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Medicine 3 > GIM 3 > Flashcards

GIM 3 Flashcards

1
Q

What organs does the portal vein supply the liver from?

A

Stomach, spleen, intestine, pancreass

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2
Q

Where do bile pigments (e.g. bilirubin) originate from?

A

Breakdown products of haemoglobin conjugated with glucuronic acid

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3
Q

What is urobilinogen and how is it secreted?

A

Bile pigments acted on by colon bacteria.
Some taken back into blood and excreted by kidney as urobilin (yellow pigment of urine).
Some converted into stercobilin (brown pigment of faeces)

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4
Q

How is bile directed to storage in the gall bladder?

A

Hepatocytes secretions build up pressure and bile flow is forced towards the duodenum. Flow into duodenum is prevented by closure of Sphincter of Oddi and enters gall bladder instead.

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5
Q

What happens to bile during storage in the gall bladder?

A

Bile salts and pigments concentrated due to salt and water reabsorption in gall bladder

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6
Q

How does bile enter the duodenum after a meal?

A

Neural influences and CCK relaxes Sphincter of Oddi and contracts gall bladder

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7
Q

What are gall stones?

A

Cholesterol crystallisation from bile salts

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8
Q

How is the liver related to metabolism of carbohydrates?

A

Converts fructose and galactose to glucose
Converts some glucose to glycogen for storage
Converts some glucose to triacylglycerol

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9
Q

What does the liver do to absorbed fats?

A

Combines fats with protein and released as lipoproteins

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10
Q

What are the 2 phases of liver detoxification?

A

Phase 1 - oxidation/reduction

Phase 2 - conjugation

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11
Q

What causes jaundice?

A

Bilirubin accumulation in plasma.

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12
Q

What are the signs and symptoms of jaundice?

A

Yellowing of skin, sclera and mucous membranes. May produce kernicterus - deposits of pigment in brain leading to nerve degeneration

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13
Q

How do you treat jaundice?

A

Light - breaks down pigment

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14
Q

What are the different types of jaundice?

A

Haemolytic jaundice - excessive haemolysis of red blood cells
Intrahepatic jaundice - defect in uptake, conjugation or secretion of bilirubin by hepatic cells
Obstructive jaundice - blockage of bile ducts
Physiological jaundice of newborn - babies have poor capacity for conjugating bilirubin

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15
Q

What is hepatitis?

A

Infection/inflammation of the liver (acute or chronic)

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16
Q

What is cirrhosis?

A

Necrosis of liver cells - replaced by fibroblasts

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17
Q

What are the pacemaker cells of the gut called?

A

Interstitial cells of Cajal. Initiate basal electrical rhythm

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18
Q

How does parasympathetic activation increase gut motility?

A

Acetylcholine acts on muscarinic receptors

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19
Q

How does sympathetic activation decrease gut motility?

A

Directly - noradrenaline on beta-adrenoceptors

Indirectly - noradrenaline on alpha2-adrenoceptors decreases release of ACh

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20
Q

How is peristalsis initiated?

A

Mechanoreceptors in pharynx detect food bolus. Persitaltic wave initiated and controlled by vagus nerve.

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21
Q

What is the purpose of peristaltic waves in the stomach?

A

To mix gastric contents and to empty contents into duodenum.

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22
Q

What is vasoactive intestinal polypeptide (VIP)?

A

Peptide hormone responsible for peristaltic relaxation. Stimulated by oesophageal and gastric distension.

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23
Q

What slows the rate of gastric emptying into the duodenum?

A

Osmolarities of chyme greater and smaller than 200 mOsm

Excess acid in the small intestine

Fat in upper small intestine

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24
Q

What increases the rate of gastric emptying into the duodenum?

A

Greater volume of gastric contents

Smaller fragment size

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25
Q

What is the purpose of segmenting contractions in the small intestine? What muscle type does it occur in?

A

To mix intestinal contents with secretions and increase exposure to mucosal surface. Circular muscle.

26
Q

How do contractions ensure food moves oral to anal?

A

Basal electrical rhythm in duodenum is 12/min and 9/min in terminal ileum

27
Q

How is small intestine motility controlled?

A

Myogenic mechanisms (stretch)
Myenteric plexus (local regulation)
Extrinsic nerves
Local chemicals

28
Q

Describe large intestinal motility

A

Mostly slow and non-propulsive with 3/4 powerful contractions per day for defecation

29
Q

What is cholestasis?

A

When bile cannot flow from liver to duodenum.

30
Q

Why are bilirubin levels used in a liver function test?

A

Liver conjugates bilirubin to make it water soluble and excretes it as bile. High levels of bilirubin mean liver function impaired. Increased in cholestasis, hepatocellular damage and haemolysis.

