liver disease
47
Tests for UC and Crohns
Raised CRP and WCC. Also increased sedimentation rate. Anaemia (decreased vitamin B12) Malabsorption (decreased albumin) Radiology Barium enema Biopsy
48
Coeliac disease
Ingestion of gluten causes inflammatory response. Stopping gluten stops this.
49
Immunology of coeliac disease
Prolamins are indigestable in the gut and therefore just sit there and cause a CD4+ T cell mediated inflammatory response.
50
Symptoms of coeliacs
``` Fatigue and tiredness GI symptoms may be absent or mild Malabsorption Raised MCV Iron deficiency Possible IgA deficiency ```
51
Who is most commonly affected by coeliacs
Middle aged females.
52
Tests for coeliacs
Anti-tissue transglutiminase Endomysal test Small bowel biopsy Anaemia, follate deficiency,iron deficiency
53
Treatment of coeliacs
Don't eat gluten | Vitamins
54
Presentation of ischaemic bowel
``` ACUTELY UNWELL Presents as sudden onset abdominal pain Vomiting Abdominal distension Absent bowel sounds Tender stomach ```
55
Ischaemic intestine
Surgical emergency | Gangrenous bowel needs removal
56
Ischaemic colitis
May present with blood in poo, accompanied by diarrhoea
57
Tests for ischaemic colitis
AXR- may show thumbprinting Most likely to occur in splenic flexure Flexible sigmoidoscopy- first line Biopsy reveals epithelial cell apoptosis
58
Treatment of ischaemic colitis
Surgery | May only need symptomatic relief