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micro/immuno? wrap up > environmental disease 2 > Flashcards

environmental disease 2 Flashcards

1
Q

3 features of fetal alcohol syndrome

A
  1. Specific dysmorphic facial features.
  2. Growth retardation.
  3. Central nervous system (CNS) abnormalities:wide range of neurobehavioral problemsincluding impairment of self-regulation,cognition, and adaptive functioning:
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2
Q

3 conditions that cause hepatic steatosis?

A

alcohol

obesity

uncontrolled diabetes

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3
Q

how does alcohol cause hepatic steatosis?

3 ways

A

How does alcohol cause hepatic steatosis?

“(1) shunting of substrates away from catabolism

   and toward lipid biosynthesis because of the

   generation of excess **reduced nicotinamide-**

** adenine dinucleotide** resulting from

   metabolism of ethanol by **alcohol**

** dehydrogenase and acetaldehyde**

** dehydrogenase **

(2) impaired assembly and secretion of
* *lipoproteins**
(3) increased peripheral catabolism of fat “

basically TOO much NADH. therefore: pyruvate uses this NADH –> lactic acid instead of continuing down the ETC and being converted to acetyl coA

                                                              Robbins Basic Pathology, page 623
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4
Q

see neutrophils in liver with steatosis. what you you have?

A

steatohepatitis

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5
Q

how does alcohol cause steatohepatitis? 5 ways

A

Acetaldehyde (a major metabolite of ethanol) induces lipid

peroxidation and acetaldehyde-protein adduct formation,

which may disrupt cytoskeleton and membrane function

Alcohol directly affects cytoskeleton organization (as illustrated by

Mallory-Denk bodies), mitochrondrial function and membrane fluidity

Reactive oxygen species generated during oxidation of ethanol

by the microsomal ethanol oxidizing system react with and damage

membranes and proteins…

Cytokine-mediated inflammation and cell injury is a major

feature of alcoholic hepatitis and alcoholic liver disease in general.

TNF is considered to be the main effector of injury;

IL-1, IL-6 and IL-8 may also contribute.”

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6
Q

cocaine blocks dopamine reuptake in CNS.

what are the three effects?

HEP

A

euphoria

paranoia

hyperthermia

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7
Q

cocaine in the cardiovascular system

what are the effects of NE?

A

HTN, cardiac arrhythmia, myocardial infarct, cerebral hemorrhage and infarct

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8
Q

Estrogen therapy, with or without progestins, is referred to as hormone replacement therapy (HRT). HRT with estrogens and progestins is associated with an increased risk of________ HRT, with or without progestins, increases the risk of _________

know: Does HRT protect against ischemic heart disease?

what do they have a protective effect against?

what do they increase risk of?

A

Estrogen therapy, with or without progestins, is referred to as hormone replacement therapy (HRT). HRT with estrogens and progestins is associated with an increased risk of breast cancer. HRT, with or without progestins, increases the risk of thromboembolism.

HRT does not protect against ischemic heart disease

protective effect against endometrial and ovarian cancers

increase risk of thromboembolism and hepatic adenomas.

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9
Q

Acetaminophen is metabolized to ________ (N-acetyl- p-benzoquinoneimine) through the hepatic P-450 system. With very large doses, excess _______ leads to centrilobular hepatic necrosis.

A

Acetaminophen is metabolized to NAPQI (N-acetyl- p-benzoquinoneimine) through the hepatic P-450 system. With very large doses, excess NAPQI leads to centrilobular hepatic necrosis.

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10
Q

Marijuana contains the psychoactive substance Δ 9-tetrahydrocannabinol ______

A

Marijuana contains the psychoactive substance Δ 9-tetrahydrocannabinol (THC).

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11
Q

what is described?

Distinctive

form of

fibrosis of

the liver with

regenerative

nodules of hepatocytes, not properly connected to hepatic arterial supply, portal venous circulation or biliary system, and surrounded by fibrous tissue

A

cirrhosis

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12
Q

what % of alcoholics get cirrhossi? how long does it take?

A

15%; 15 years;

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13
Q

How can you differentiate cirrhosis due to alcoholism from

cirrhosis due to non-alcoholic fatty liver disease (NAFLD)?

A

History

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14
Q

hepatocellular carcinoma is the cause of death in what % of alcoholic liver disease?

A

3-6%

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15
Q

what are all below:

  1. Intoxication
  2. Accidents
  3. Murder
  4. Suicide
  5. Pancreatitis
  6. Liver disease (steatosis, hepatitis, cirrhosis)
  7. Gastritis (erosive, hemorrhagic and ulcerative)
  8. Alcoholic cardiomyopathy
  9. Peripheral neuropathy
  10. Fetal alcohol syndrome
  11. Cerebral atrophy
  12. Cerebellar degeneration
  13. Cancer of the mouth
  14. Cancer of the larynx
  15. Cancer of the esophagus
  16. Breast cancer
  17. Liver cancer
A

toxic effects of ETOH

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16
Q

what are mallory denk bodies?

A

tangled skins of deranged cytoskeletal cytokeratin intermediate filaments

17
Q

what is kwashikor?

what does lack of protein cause?

A

This is kwashiorkor, protein starvation

with less inadequate carbohydrate nutrition.

Lack of protein for lipoprotein synthesis

causes lipid to accumulate in hepatocytes.

