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GI - Y2 > L15 - Alcohol > Flashcards

L15 - Alcohol Flashcards

1
Q

Hepatic stellate cells

A

Fat containing myofibroblasts.

Myofibroblasts
- contractile cell, contraction stimulated by endothelin-1

Increase in platelet derived growth factor will activate hepatic stellate cells into myofibroblasts

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2
Q

Steatosis

A

Accumulation of fat in hepatocytes

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3
Q

Cholestasis

A

Decrease in bile flow due to impaired secretion by hepatocytes or to obstruction of bile flow.

Substances normally excreted in bile are retained e.g. billirubin

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4
Q

Hepatocyte integrity measured by:

A

Serum

  • aspartate aminotransferase AST
  • alanine aminotransferase ALT
  • lactate dehydrogenase LDH
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5
Q

Function of Kupffer cell and lymphocytes

A

Release cytokines and chemokines which moldulate the expression of genes in stellate cells that are involved in fibrogenesis.

e.g. TGF-b

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6
Q

Cirrhosis

A

Diffuse transformation of entire liver into regenerative parenchymal nodule surrounded by fibrous bands and variable degrees of vascular shunting.

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7
Q

Impaired oestrogen metabolism and consequent hypereoestrogenemia in male patients with chronic liver failure can lead to:

A

Palmar erythema
- reflection of local vasodilation
Spider naevi
- central pulsating dilated arteriole from which small vessels radiate

Gynecomastia
Hypogonadism

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8
Q

Describe portal hypertension in liver

A

Increased resistance to portal blood flow.
- alteration in sinusoidal endothelial cells that contribute to the intrahepatic vasoconstriction; associated with portal hypertension

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9
Q

What other factors can cause vasoconstriction

A
  • decreased nitric oxide
  • increased endothelin-1
  • angiotensinogen
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10
Q

Four major clinical clinical consequences of portal hypertension

A
  1. Ascites: accumulation excess fluid in peritoneal cavity
  2. Formation of portosystemic venous shunt
  3. Congestive splenomegaly
  4. Hepatic encephalopathy
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11
Q

Morphology of hepatic steatosis

A
  • lipid droplets accumulate in hepatocytes
  • lipid begins as small droplets
    coalesce into large one which distend the hepatocyte
  • nucleus pushed aside
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12
Q

Describe alcoholic (steato-) hepatitis

A

Hepatocyte swelling and necrosis
- accumulation fat, water and proteins which are normally exported

Inflammation induces production and accumulation of ECM (collagen) from Hepatic stellate cells.

Mallory Denk bodies
- clumped eosinophil material in ballooned hepatocyte

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13
Q

Steatofibres

A

Alcoholic steatofibrosis

- fibrosis begin with sclerosis of central vein

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14
Q

Why are females more susceptible to hepatic injury

LPS - lipopolysaccharide

A
  • oestrogen increases gut permeability to endotoxins
  • increased expression of LPS receptor CD14 in Kuppfer cell.
  • predisposes to increase production of pro-inflam cytokines and chemo kines
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15
Q

Hepatocellular steatosis occurs because

A
  • normal substrates shunted away from catabolism to lipid biosynthesis, hence increase in reduced NADH
  • impaired assembly and secretion of lipoproteins
  • increased peripheral catabolism of fat, releasing free fatty acids into circulation
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16
Q

What does the alcohol metabolite acetylaldehyde induce

A
  • lipid peroxidation
  • protein adduct formation

Disrupts cytoskeleton and membrane function.

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17
Q

Patients resistant to insulin

A
  • increase in visceral adipose tissue
  • decrease in adiponectin (lipid hormone)
  • increase in inflammatory cytokines TNF-a , IL-6
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18
Q

Autophagy

A

Body’s way of cleaning out damaged cells

19
Q

Diminished autophagy contributes to

A
  • mitochondrial injury
  • formation of Mallory Denk bodies
  • Kupffer cell production of TNF-a, TGF-R
  • activates stellate cell
  • deposition of scar tissue
20
Q

Haemochromatosis

A
  • caused by excessive iron absorption

- iron deposited in parenchyma in organs such as liver, pancreas, heart joint and endocrine organs

21
Q

Ethanol oxidation results in increased ratio of…

A

NADH to NAD+

  • inhibits oxidation of lactate to pyruvate
  • pyruvate susbtrate for hepatic gluconeogenesis
  • hence risk of hypoglycemia
  • NAD+ needed as a co-factor,
22
Q

Describe the NADH/NAD+ shift

When NADH increases

A
  • inhibits beta oxidation of fatty acids
  • promotes triglyceride synthesis
  • excess of triglyceride deposited in liver
  • secreted into plasma as VLDL
23
Q

Chronic alcohol consumption has what effect on proteasome activity

A

Decreases proteasome activity.
Can de-regulate hepatocyte signalling by inhibiting Janus Kinase signal transduer and activation of transcriptor JAK-STAT (acute phase response fo antiviral defence)

Accumulation of protein in liver –> enlargement

24
Q

Increased secretion of chemokine IL8 and monocyte chemo-attractant protein 1 by hepatocytes leads to…

A

Leads to liver infiltration by neutrophils.