31
Q

What are the aminotransferases used in liver function tests and why are they useful for testing liver function?

A

Aspartate (AST) and alanine (ALT) transaminase. Leak out from damaged cells so markedly raised in hepatocellular damage

32
Q

Why is alkaline phosphates used in liver function tests?

A

Present in canalicular and sinusoidal membranes of liver and markedly raised in cholestasis and metastatic infiltration of the liver

33
Q

Why is international normalised ratio (INR) used in a liver function test?

A

Uses prothrombin time to show coagulation activity. High INR shows liver damage (blood is taking longer to clot)

34
Q

What is bilirubin in the urine and pale stools a sign of?

A

Obstructive jaundice - liver can convert bilirubin to soluble form but cannot excrete it in bile

35
Q

What are goblet cells?

A

Exocrine glands that secrete mucus

36
Q

What are enteroendocrine cells?

A

Cells of the GI tract that produce hormones and have paracrine, neurocrine and endocrine effects

37
Q

What is the epithelium type in the stomach?

A

Gastric columnar mucosa

38
Q

What does the pKa of a drug tell us?

A

The pH at which the ratio when the drug is charged:uncharged is 50:50

39
Q

Are weak acid or weak base drugs more likely to enter brain

A

Weak base drugs because they are largely present in unionized form at blood pH

40
Q

Why is drug ionisation related to absorption?

A

Drugs that are ionised cannot pass into cells as they cannot get across the lipid bilayer. Unionised drugs can diffuse into the cells.

41
Q

What is found in the portal field in the liver?

A

Portal vein
Hepatic artery
Bile duct
Lymphatic vessels

42
Q

What is a liver sinusoid?

A

Highly porous vascular channel derived from fusion of terminal branches of hepatic artery and portal vein

43
Q

What are liver canaliculi?

A

Intercellular gutters between hepatocytes

44
Q

What are the three concepts of organisation inside the liver?

A

Classic lobule - drained by central vein
Portal lobule - drained by bile duct
Acinus - supplied by terminal branches of hepatic artery and portal vein

45
Q

What are Kupffer cells?

A

Resident macrophages in the liver

46
Q

What are hepatic stellate cells?

A

Store 80% of the body’s retinol (vit A) and produce the EDM scaffold that holds the space of Dissé open

47
Q

What is the space of Dissé?

A

The space between a hepatocyte and a sinusoid containing blood plasma

48
Q

What are peribiliary glands?

A

Secrete mucin, stem cell niche, contribute to regeneration of biliary epithelium after injury

49
Q

What are the two types of gland in the pancreas?

A 
Exocrine glands
Endocrine glands (islets of Langerhans)
50
Q

What are the clinical features of viral hepatitis?

A 
Malaise
Anorexia
Nausea
Abdominal discomfort
Fever
Pale stool/dark urine
Jaundice
51
Q

Describe the makeup of hepatitis A

A

+ve single stranded RNA

52
Q

How is hepatitis A transmitted

A

Faecal-oral transmission (contaminated food or water)

53
Q

What are the consequences of hepatitis A infection?

A 
Asymptomatic infection
Acute icteric (jaundice) hepatitis
54
Q

How is hepatitis B transmitted?

A

Mother to baby
Sexual
Parenteral (unsafe injections, transfusion)

55
Q

What is the main transmission of hepatitis C?

A

Blood-borne virus

56
Q

What is emesis?

A

Vomiting

57
Q

What are the different types of anti-emetic drugs that can be used?

A

H1-receptor antagonists - promethazine, act on vestibular nuclei to help motion sickness
Anti-muscarinic agents - hyoscine
Dopamine antagonists - metoclopramide, effective against anti-cancer drug emesis
5-HT antagonist - ondansetron, anti-cancer drugs

58
Q

How do enterotoxigenic bacteria cause diarrhoea?

A

Adhere to brush border, increase cAMP, increased Cl- and Na+ secretion, increased water secretion

59
Q

How do you treat diarrhoea?

A

Oral rehydration therapy - replace lost electrolytes.

60
Q

How do antimotiliy agents help treat diarrhoea?

A

Opioid drugs that inhibit presynaptic release of ACh. Reduces GI motility and increases transit time to promote water reabsorption (codeine and loperamide)

61
Q

How do laxatives treat constipation?

A

Through osmotic effect and by stimulating GI motility (e.g Mg2+, lactulose)

62
Q

How do you treat IBS?

A

Antispasmodic agents (antimuscarinics to inhibit parasympathetic activity), amitriptyline (alters nerve sensitivity in GIT)

Medicine 3 (8 decks)

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