18
Q

what is: __________is starvation with deprivation of all nutrients in proportion.

A

Marasmus is starvation with deprivation of all nutrients in proportion.

19
Q

________ is a psychiatric disease with self-induced starvation

due to an obsession with thinness (and misperceived obesity).

A

Anorexia nervosa is a psychiatric disease with self-induced starvation

due to an obsession with thinness (and misperceived obesity).

20
Q

_____ is a state of profound loss of lean body mass and fat

due to cytokines, principally _______.

A

Cachexia is a state of profound loss of lean body mass and fat

due to cytokines, principally TNF.

21
Q

in the hypothalamus, which neurons does leptin stimulate to reduce food intake?

inhbiti to reduce food intake?

A

“With abundant adipose tissue, leptin secretion is stimulated, and the

hormone travels to the hypothalamus, where it reduces food intake by

** stimulating POMC/CART** neurons and inhibiting NPY/AgRP neurons.

…Leptin also increases energy expenditure by stimulating physical

activity, energy expenditure and thermogenesis.”

                                                     Robbins Basic Pathology, page 304
22
Q

which gut peptide is a satiety signal

A

“Peptide YY, which is released post-prandially by endocrine cells

in the ileum and colon, is a satiety signal.”

23
Q

which peptide increases food intake?

A

Ghrelin is produced in the stomach and is the only known gut peptide

that increases food intake.”

“Ghrelin secretion stimulates appetite,

and it may function as a

‘meal-initiating’ signal.”

24
Q

intestines produce which satiety peptide?

stomach produces which petpidet that increases hunger?

pancreatic beta cells release which peptides?

adipose cells release which peptides?

A

intestines: PYY
stomach: Ghrelin

pancreatic Beta cells: insuling

fat cells: leptin

25
Q

“In children, ___________ may take the form of metastatic calcifications

of soft tissues such as the kidney; in adults, it causes bone pain and

hypercalcemia.”

A

“In children, hypervitaminosis D may take the form of metastatic calcifications

of soft tissues such as the kidney; in adults, it causes bone pain and

hypercalcemia.”

26
Q

BMI normal weight?

overweight?

obesity?

morbid obestity?

A

The recommended classifications for BMI adopted by the National Institute of Health (NIH) and World Health Organization (WHO) and endorsed by most expert groups are:

Normal weight — BMI ≥18.5 to 24.9 kg/m2

Overweight — BMI ≥25.0 to 29.9 kg/m2

Obesity — BMI ≥30 kg/m2

Morbid Obesity — BMI ≥40 kg/m2 (also called severe or extreme obesity)

                                       Condensed from Up-to-Date, accessed 2/13/2014
27
Q

in sarcoid, what do the macrophages in granulomas have that increases amts of vitamin D?

A

activated macrophages in granulomas have the enzyme for converting vitmain D to its most active form w/out feedback control

28
Q

what is the overweight BMI cut off for ASians? Obestiy?

A

Overweight: BMI: 23-24.9

Obesity: BMI >25kg/m2

29
Q

t/f.

Patients with abdominal obesity (also called central adiposity, visceral, android, or male-type obesity) are at increased risk for heart disease, diabetes, hypertension, and dyslipidemia.

A

true

30
Q

how does insulin resistance lead to the accumulation of triglycerides in the hepatocytes:

A

• impaired oxidation of fatty acids•

increased synthesis and uptake of fatty acids•

decreased hepatic secretion of very-low-density lipoprotein cholesterol

31
Q

how do we remove cholesterol from the body

A

Bile formation is the only significant pathway for elimination of excess

cholesterol from the body

32
Q

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Adipocytes make estrogen, which contributes to gallstone formation because estrogen increases<!--EndFragment-->

A

A.Hepatic uptake and synthesis of cholesterol

33
Q

name 4 substances that regulate the metabolic syndrome

A

IL-1

IL-6

IL-18

TNF

34
Q

what is adiponectin?

what makes it?

how does it work?

which syndrome is it reduced in?

A

Adiponectin is an anti-inflammatory

cytokine produced exclusively by

**adipocytes. **Adiponectin enhances

insulin sensitivity and inhibits many

steps in the inflam-

matory process.

Adiponectin is reduced

in the metabolic

** syndrome.**

35
Q

which joints are most affected by osteoarthritis in obese pts?

A

The weight-bearing joints

(knees and hips) are the

ones most affected by

osteoarthritis in obese

patients, and even more

weight is directed onto a

smaller joint in the knee

than the hip.

36
Q

what are 5 possible mechanism by which obesity induces cancer?

LIME IGF-1

A

(1) Fat tissue produces excess estrogen, associated with the risk of breast, endometrial, and some other cancers.
(2) Obese people often have increased levels of insulin and insulin-like growth factor-1 (IGF-1) in their blood.
(3) Fat cells produce hormones, adipokines, that may stimulate cell growth. Leptin, more abundant in obese people, seems to promote cell proliferation.
(4) Fat cells may also have direct and indirect effects on other tumor growth regulators, including mammalian target of rapamycin (mTOR) and AMP-activated protein kinase.
(5) Obese people often have chronic low-level inflammation.

37
Q

t/f.

cancers due to obesity are more fatal than average

A

true

micro/immuno? wrap up (14 decks)

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