Nutritional, Environmental Disorders Flashcards
How do you get lead poisoning
Lead is absorbed via lungs or GI and follows calcium into bones
Threshold
Symptoms lead poisoning
GI (“lead colic”), CNS (irritability, ataxic, drowsy), microcytic hypochromic anemia w/ basophilic stippling, increased bone density at growth plates, peripheral neuropathy (foot drop, GI colic), nephropathy (Falconi syndrome)
Falconi syndrome
Impaired proximal renal tubular reabsorption of AA, phosphate, glucose
Mercury poisoning sources, symptoms
Dental amalgams, contaminated fish
Tremor, gingivitis, bizarre behavior, kidney damage
Cancer a/w:
Aromatic amines, benzene, nickel, vinyl chloride
AA: bladder
Ben: multiple myeloma, leukemia
Nickel: sinus, lung
VC: angiosarcoma of liver
Arsenic poisoning symptoms, diseases caused
GI pain, heart, CNS (2-8 wk post)
Chronic: skin cancer on palms, soles
Cadmium poisoning: sources, symptoms/diseases
Mining, electroplating nickel-cadmium batteries -> contaminated soil/water
Subtle renal disease, calcium loss -> osteomalacia/ porosis
Problems for chimney sweeps in old times
Soot -> scrotal cancer
Cancers caused by smoking
Oral (lip, in mouth), larynx, lung, pancreas, esophagus, bladder, kidney, uterine cervix
Component of cigarette smoke causing cancer
Polycyclic aromatic hydrocarbons
Most and least common lung cancers from smoking & an in between
Most: small cell (oat cell)
Least: bronchioalveolar adenocarcinoma
Mid: non-small cell bronchioalveolar
Heart disease, lung cancer, emphysema risk with cessation of smoking
HD: greatly reduced w/in 5 years
Lung: decreases 21% in 5 yr, risk lasts for 30 y
Emp: never goes away but won’t get worse
Acute alcoholic injuries
Drunkenness, fatty change of liver, acute alcoholic hepatitis
Chronic alcoholic injuries
Cirrhosis, alcoholic cardiomyopathy, acute/ chronic pancreatitis, alcohol dependence/ withdrawal
Reversible injury associated with drinking & cause
Acute fatty change of the liver d/t TG synth (can’t put all EtOH 2-C frags into Krebs) -> dec lipid secretion by liver
GGT goes up, not AST/ALT, alkaline phosphatase
*Lasts for days, may cause sudden death d/t metabolic derangement
Other causes of fatty liver
Glucose/sugar shunted from Krebs to fat production bc ADH makes too much NADPH (while DH EtOH) & H2 has to go somewhere
*Also oxidizing EtOH = free radicals, acetaldehyde
Acute alcoholic hepatitis
Rare rxn; throw up a lot -> death
*Must be genetically susceptible
Lab dx alcoholic hepatitis
Mallory bodies (pink clumped precytokeratin filaments) with neutros around Mallory body hepatocytes & neutros, eos, lymphs in portal triad
Fibrosis b/t portal triads (bridging) -> cirrhosis
AST, ALT, GGT, alk phos elevated
Portal HTN & esophageal varices
Cirrhosis prevents connection of nodules to central veins = congestion
Blood backs up into coronary vein -> esophageal veins
Also spleen enlargement
Alcoholic cardiomyopathy
Form of dilated cardiomyopathy, can cause splinter hemorrhages
D/t myocyte toxicity by loosening BM dystrophin
EtOH shortest SCFA, which heart lives on, but this messes it up
Acute and chronic pancreatitis findings
Acute: Ranson’s criteria
Chronic: toothpaste-y stuff in ducts, stones, chain of lakes, grittiness on sectioning, possible fat saponification
Ranson’s criteria
At admission: >55 y, WBC >16, glucose >200, serum LDH >350, AST >250
After 48 hr: hematocrit falls >10%, urea rises >5mg/L, arterial PO2 -4, estimated fluid sequestration >6L
Fetal alcohol syndrome features
Short palpebral fissures, flat midface, short nose, flat philtrum, thin upper lip, micrognathia, minor ear abnormalities, low nasal bridge, epicanthal folds
MR, social problems
Infections from IVDA
Infections: Hep B, C, AIDS, endocarditis
Talc granulomatosis
Characteristics of cocaine
Acute HTN surge, vasoconstriction (paradoxical inotrope), possible stroke
Acute OD: seizure, cardiac arrhythmia, death
Chronic overuse: temp 105
Features of ASA OD
Metabolic acidosis, resp alkalosis, tinnitus, high anion gap, vomiting
