Tobacco, Alcohol Flashcards by isabelle courtney | Brainscape

Q

Explain why nicotine is so addictive, what does it stimulate?

A

Nicotine stimulate the release of catecholamines from sympathetic neurons leading to a heightened “Pleasure response”

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Q

Describe the features of Thromboangiitis Obliterans (Beurgers disease)

A

A condition 100% due to smoking, usually seen in heavy smokers younger than 35

Chronic smoking leads to direct endothelial cell toxicity or an autoimmune response to the tobacco

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Q

Describe the signs of Thromboangiitis Obliterans (Beurgers disease)

A

Segmental thromboses of small-med arteries which leads to vasculitis & luminal thrombosis
Intermittent claudication which leads to gangrene of digits
Can cause fibrosis surrounding vein & nerve

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Q

Patient with a blood alcohol of 20mg/dL will present with

A

Lowered inhibitions & slight intoxication

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Q

Patient with a blood alcohol of 80mg/dL will present with

A

Decreased complex cognitive functions & motor control (drunk driving)

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Q

Patient with a blood alcohol of 200mg/dL will present with

A

Drowsiness
Slurred speech
Motor incoordination
Irritability (try to fight + uncooperative)
Poor judgement

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Q

Patient with a blood alcohol of 300mg/dL will present with

A

Stupor
Light coma
Depressed vitals

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Q

Patient with a blood alcohol of 400mg/dL will present with

A

Coma &/or
Death

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Q

Coma &/or
Death

What is the blood alcohol level?

A

400mg/dL

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Q

Stupor
Light coma
Depressed vitals

What is the blood alcohol level?

A

300mg/dL

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Q

Drowsiness
Slurred speech
Motor incoordination
Irritability (try to fight + uncooperative)
Poor judgement

What is the blood alcohol level?

A

200mg/dL

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Q

Decreased complex cognitive functions & motor control (drunk driving)

What is the blood alcohol level?

A

80mg/dL

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Q

Lowered inhibitions & slight intoxication

What is the blood alcohol level?

A

20mg/dL

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Q

Describe how increased alcohol intake impacts the ethanol metabolism pathway

A

More alcohol in means higher ethanol metabolism which depletes NAD & accumulates NADH

The skewed NADH(high) & NAD(low) ratio leads to the following:

Ketoacidosis (more acetyl-coA into ketogenesis)
Hepatosteatosis (more DHAP & acetyl-coA into lipogenesis)
Lactic acidosis (more pyruvate is made into lactate)
Fasting Hypoglycemia (inhibited TCA means less gluconeogenesis)

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Q

Alcohol abuse progresses in stages of liver damage what is the order or liver damage?

A

Fatty change aka hepatic steatosis
Alcoholic hepatitis (reversible)
Alcoholic cirrhosis (irreversible)

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Q

Describe the features of alcohol induced fatty change (aka hepatic steatosis)

A

Usually asymptomatic for the most part but will present with:

Hepatomegaly (NO inflammation or necrosis)

Reversible

Q

Describe the pathophysiological changes in liver fatty change (aka hepatic steatosis)

A

Alcoholics don’t usually eat enough or their absorption is impaired so their bodies burn through fat and resupply it in the liver:

More peripheral fat catabolism to increase free fatty acids going to the liver
skewed NADH/NAD ratio increases lipogenesis in the liver
Mitochondria don’t oxidize fat as much
Lipoproteins can’t be moved out of the liver (because the accumulated acetaldehyde binds tubulin)

All this reduce body fat but increase liver fat

Q

Describe the features of alcohol induced hepatitis

A

Usually from acute alcohol intake (i.e 1-2 days after binge drinking):

Tender/painful liver
Hepatocellular necrosis (Mallory bodies & PMNs)
Central hyaline sclerosis

This is reversible but also a precursor to cirrhosis

Q

Describe the features of alcoholic cirrhosis

A

A shrunken & nodular liver that can be classified base on nodular size

micronodular >3mm
macronodular <3mm
mixed cirrhosis

Necrosis & fibrosis surrounding regenerative nodules (because necrosis damages hepatocytes framework)
Sclerosis around the central vein (increased portal hypertension: esophageal & rectal varices, ascites, & caput medusae)

Q

Alcohol:

Describe the features of thiamine (B1) deficiency (not asking for symptoms here!)

A

Alcohol reduces B1 absorption & inhibits the TCA cycle. This means the patient will present with fasting hypoglycemia but make sure to give B1 before dextrose or it can cause some serious damage!

Q

Alcohol:

Describe the cardinal signs of Thiamine (B1) deficiency in alcoholics

A

The main cardinal signs:
- Heart failure
- Polyneuropathy
- Edema

Q

Alcohol:

Describe the alternative signs of Thiamine (B1) deficiency in alcoholics

A

Wet beriberi
- Cardiac failure (aka cardiomegaly & reduced ejection fraction)
- Edema (hyperdynamic failure)

Others
- Weight loss
- Muscle wasting
- Wernicke’s encephalitis (Dementia, Ophthalmoplegia, & Ataxia)

Q

What are two cases where severe thiamine (B1) deficiency can happen?

A

Chronic alcoholism
&
A polished rice diet
(no vitamins in polished/white rice)

Q

Alcohol:

Describe ALL the symptoms associated with thiamine (B1) deficiency

A

Polyneuropathy
Wet beriberi (cardiomegaly & edema)
Weight loss
Muscle wasting
Wernicke-Korsakoff syndrome
Alcoholic cardiomyopathy (normal thickness, cold/clammy extremities, & low ejection fraction)

Q

Describe the features of Wernicke-Korsakoff syndrome

A

Only from B1 deficiency, hypoglycemic patients get worse if they’re not given B1 before dextrose.

Signs:
- Wernicke’s encephalopathy (Dementia, Ophthalmoplegia, & Ataxia)

It can progress to Korsakoff’s syndrome:
- Irreversible memory loss
- Confabulation
- Personality changes

It DOES respond to B1 replacement

Q

Describe the signs of Korsakoff syndrome

A

A progression of Wernicke’s encephalopathy in thiamine deficient & direct toxicity:

Irreversible memory loss
Confabulation (unintentional false memories)
Personality changes

It DOESN’T respond to B1 replacement

Q

Describe why females are more prone for developing an alcohol disorder

A

They absorb alcohol faster because their endoplasmic reticulum hyperplasia

Q

_________ have type 2 ADH and are more prone for developing what condition?

A

Asians tend to have type 2 ADH causing them to develop liver cirrhosis

Q

Describe the features of Polymorphic ALDH2

A

It causes the highest accumulation of acetaldehyde

Signs:
- nausea
- tachycardia
- flushing
- Hyperventilation

Q

Describe the physiological changes in Wernicke’s encephalitis

A

Necrosis of mamillary bodies in hypophysis
Necrosis of periaqueduct gray matter
Accumulation of hemosiderin in brain matter

Q

Describe the features of alcoholic cardiomyopathy

A

alcohol metabolites like acetaldehyde can cause dilated congestive cardiomyopathy

Histo slides will show interstitial fibrosis with myocyte hypertrophy