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Multisystem Path > Environmental Path 3 > Flashcards

Environmental Path 3 Flashcards

1
Q

Let’s talk about the metabolism of alcohol

A
  1. Stomach/SI - Absorb ethanol without altering it
  2. Distributed to all tissues in blood
    2a. Oxidized in blood by: alcohol dehydrogenase, catalase, and microsomal ethanol-oxidizing system
    2b. AD = cytosol of hepatocytes
    2c. MEOS = During high alcohol consumption
    2d. Catalase = minor importance, only 5% of ethanol in liver (uses hydrogen peroxide)
  3. Acetaldehyde made by metabolism, converted to acetate by acetaldehyde dehydrogenase, acetate used in mitochondrial respiratory chain
  4. 10% excreted unaltered in sweat, breath, urine
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2
Q

Let’s talk about how the sx of alcohol change depending on how much you have.

A
  1. 80 mg/dL (3 beers, 15 ounces wine, 4-5 ounces 80 proof liquor) = Drunk driving
  2. 200 mg/dL = Drowsiness
  3. 300 mg/dL = Stupor
  4. > 300 mg/dL = Respiratory arrest/coma eventually
  5. 700 mg/dL = Limit chronic alcoholics can tolerate due to 5-10x increase in CYP induction
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3
Q

What are the toxic metabolites in alcohol? Just list them now, more detail in next cards

A
  1. Acetaldehyde
  2. Decreased NAD
  3. ROS
  4. Endotoxin
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4
Q

Acetaldehyde. Tell more more.

A

Source: Ethanol oxidation
Sx: Flushing, Nausea, Tachycardia, Hyperventilation
Genetics: Acetaldehyde is high if acetaldehyde DH enzymes are low
Asians = ALDH22 instead of 21 = inactive form of enzyme = High Acetaldehyde

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5
Q

Decreased NAD. DO TELL ME MORE PLEASE

A

Source: AD reduces NAD to NADH. NAD needed for fatty oxidation and conversion of lactate to pyruvate. Leads to fatty accumulation in the liver and lactic acidosis (high lactate and fat)

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6
Q

Where are all these ROS coming from?

A

Source: CYP2E1 of ethanol makes ROS = lipid peroxidation in hepatocyte membranes

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7
Q

What’s this endotoxin you speak of?

A

Source: Alcohol hits gram negatives in gut causing release of LPS endotoxin to stimulate TNF and other cytokines from macrophages and kupffer cells leading to hepatic injury

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8
Q

What are we saying the effects of acute alcoholism are?

A

Fatty change: Accumulation of fat in hepatocytes
GI: Gastritis and ulcers
CNS: Depressed then stimulated = Disordered intellect and motor behavior. Eventually depressed again at cortical and medullary centers including those for respiration

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9
Q

What about that chronic alcoholism? More is better eh?

A

Ha, no.
Liver: Hepatitis, cirrhosis → Portal HTN and incr. risk of hepatocellular carcinoma

GI: Massive bleeding from ulcers or esophageal varices (associated with cirrhosis)

B1 Deficiency (Thiamine): Causes peripheral neuropathies and Wernicke Korsakoff syndrome. Eventually cerebral atrophy, cerebellar degeneration, optic neuropathy

CV: Dilated cardiomyopathy, HTN, decreased HDL → Increased chance of CAD

Endocrine: Pancreatitis (acute + chronic)

Pregnancy: FAS → Microcephaly, growth retardation, facial abnormalities, reduced mental function. Avoid alcohol in first trimester

Cancer: Acetaldehyde-DNA adducts or ALDH2*2 alleles (esophageal CA) → Oral, esophageal, liver, breast (females)

Nutrition: Alcohol = energy = empty calories = nutritional deficiencies

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10
Q

So no more alcohol for us ever again in the rest of our lives??? WAHHHHH

A

Nope, you just need to pick the right stuff:

250 mL of wine per day = Good

  1. Increased HDL
  2. Reduced platelet aggregation
  3. Lower fibrinogen levels

AW YEAH

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11
Q

Normal dosing for Acetaminophen

A

Normal dose = 0.5 g

Overdose = 15-25 g

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12
Q

Discuss the metabolism of acetaminophen?

A

95% detoxified in liver by phase II enzymes → excreted in urine as glucuronate or sulfate conjugates.

5% by CYP2E, producing NAPQI, a toxic metabolite. NAPQI usually gets conjugated with Glutathione. If gluthione is depleted (chronic alcholism) NAPQI accumulates and damages hepatocytes → centrilobular necrosis → liver failure

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13
Q

So what’s this NAPQI you speak of? Why is it so bad?

A

Covalent bonding to hepatic proteins → damage to cell membranes and mitochondrial dysfunction

Depletion of glutathione (GSH) → Hepatocytes more prone to damage by ROS

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14
Q

What are the sx of acetaminophen overdose?

A
  1. N/V/D
  2. Shock
  3. Jaundice
  4. Liver failure
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15
Q

Tx of acetaminophen overdose?

A

Within 12 hours = N-Acetylcysteine = Restores GSH levels.

Liver centriolobular necrosis = Liver Transplant

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16
Q

Discuss the pathophys involved with aspirin toxicity?

A

Stimulation of Respiratory System in Medulla → Alkalosis → Metabolic Acidosis → Pyruvate and lactic acid accumulation due to uncoupling of oxidative phosphorylation and Krebs Cycle inhibition. This metabolic acidosis enhances formation of non-ionized forms of salicylates which diffuse into the brain → Anything from nausea to coma

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17
Q

What are the sx associated with aspirin toxicity? (defined as 3g+/day

A

CNS: Headaches, dizziness, tinnitus, hearing impairment, confusion, drowsiness, seizures, coma

GI: N/V/D, erosive gastritis → bleeding and ulcers

CV: Acetylation of platelet cyclooxygenase and irreversible block of Thromboxane A2 production (needed for platelet aggregation → Excessive bleeding → Petechial hemorrhages of skin and internal viscera

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18
Q

What can happen with you’re doubling up on aspirin and acetaminophen

A

Taken chronically → Tubulointerstitial nephritis with renal papillary necrosis (analgesic nephropathy)

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19
Q

Cocaine. Talk about the composition and types of this drug.

A

Extracted from coca leaves → water soluble powder.

Mixed with Talcum powder or lactose. Snort or dissolve in water and inject.

Crack = crystallized cocaine → Heat (causes it to crackle hence the name) and inhale vapors → far more potent than cocaine but same effects

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20
Q

Addiction with cocaine?

A

Psychological addiction, NOT physical. Withdrawal is profound.

21
Q

CV sx associated with cociane?

A
  1. Sympathomimetic, blocks reuptake of Epi and NE and stimulates release of NE presynaptically → Tachycardia, HTN, peripheral vasoconstriction.
  2. Enhances platelet aggregation and thrombus formation → Coronary artery vasoconstriction → Myocardial ischemia.
  3. Enhanced sympathomimetic activity + ion transport disruption (Na+, K+, Ca2+) → Lethal arrhythmias
  4. Development of dilated cardiomyopathy (doesn’t say why)
22
Q

CNS effects of cocaine?

A

Blocks reuptake of Dopamine → euphoria and hyperpyrexia (very high fever due to dopaminergic pathways of body temperature control) and seizures

23
Q

What about cocaine during pregnancy?

A

Decreases in blood flow to placenta → Fetal hypoxia, degeneration of neural development and potentially spontaneous abortion

24
Q

What lab will be + for a cocaine user

A

(+) BE (benzoylecgonine)

25
Q

What’s the deal with heroin? Where does it come from?

A

Poppy plant, closely related to morphine.
Cut with Talc or quinine.
Administered intravenously or subQ

26
Q

CNS effects of heroine?

A

Euphoria, hallucinations, somnolence, sedation

27
Q

Can you get sudden death from heroin?

A

Yes,

  1. Profound respiratory depression
  2. Arrhythmia
  3. Cardiac arrest
  4. Severe pulmonary edema
28
Q

What are the effects of cocaine in the lungs?

A

Edema, septic embolism (from endocarditis) lung abscess, foreign body granulomas from Talc, opportunistic infections. Note, granulomas can be found elsewhere like spleen, liver and lymph nodes

Imaging: Talc crystals under polarized light, sometimes in giant cells

29
Q

What kind infections are common with heroin use?

A
  1. Right sided tricuspid - S. Aureus
  2. Viral hepatitis: most common infection
  3. HIV due to needle sharing
30
Q

What skin shit happens with heroin use?

A

Cutaneous lesions from subQ injections, hyperpigmentation over injection sites

31
Q

Kidney stuff with heroin?

A
  1. Amyloidosis from skin infections
  2. Segmental glomerulosclerosis.
  3. Proteinuria
  4. Nephrotic syndrome
32
Q

What lab will you see with heroin use?

A

6-MAM (monoacetylmorphine)

33
Q

How do you treat a heroin overdose?

A

methadone therapy

34
Q

What bad things do burns cause?

A
  1. Shock: Shift of body fluids into interstitial compartment 2. Pulmonary and generalized edema→ Vascular leakiness
  2. Hypermetabolic state→ heat loss and need from nutritional support.
  3. Infection→ most common organism=*Pseudomonas aeruginosa, MRSA, Candida.
  4. Airway and lung injury from inhalation → complete or partial airway obstruction
35
Q

Classification of burns

A

1* Superficial: confined to epidermis,
2* Partial thickness burns: injury to top of dermis, wet and pink
Deep partial thickness: through all dermis, dry and red
3* Full-thickness: extension to subcutaneous tissue, white/brown and leathery, no pain
4* into muscle tissue or bone, black charred

36
Q

What kind of injuries do we see in hyperthermia

A
  1. Heat cramps: from loss of electrolytes from sweating. A/w vigorous exercise
  2. Heat exhaustion: most common. From failure of cardiovascular system to compensate for hypovolemia caused by dehydration. Onset is sudden with prostration and collapse
  3. Heat stroke: A/w high temp, high humidity and exertion. At risk: older people, people undergoing physical stress, people with CV dz.
37
Q

More on heat stroke. What is the pathophys involved here

A
  1. Body temp>40C→ multiorgan dysfunction.
  2. Generalized vasodilation→ peripheral blood pooling and ineffective circulation.
  3. Sustained contractions of skeletal muscle contractions→ muscle necrosis and rhabdo.
38
Q

Why are there sustained muscle contractions seen in heat stroke?

A

RYR1 nitrosylation disruption: RYR1 is responsible for regulating Ca2+ release in sarcoplasm in skeletal muscle. Heat stroke causes RYR1 dysfunction allowing Ca2+ to leak into cytoplasm, stimulating muscle contraction.

39
Q

What is malignant hyperthermia?

A

Inherited mutation in RYR1. Rise in body temp in response to anesthetics

40
Q

What are the direct effects of hypothermia?

A

crystallization or intra and extracellular water→ high salt concentrations → cell injury

41
Q

What are the indirect effects of hypothermia?

A

Changes in circulation depending on the rate of chilling:
1. Slow chilling: vasodilation and increased vascular permeability→ edema and hypoxia (Ex: Trench Foot + gangrene)

  1. Rapid chilling: vasodilation and increased blood viscosity → local ischemic injury and peripheral nerve degeneration. Gangrene can be seen. Vascular injury and edema seen as temp returns to normal.
42
Q

What happens in a low voltage (120 or 220v: home or workplace) electrical injury?

A
  1. With low resistance (wet skin) can cause ventricular fibrillation.
  2. Sustained current (caused by alternating current leading to tetanic muscle spasm→ prolonged grasp of wire) can cause burns (entry/exit sites and internal)
43
Q

What do high voltage (high-power lines or lightning) injuries cause?

A

Same mechanism as above but stronger. More likely to cause paralysis of medullary centers and extensive burns.

44
Q

What is at risk for damage from ionizing radiation?

A

Rapidly dividing cells and fetus

45
Q

So there is ionizing radiation. Is there non ionizing radiation?? If so, how are they different?

A

YEAH! Here’s the difference:

Nonionizing: UV, infrared light, microwave, sound→ can cause atoms in molecule to vibrate but can’t displace electrons

Ionizing: X-ray, gamma rays, high-energy neutrons, alpha particles (2p+ 2n), beta particles (e-)→ can remove bound electrons. Electrons hitting other molecules releases more electrons→ known as ionization

46
Q

Where do we get exposed to ionizing radiation?

A
  1. Medical imaging (CT, X-ray)
  2. Cancer tx
  3. Diagnostic and therapeutic radioisotopes
47
Q

What determines the biological effect of ionizing radiation?

A
  1. Rate of delivery: breaks from radiation–> cell recovery
  2. Field size: large dose to small field better than small dose to large field
  3. Cell proliferation: ionization causes DNA damage. Rapid cell proliferation will increase # of cells damaged. ^damage–> bone marrow, gonads, GIT mucosa, lymphoid tissue
  4. Oxygen effects/hypoxia: Radiolysis of H2O→ free radical production→ ROS formation → DNA damage. Tissue with poor oxygen supply (center of rapidly growing tumors) are less susceptible to effects of radiation.
  5. Vascular damage: endothelial cells sensitive to radiation→ occlusion of vessels → impaired healing, fibrosis, chronic ischemic atrophy
48
Q

Sx of ionizing radiation?

A

Fibrosis, mutagenesis, carcinogenesis, teratogenesis.

Multisystem Path (11 decks)

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