Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology lectures > 22nd lecture (Effects of tobacco, and other drugs) > Flashcards

22nd lecture (Effects of tobacco, and other drugs) Flashcards

1
Q

which plant is used to make tobacco?

A

nicotiana tabacum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Most common method of tobacco consumption?

A

Smoking and inhaling and having the substances absorbed through the alveoli in the lungs or oral mucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why is nicotine addictive?

A

it binds to brain receptors mimicking dopamine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the acute immediate affects of nicotine?

A

It increases Heart rate
constriction of cutaneous blood vessels
muscular, hormonal and metabolic effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what damage does nicotine cause?

A
  • vessel damage as the carbon monoxide, to increased platelets stickiness and aggregation and damage to the lining of the blood vessels.
  • It has no direct carcinogenic activity itself, it enables the formation of tobacco-specific nitrosamines, which are potent carcinogens.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what does tobacco made of? what are the effects?

A
  • over 4000 potentially noxious chemicals
  • The toxic affects on the cilia and irritative to mucosa. (formaldehyde, oxides of nitrogen, Hydrogen Cyanide)
  • It also causes hypoxia to some extent due to impaired oxygen transport due to CO.

Carcinogenesis: Tar, PAH, benzopyrene, nitrosamine, metals-niccel, arsenic, cadmium, chromium, lead.

Tumor promotion is done by Phenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the tobacco induced diseases?

A
  • direct irritant effect on the tracheobronchial mucosa
  • carcinogenesis
  • atherosclerosis (Myocardial infraction)
  • Maternal smoking increases the risk of spontaneous abortions, growth retardation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe the appearance of the lungs in heavy smokers?

A

The superficial lymph vessels are filled with Tar and exogenous pigmentation and appear black.
COPD is the most common in smokers as the lung tissue is lost and shrinks. The increased pulmonary tissue resistance leads to pulmonary sclerosis artery due to the hypertension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what factors increases the risk of cancer in smokers?

A

the number of packages smoked per day.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does a smoker get squamous cell carcinoma if there are no such squamous cells in the lung?

A

the lung undergoes dysplasia and then neoplasai and then cancer develops. Metaplasia due to constant irritation of the tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what causes acute myocardial infraction in smokers?

A

coronary thrombosis, mural thrombosis. acute coronary syndrome, Thrombotic plaque formation, and enclosement of the coronary arteries.
CO and nicotine activates throbocyte activation, also the hypoxia also increases the risk of the coronary arteries closing up.
3-5 days old myocardial infraction (yellow necrosis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

burgeons disease definition

A

Buerger’s disease affects blood vessels in the arms and legs. Blood vessels swell, which can prevent blood flow, causing clots to form. This can lead to pain, tissue damage, and even gangrene (the death or decay of body tissues).
Smokers who have YD88G mutation are sensitive to the inhalated smoke causing increased IL33 cytokine production somehow activate and damage the vessels that are infiltrated by lymphocytes forming an acute vasculitis or a thromboangiitis obliterans; inflammation and thrombosis at the same time.

thromboangiitis obliterans = burgeons disease; the results in gangrene. This could cause the loss of hands and feet.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are some of the aggressive diseases in cigarette and pipe smokers.

A

oral and tongue cancers are very aggressive. esophagus cancer can close the esophagus, its difficult to operate and a stent has to be inserted to keep it open, but the patient will die later on.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does smoking cause stomach ulcers?

A

One of the effects of smoking is vasospasm which can cut of circulation to the stomach and the duodenum leading to ulcer formation due to necrosis. Peptic and gastric ulcers form which can bleed and most often the bleeding of the ulcers causes the death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when using a waterpipe that gives the user a 100-200 times volume of smoke inhaled with a single cigarette what is the headache causes by after its use?

A

acetaldehyde: it is toxic to cells and can shrink them, possible cutting off/limiting blood flow to the brain. The p450 system (CYP2E1 enzyme) breaks down ethanol to water and acetaldeyde, in some populations of the world this does not work right and they could get drunk. Catalase may also break down ethanol. But certain drugs affects can enhance the alcohols affect as they may block certain enzymes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Toxic effects of alcohol metabolism?

A

Toxic effects result from ethanol metabolism; since fatty oxidation requires NAD+, is deficiency causes fat accumulation in the liver of alcoholics as ethanol decreases NAD+ and increases NADH.