Features of acetaminophen OD & tx
Throw up once, okay for one day (liver depleting GSH), come back dying of hepatic failure with drug level
Solar elastosis
Elastic replaced by scar tissue
Non-ionizing EM radiation at 1-10^18 Hz
Long wavelength, low freq
Electric power, radio waves, microwaves, infrared, UV light
Vibration and rotation of atoms in biologic molecules
Non-ionizing EM radiation at 10^18-10^27 Hz
Short wavelength, high freq
X-ray, gamma ray, cosmic rays
Ionize target molecules and eject electrons
Hematopoietic syndrome d/t radiation
200 rad (2Gy) to 700 rad of photons -> radiation-sensitive BM stem cells depleted = pancytopenia with anemia, infections, bleeding Attrition of gonadal stem cells
Gastrointestinal syndrome d/t radiation
1000 rads, depletes GI mucosa = malnutrition, malabsorption, electrolyte imbalance, septicemia
CNS syndrome d/t radiation
Several thousand rads, generalized endoth damage w/ vascular leakage = neuro symptoms, cardiovascular sx
*Rapidly fatal (hr to days)
Local vascular damage d/t radiation mechanism
Radiation fibroblasts: scarring with 2’ tissue disorganization, atrophy
Telangiectasia, ulceration, erosion, ischemic
Vascular stenosis d/t sclerosis, mural fibrinoid material, intimal foam cell accumulation, thrombosis
Marasmus vs. kwarshiorkor
M: wasting d/t insufficient calories; fretful, desperate for food; no SQ fat, die of infxns
K: protein malnutrition; rash, scaly skin, distended abd, anemic, apathetic; fatty liver, edema
Central vs. peripheral fat (apple vs. pear)
Apple: internal fat, assc. with DM2, dyslipidemias, cancer, HTN, heart/kidney disease
Unexpected effects of BMI >35
Non-alc fatty liver, gallstones, sleep apnea (Pickwickian syndrome), arthritis, cancer (esoph, GB, colon, thyroid, kidney, endometrium)
Enzymes required for absorption of fat-soluble vitamins
Bile & panc enzymes (triggered by fat)
ApoE-R (vit A)
Stored in fat, liver
Vitamin A functions
Fight infections, normal columnar and transitional epithelium (skin follicles, resp tree, kidney/ureters), normal growth
Vit A and cancer; why?
Inverse relationship because retinoids modify cellular diff/prolif
Vit A teratogen
Retin-A, a beta-carotenoid (alpha non-teratogenic)
Vit A deficiency
Night blindess -> perm blindness via keratostomia, corneal ulcer, corneal/scleral thickening (Bitot spot)
Mucosa/skin -> keratin = stones, tumors
Follicular hyperkeratosis
Vitamin A deficiency causes (aside from poverty)
GI disorders/ malabsorption: sprue, celiac, CF, steatorrhea, cirrhosis, chronic hepatitis, other liver problems
*Nursing women may deplete stores
Vit A sources
Eggs, milk, butter, fish, polar bear liver (too much)
Carotenoids from yellow veg, leafy greens (carrots, yellow squash, red, yellow peps, spinach, salad)
Vitamin A toxicity
HA, n/v, blurred vision, papilledema, stupor, alopecia, weight loss
Overstimulated osteoclast -> bone/jj pain, bone resorption, fx, symmetrical hyperostosis
Vit D deficiency
Weak bones, lose mm strength, lose immune fxn, cancer (colon, breast, pancreas, prostate)
High inflammation levels
Vit D effect on small intestine?
D-OH-2 triggers Ca2+ absorption
Structure of vit D
Prohormone, modified by liver and kidney to become D-OH-2 and active
Skeletal vit D functions
Maintain Ca/phosphorus homeostasis (absorb Ca in small int and reabsorb in kidney) to maintain blood Ca, too much -> bone to make stronger (PO4 follows, so low vit = low Ca and PO4)
Nonskeletal vit D functions
Steroid hormone made from chol produced by breast, prostate, colon, MFs, squamous cells
Regulates expression of genes, many imp in cancer
Low it D blood levels
D-OH-2 below 20 ng/ml assc with 30-50% increase in breast, prostate, colon cancers
Synthesis of vit D
Skin 7-dehydro-chol + UVB = vit D3 (chole)
Food vit D in liver -> D-OH-1 (ergo)
Vit D-OH-1 in kidney -> vit D-OH-2 *active
How to become vit D deficient & prevention
Not enough sunlight (more melanin, clouds, sunscreen)
Low D in diet
Bad kidneys (no conversion)
*Cod liver oil (except renal)