25
Q

Describe speed of ingestion of alcohol

A

Slowly absorbed from stomach.

Rapidly absorbed from the small intestine.

26
Q

Which enzymes metabolise the ethanol consumed?

A
  • Alcohol dehydrogenase ADH

- Mitochondrial acetylaldehyde dehydrogenase ALDH

27
Q

First step in the metabolism of alcohol?

A

Oxidation of ethanol to acetylaldehyde catalysed by ADH.
Uses NAD+ and reuslts in generation of reduced NADH.

Acetylaldehyde - acetate

  • also requires NAD+
  • results in reduced NADH
28
Q

Why might alcohol consumption cause tachycardia and increase in BP?

A
  • stimulation of the hypothalamus

- increased release of sympathetomimetic amines and pituitary adrenal hormones.

29
Q

What happens to the acetate produced?

A

Further oxidized to CO2 and H20. Example of mitochondrial extrahepatic oxidation.

Acetate entering the citric acid cycle generates even more NADH.

30
Q

Describe how metabolism of alcohol is faster in heavy drinkers?

A
  • high blood acetate levels
  • brings the microsomal ethanol oxidising system into play
  • dependent on liver enzyme cytochrome P450IIE1 , which may increased after chronic drinking
31
Q

Why does drinking alcohol warm people up for a short time?

A

Rapid NADH production from alcohol.

Increases energy availability and body temperature.

32
Q

Describe how excess NADH can lead to acidosis?

A
  1. Pyruvic acid —NADH— lactic acid
  2. low [pyruvic acid] results in inhibition of hepatic gluconeogenesis.
  3. Glucose production reduced.
  4. Hypoglycaemia risk
  5. Over production of lactic acid blocks uric acid excretion by the kidneys.
33
Q

Effects of excess NADH?

A
  1. Inhibition of lipolysis and increases lipogenesis.
  2. Accumulated fatty acids, converted into ketones and lipids.
  3. Heavy drinkers tend to be overweight.
34
Q

Summarise how alcohol damages the GI tract?

A
  1. Inflammation of tongue, stomach, pancreas, liver and intestines.
  2. Breakdown products lead to fat deposition, fibrosis and scarring of the liver.
  3. Impaired digestion and absorption of food.
  4. Diarrhoea
35
Q

Describe effects of alcohol on pancreas?

A
  1. Stimulation of CCK and secretin release from duodenum
  2. Changes in pancreatic blood flow and secretion
  3. Generation of free radicals from ethanol metabolism leading to necrosis.
36
Q

How might non-oxidative metabolism lead to pancreatitis?

A

Non-oxidation metabolism of alcohol via carboxylesterase.
Results in fatty acid ethyl esters forming.
Results in calcium spike overload, mitochondrial dysfunction, necrosis –> Pancreatitis

37
Q

Will oxidative metabolism lead to pancreatitis?

A

Oxidative metabolism
- alcohol dehydrogenase
- cytochrome P450
Acetate

No calcium spikes.
No pancreatitis.

38
Q

Summarise signs of necrosis

A
  • Jaundice
  • Fluid in belly (ascites)
  • vomitting blood (haemetemesis)
  • confusion (hepatic encephalopathy)
  • spider naevi
  • gynaecomastia (reduction in testosterone production)
39
Q

Oesophageal varices

A

Abnormal dilation of veins due to increase in portal vein pressure.

40
Q

Effect of alcohol on brain

A
  • alcohol increases dopamine release to cause euphoria
  • inhibits glutamate receptor function.
  • potentiates GABA-A receptor function
  • increases release of serotonin (5HT)
41
Q

5HT plays major role in

A

Sleep-wakefullness cycle, mood and emotion

42
Q

GABA

A

Major inhibitory neurotransmitter in brain.
Receptor sub types.
a5 - memory impairing effects
a2,a3 - relaxation and pleasure mediating effects
a1 - sedation, anaesthesia and unsteadiness

43
Q

Describe production of No in a cirrhotic liver?

A

Normally NO vasodilator synthesised by sinusoidal endothelial cells.
Production of NO decreased. in cirrhotic liver. Intraheptatic vasoconstriction occurs in CL and accounts for some increased intrahepatic resistance.

GI - Y2 (18 decks)

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