  • acetaldehyde toxicity
  • Endotoxin release from GI bacteria (stimulates TNF release of kuppfer cells)
  • ROS generation (lipid peroxidation of membranes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the order in which the damage to the liver occurs in alcoholics?

A
  • Fatty change
  • Alcoholic hepatitis
  • Fibrosis
  • Cirrhosis
  • Hepatocellular carcinoma (HCC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what damage occurs to the GI tract and pancreas in alcoholics?

A 
GI
-Gastritis
-Bleeding (gastric ulcer, esophageal varices)
Pancreas
-Acute pancreatitis
-Chronic pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what affects does alcohol have on the following systems:

  • Cardiovascular effects
  • Neurologic effects
  • Malnutrition
  • Effects on fetus
  • Carcinogenesis
A 
-Cardiovascular effects
Alcoholoic cardiomyopathy (DCM)
Decreased levels of HDL
Hypertension
-Neurologic effects
Thiamine deficiency
Peripheral neuropathies
Wernicke Korsakoff syndrome
-Malnutrition
Ethanol empty calories
Deficiencies , B vitamins
-Effects on fetus
Fetal alcohol syndrome
-Carcinogenesis
Oral cavity , esophagus , liver , breast
20
Q

what is digested blood called during gastric failure?

A

Digested bleeding is called Melena

21
Q

what is Spontaneous bacterial peritonitis (SBP)?

A

infection of ascitic fluid without an apparent source.
Somehow the bacteria can spread outside the GI tract without perforation of the GI tract. This could be due to the liver failure combined with possible ulcer in the GI tract.

22
Q

what is typical sign of liver failure?

A

Jaundice (yellow skin)

23
Q

Describe secunder diltative cardiomyopathy?

A

is a disease of the heart muscle, usually starting in your heart’s main pumping chamber (left ventricle). The ventricle stretches and thins (dilates) and can’t pump blood as well as a healthy heart can.
Can be causes by alcoholism due to its direct toxic affect on the heart muscle.

24
Q

describe lobar pneumona?

A

edema is seen, which is not pus but fibrin since the pneumococcus bacteria to which alcoholics are sensitive to.

25
Q

Affects on the fetus by alcohol?

A
  • growth retardation
  • Facial anomalies: Microcephaly, short palpebral fissures, maxillary hypoplasia, psychomotor disturbances, reduction of mental function.
26
Q

what are the neurological affects of alcohol?

A
  • Thiamine deficiency
  • wernicke-Korsakoff syndrome
  • wernicke encephalopathy (confusion, abnormalities in eye movement, ataxia.
  • Korsakoff syndrome: irreversible profound memory disturbances.
27
Q

what are the statistics of injury by therapeutic drugs?

A
  • 7-8% of patients have adverse reaction to drugs
  • 10% of such reactions prove fatal reactions to drugs.

Aspirin overdose is common (respiratory alkalosis and metabolism acidosis)

28
Q

what are the clinical affects of aspirin overdose? And acetaminophen overdose?

A
  • suicide
  • respiratory alkalosis and metabolism acidosis
  • Chronic toxicity (salicysm)
  • headache, dizziness, ringing in the ears (tinnitus), difficulty in hearing, mental confusion, drowsiness, nausea, vomiting and diarrhea.
  • Acute erosive gastritis: gastric mucosa is filled with small erosion.

Acetaminophen overdose

  • centriloblar hepatic necrosis
  • liver failure - transplantation (this is the only cure)
29
Q

describe Thalidomid? (contergan)

A
  • it was used against nausea and to alleviate morning sickness in pregnant women
  • 10,000 cases were reported to infants with phocomelia (small arms and legs)
  • negative effects of thalidomide led to the development of more structured drug regulations and control over drug use and development.
30
Q

Describe obesity?

A

a state of increased body weight, caused by adipose tissue accumulations, that is of sufficient magnitude to produce adverse health effects.
BMI is used to measure it.

31
Q

How is BMI calculated?

A

(weight in kilograms)/(height in meters)2, or kg/m2.

BMI greater than 30kg/m2 imparts a health risk.
25-30 = overweight
over 30 = obese.
over 40 = morbidly obese.

32
Q

what is the etiology of obesity?

A

Genetic factors:

  • sex
  • genetic syndromes (prader-willi syndrome, Laurence-moon-biedl syndrome, hypogonadism, klinefelter-syndrome.
  • Leptin gene or leptin receptor gene

Environmental factors:

  • excessive food intake
  • physical inactivity
  • socio-cultural and economic factors
  • metabolic imbalances
  • -hypothyroidism
  • -cushing’s disease
33
Q

Describe laurence-moon-bardet-biedl syndrome

A
  • -autosomal recessive genetic disorder
  • Obesity
  • Retinal degeneration
  • Extra digits on the hands and feet
  • Intellectual impairment
  • -Gene responsible on chromosome 16.
34
Q

describe the localization of fat in the context of apple and pear obesity?

A

APPLE: central or visceral, obesity, in which fat accumulates in the trunk and in the abdominal cavity (above the waist,)
PEAR: accumulation of fat int he diffuse distribution in subcutaneous tissue (bellow the waist).

35
Q

how is hunger regulated in mammals.

A

Leptin produced by the fat cells and inhibits the hypothalamus and the patient looses his hunger at the time.
Feedback from the fat cells to the brain
BMI and body fat stores are directly related to leptin secretion.

the hormone crosses the BBB and travels to the hypothalamus, where it reduces food intake by stimulating POMC/CART neurons and inhibiting NPY/AgRP neurons.

36
Q

describe adiponectin?

A

Adiponectin is a fat burning molecule. Directs fatty acids to muscle for their oxidation. It decreases the influx of fatty acids (FFA) to the liver and the total hepatic triglyceride (TG) content, decreases glucose production in the liver, causing an increase in insulin sensitivity.

Anti-diabetic, anti-inflammatory, anti-atherogenic, anti-proliferative and cardioprotective effects.

37
Q

Describe Ghrelin?

A
  • produced in the stomach and the arcuate nucleus of the hypothalamus.
  • It increases food intake
  • Stimulates the NPY/AgRP neurons in the hypothalamus

Full stomach = decreased Ghrelin = Decreased appetite.

38
Q

Describe peptide YY (PYY)

A
  • secreted from endocrine cells in the ileum and the colon
  • it decreases appetite and augments a sense of fullness, thereby decreasing food intake
  • stimulates POMC/CART neurons in the hypothalamus.
39
Q

Clinical consequences of obesity?

A
  • Type 2 diabetes mellitus
  • cardiovascular disease
  • cancer

Central obesity stands at the center of the metabolic syndrome:

  • abnormalities of glucose
  • lipid metabolism
  • hypertension
  • systemic proinflammatory state. (obesity is always a certain inflammatory and pro-inflammatory state because of previously mentioned cascade systems, peptide YY, ghrelin, adiponectin)
40
Q

Clinical consequences of obesity?

A
  • obesity is associated with insulin resistance and hyperinsulinemia T2DM
  • obese persons generally have hypertriglyceridemia and low HDL cholesterol levels
  • nonalcoholic fatty liver disease
  • Choleslithiasis (gallstones)
  • hypoventilation syndrome (OHS)
  • degenerative joint disease (osteoarthritis)
  • C-reactive protein (CRP) and porinflammatory cytokines like TNF levels elevated.
41
Q

how does fatty liver cause cirrhosis?

A

no all fatty livers are caused by alcohol. Inflammation is carried with the liver fat deposition and over time the chronic inflammatory state will cause scar tissue to form in the liver and cirrhosis will happen.

42
Q

How does gallstones (cholelithiasis) occur?

A

obesity almost always leads to gallstone formation.

43
Q

what happens to the joints in obesity?

A

osteoarthritis (degenerative joint disease) excessive pressure on the joints.

44
Q

There is a statistical correlation between cancer and obesity, what are the common cancer in certain genders.

A

Males: esophagus, thyroid, colon, kidney (obesity causes 14% cancer death in men)
Females: esophagus endometrium, gallbladder, kidney (obesity causes 20% of cancer death in women)

45
Q

mechanism of cancer being caused by obesity.

A

ALL of the following factors causes cancer:

  • elevated insulin levels-rise in levels of free insulinlike growth factor-1 (IGF-1)
  • effects on steroid hormones
  • reduced adiponectin secretion
  • Proinflammatory state

Pathology lectures (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions