TURNERS: 45,X0 (Gonadal dysgenesis)

Serum Estrogen: Decreased

Serum GnH: Increased FSH and LH
Growth Hormone Therapy Effective as early as 9 months of age
As soon as growth failure is demonstrated, very low dose (0.3mg/kg/wk)
o Most effective administered daily; monitor IGF1 levels
< 9 can use GH alone; older, add non-aromatizable anabolic steroid
(oxandrolone)
Continue until satisfactory height or little bone growth potential (bone age >14
yrs)
Estr/Progest Replacement in Turner Syndrome
>90% will have gonadal failure; estrogen therapy required to induce pubertal
development
Low estr doses at age 12 prevents premature epiphyseal fusion, permit
normal puberty pace without compromising effects of GH on height
Start 1/10-1/8 adult dose, increase gradually over 2-4 years
Achieve normal range estradiol in young adult
Other Considerations
Progesterone: wait at least 2 yr after starting Estrogen or wait for breakthrough bleeding
Avoid OCPs in puberty; estrogen levels are too high, progesterone interferes with breast and uterine
development
Discontinue OCPs at normal menopause age
METHOD OF ACTION
SIDE EFFECTS
FIRST LINE DRUG OF CHOICE
METABOLIC SYNDROME lots of questions [Obesity & nutrition lecture]
34.5% US adults have metabolic syndrome
DIAGNOSTIC CRITERIA (DEFINITION):
Any 3 or more of:
o Elevated waist circumference (40 inches for men, 35 inches for
women)
o Elevated triglycerides (150 or higher) or tx for hypertriglyceridemia
o Reduced HDL (<40 men, <50 women)
o Elevated BP 130/85 or being treated for HTN
o Elevated fasting glucose (>100) or being tx for elevated glucose
Nutrition: know recommended intake
Carbohydrates: recommended 45-65% of calories, 4 Calories/gram
Protein: recommended 10-35% of calories, 4 Calories/gram
Fats: recommended 20-35 % of calories, 9 cal/gram
Cholesterol: AHA recommends 300mg/day
Fiber: Recommended 25-35 grams/day for an adult
Alcohol: 7 Calories/gram
Ghrelin: stomach shrinks; activates feeding/satiety centers
Ghrelin, incretin, leptin
Orlistat (blocks TG uptake), decr circulating lipids, ADR = diarrhea

HYPOTHALAMUS/PITUITARY
REPLACEMENT
GH: must be HUMAN growth hormone
know its a protein hormone: means it MUST be given by injection (broken down in GI)
See GH graph (levels at different ages)high in childhood
Know that it must be replaced to an age-appropriate level (less will have no effect)
GH admin has no effect if the pt is not deficient
Peds: must measure GH level & determine deficit before replacing
GH resistance: replace IGF1 instead
Major ADR of GH and IGF1: side-effect of hypoglycemia because of insulin-like effects
Acromegaly: usually due to GH secreting adenomas; usually express somatostatin (SS) Rs 2&5
Can also be due to dopamine agonists PRL and DA are similar in structure, but MOA unknown
Tx: SS analogue (octreotide)works on SS-Rs 2&5
Pegvisomant: binds GH-R (competitive inhibition), so no IGF1 production; works on target tissues
GH tx with Turner syndrome (can also have elevated FSH)
GH therapy as soon as GH deficit demonstrated, as early as 9mos
monitor tx through IGF1 levels
At puberty, lower GH levels and add estrogen (very low doses; titrate uptoo much will cause closure
of epiphyses)
For reproductive lifespan, admin oral contraceptives
Prolactin: primary inhibitor is DA; TRH also stimulates prolactin (not strongly, DA effect predominates)
Hyperprolactinemia: decreased fertility/amenorrhea, galactorrhea (usually due to pit adenoma)
Bromocriptine (daily administration) is drug of choice (even though older and more ADRs)
Cabergoline: weekly admin, used if bromocriptine not tolerated
Panhypopituitarism: replace cortisol, thyroxine; if in peds, GH too
If complete resection, also replace ADH (Desmopressin: longer DOA, fewer ADRs)
SIADH (really review this)
most common in small cell carcinoma (paraneoplastic syndrome)
Demeclocycline & ADH receptor antagonists
THYROID (this is the important one)
primary = organ/gland; 2ary = pituitary; 3ary usually hypothalamus
levothyroxine (important drug)
(liothyronine: not on this test)
To treat newly diagnosed hypothyroidism: Start w/lowest dose and slowly
increase, checking blood levels every 6-8 weeks
Hyperthyroidism: thyroiditis (if due to infection, treat infection)
Graves is most common
THYROID STORM: medical emergency; 50% lethal WITH tx
Biggest prob is CV effects: tx with B-blockers, diogox
antithyroid drugs: iodide salts (used prior to surgery; MOA not understood, but temp inhib of
synthesis)
beta-adrenergic antagonists (decr. sympathetic sx)
Diuretics, digitalis and O2 to combat congestive heart failure
Reduce secretion and production of thyroid hormones: PTU (blocks peripheral T3-T4 conversion)
Fluid replacement, glucose, electrolytes
Hydrocortisone to prevent symptoms of adrenal insufficiency

In a person w/hyperthyroidism, to avoid later hormone replacement:

Concurrent administration of propylthiouracil, SSKI [potassium iodide],
and dexamethasone to the patient with severe thyrotoxicosis effects a
rapid reduction in serum T3-T4, often to within the normal range in 24 to
48 hours.
Most common tx in US: radioactive I (I131): ADR hypothyroidism
Exclusion criteria: pregnancy and/or physical immaturity
Thioamides: PTU, methamazole (both inhibit TG iodination)PTU also inhibits T3-T4 conversion

XY SYNDROMES: know definitions (Names and XXY, X0, etc.)

PCOS
Most common reproductive/fertile disorder in US
LH is always higher than FSH in women w/PCOS
LH levels 2-3x higher than FSH are diagnostic (though not always
present)
usually req USd showing polycystic ovaries
metabolic disorder + hyperandrogenicity
if pregnancy is not desired, combination hormonal contraceptive or Depo (medroxyprogesterone)
first-line tx in presence of metabolic syndrome/insulin resist: metformin (this is NOT an offlabel use)
Clomiphene: partial agonist at Estr-R
Prevents normal FB inhibition and incr. LH (used in PCOS and infertil tx)
If metformin fails, then clomiphene
Flutamide: androgen-R antagonist (used in prostate ca)
Finasteride: 5a-reductase inhibitor, reduces DHT levels (used in BPH)
Spironolactone: decr androgens (aldosterone cross-reacts with androgen receptors) used in prostate ca
Ketoconazole: inhib CYP450 (Star protein precursor), thus inhib steroidogenesis; also inhib 17a-hydroxylase
AND desmolase
HER2: human epidermal growth factor receptor (tx w/trastuzumab)
CANCER DRUGS: know indiv drugs and combinations (regimens) used for specific cancers
G
F
21 & 11a-hydroxylase
17a-hydroxylase
(deficiencies not compatible with life)

Aldosterone
Cortisol

R
androgens

LEIOMYOMAS
GnRH agonists (antag can give same results: supp LH & FSH; ex. Clomiphene): agonists used before surgery
(fewer ADRs)
Danazole: antiestrogen drug of choice; decreases uterine volume; if not doing surgery, use this drug
ENDOMETRIOSIS
abnormal bleeding is presentation
hysterectomy is main and only definitive tx

if hysterectomy not desrired, can use hormonal contracep to supp GnRH release
GnRH is used for preop mgmt: used to shrink uterine endometrium
Pain relief is managed with danazole (number one tx for this): suppresses growth and reduces pain
FERTILITY
no one knows why estr switches from neg to pos feedback during LH spike
Bolus estr mimics spike, causes LH surge
LH surge = ovulation (main target of contraception & fertility tx)
ORAL/HORMONAL CONTRACEPTION
Primary MOA is inhib of LH surgePREVENTS OVULATION
progesterone is the active ingredient
Prev ovulation, thicken cervical mucus, alt/decidualize endometrium
8% failure rate with typical use
optimal use: take at same time each day, no skipped days
Reduce risk of ovarian, colorectal, endometrial cancer
Increased cervical ectopy and chalmydial infx, incr risk heopatocell adenoma
Increased estr levels have many adverse effects: increased synthesis of clotting factors (hypercoag)
most important ADR of hormonal contracep: DVTs
Smoking + OCPs = incr risk of DVTs in 40+ F
2nd-gen progestins are best in combin. w/estr
-know characteristics of each generation
-biggest reason to add estrogen/combine: controls breakthrough bleeding (progestin-only pills have this)
Ethinyl estradiol: good abs & bioavail; binds to SHBG; survives 1st-pass through liver (no native hormones
survive 1st-pass: steroids are metabolized in liver)
Yaz: ethinyl estradiol & drospironone (spirinolactone): can cause hyperkalemia
Plan B: levonorgestrel (2 doses) prevent implantation
Mifepristone: Progesterone-R antagonist; aborifacient
1. Know that the point of OCPs is to prevent ovulation
2. Types of emergency contraceptives and abortifacients
PREGNANCY
Woman spotting w/lot of blood in first trimester: Measure hCG levels, wait
48h, measure again
CANNOT BE TX if hCG continues falling (losing pregnancy)
Bleeding can be tx in 3rd trimester only
Either tocolytics (arrest contractions; #1 = MgSO4) or oxytocin/pitocin
(induces labor by incr uterine smooth muscle contrax)
Tocolytics: inhibit CA in cytoplasm or cAMP
Oxytocin: if doesnt work, can use ergot alkaloids (VERY strong; poss CV ADRs, ex. htn); can moderate effs
with MgSO4
G1 P1 1 1 1 : [full-term, preterm, miscarriages, living children]
TOXICOLOGY
treat pt, not poison
Methods: adsorption, lavage, etc.
therapeutic index: LD50/ED50: larger number = safer drug (lethal dose is large, effective dose is small)
[ED50 = effective dose]
acetominophen: glutamic oxaloacetate aminotransferase
Reactive intermediate is toxic (conj to glutathione to neutralize)

If amount overshoots avail glutathionetoxic

Tx: N-acetylcysteine (incr. avail of glutathione)
organophosphate (insecticides) = Ach inhib
chelators: metal with sulfhydryl groups
PHARMACOLOGY
For colon cancer:
Can give antimetabolite + platinum
OR topoisomerase inhibitor + molecular targeting agent
5-FU: inhibits thymidilate synthase (+ leucovorin makes more potent)
Irinotecan: Metabolized by enzyme UGT1A1
Patients with mutation *28 cannot metabolize, resulting in greater toxicity
5-FU: 8% of US population cant metabolize
Dihydropyrimidine Dehydrogenase (DPD) deficiency
Toxicity of 5-FU is much greater
Pre-screening recommended
Trastuzumab is cardiotoxic; contraindicated in cardiac patients
Lapatinib (TK inhibitor)(+capcitabine)use for HER2/neu positive cancers that have developed
resistance to trastzumab
Cancer/chemotherapy pts have nausea because of stimulation of the CTZ
(chemoreceptor trigger zone) in the area postrema of the medulla. (Esp. 5HT3
receptors, but also has DA/D2, opioid, muscarinic, & H1 receptors.)
Niacin causes hypoglycemia
Bile acid sequestrants decrease hyperglycemia
Beta blockers mask hypoglycemia
Review statins/hyperlipidemia/metabolic syndrome

Erectile dysfunction tx:

MOA of Cialis (tadalafil) & sidalefil, and others (PGE5?)PDE inhibition; vascular relaxation
Sildenafil/tadalafilPDE5 inhibitors, increase cGMP in corpus cavernosum
Which H2 blocker can cause ED? Cimetidine
ADH-R antagonists: vaptans (tolvaptan, etc.)
N-acetyl-cysteine MOA (effect on glutathione in acetaminophen toxicity)
Mechanism of action for BPH & prostate cancer drugs:
a. Finasteride: 5-alpha reductase inhibitor
b. Flutamide: Androgen receptor antagonist
c. Tamsulosin/zosins: alpha-1a selective alpha-blocker
d. Leuprolide: GnRH analogue (also goserelin, gonadorelin)
Cetuximab: EGF-R (epidermal growth factor) antibody

Bevacizumab MOA: Dont give to DM pts w/peripheral neuropathy or foot sores! Makes them worse b/c
it stops vascularization/VEGF.
Know that misoprostol is PGE1 and is given to prevent NSAID-induced ulcers, but can cause diarrhea
Loperamide is an anti-diarrheal that can cause toxic megacolon
Tx for males w/ CAH & 21-alpha-hydroxylase deficiency (hydrocortisone and fludrocortisone)
Which drug can fix diabetic gastroparesis, what is the MOA, and what are the side effects:
MetoclopramideD2 antagonist, 5HT3 receptor antagonist, 5HT4 agonist
Know MOA of Orlistat (inhibits intestinal lipases) and the major side effect (diarrhea)
Danazole: used for tx of endometriosis & leiomyomas (drug of choice if not performing surgery)
Mild androgen, inhibits release of FSH and LH growth of ectopic endometrial tissue
Wt gain, acne, breast size, deepening voice, libido, hair growth
Can suppress adrenal function
Leiomyomas: tx
Administer GnRH analogue pre-surgery to shrink tumor, then resect
Danazole: drug of choice if not performing surgery

I. DISEASES OF THE PANCREAS:

Insulin: Ultra-rapid acting insulin, Rapid-acting insulin, Intermediate-acting insulin, Extended acting insulin.
Remember that the extended acting and intermediate acting insulin are also slow acting as their onset of action
takes 1-4 hours.
Drugs to treat hypoglycemia:
d1) K+ channel agonist (Diazoxide): suppresses insulin secretion (open channel stops
Ca2+ release)
d2) Glucose (oral and parenteral)
d3) Glucagon
d4) Long-acting somastostatin analog (octreotide)
d5) Alpha glucosidase inhibitor (Acarbose)
One of my questions will relate to Metabolic syndrome, which could present itself with hypertension,
dislipidemia and hyperglycemia. Please review the effect of the drugs used to treat hypertension (Ca channel
blockers, thiazide diuretics, ACE inhibitors) on insulin secretion. Same for statins and antilipid drugs.
PARATHYROID, BONE AND CALCIUM:
Liver: Vit D 25-OH Vit D (primary circulating Vit D)
Kidney: 25-(OH) Vit. D 1,25-(OH)2 Vit. D (100-1000x affinity) ACTIVE FORM
Replace Vit. D deficiencies in people with renal/liver failure with the appropriate form
(D3 wont work):
1,25-dihydroxy Vit D w/renal failure, 25-OH Vit D w/liver failure

Thiazide diuretics: lower urinary calcium excretion

Loop diuretics: used with saline infusion to manage moderate hypercalcemia
High-dose glucocorticoids: Inhibit intestinal Ca2+ reabsorption; used in severe hypercalcemia, esp Vit D tox
Cinacalcet (calcium sensor mimetic): Binds to Ca2+ sensing receptor in PTh cells, mimics rise in blood
calcium dose-dependent decrease in PTH secretionreduces blood Ca2+ levels; used in severe
hypercalcemia
Tamoxifen
Competitively inhibits Estrogen Receptor (ER) and stimulates ER .
Response: 50% in ER+ tumors, 70% in ER+/PR+ tumors.
Agonist activity in bone protects against bone breaks
Cardioprotective
ADRER agonist in endometrium: increases endometrial cancer.
ADRHot flashes, cataracts, nausea.
SERM (Raloxifene)
Bone: Estrogen agonist activity decreases bone resorption in
postmenopausal women
Breast: Decreases proliferation of breast cancer cells (anti-estrogenic).
Plasma: Decreases LDL and total cholesterol
Endometrium: No effect (different to Tamoxifen, which has agonistic
action)
o Other adverse effects are similar to tamox
More effective at preventing fractures; less cardioprotrective.
Easily displaced from estrogen receptors by endogenous estrogen
Competitively inhibits Estrogen Receptor (ER) and stimulates ER.
Estrogen Supplementation
MOA: Antagonizes action of osteoclasts, decreasing bone resorption
No increase in skeletal mass, but slows loss of muscle relative to no estrogen
Indications: Estrogen Deficiency (ovariectomy/ovarian failure, natural menopause)
Exclusion recommended: personal or familial history of CVD, estrogendependent breast or endometrial cancer
Intact uterusadd progestin to decrease risk of endometrial cancer
Estrogen decreases risk of bone fracture by 50%
Increased risk for: CVD and CV events, stroke, venous thrombosis, breast
cancer
Only agent that decreases hot flashes
Second Generation Bisphosphonates
MOA: Bind to boneinhibit osteoclast functionprevent
demineralization
Osteoclast-mediated bone resorption releases the bisphosphonates
uptaken by osteoclasts
cytotoxic to osteoclasts decreased bone resorption
Noninhibitory of osteoclast induced osteoblast recruitment and attachment
increased bone mineralization
Decreased osteoclastic-mediated demineralization relative to osteoblasticmediated bone replacement.

ADRs: GERD, osteonecrosis (FDA: increased risk of atypical subtrochanteric femur

fractures, 2010)

Calcitonin
Uses: Osteopenia and osteoporosis (some patients), Paget Disease, hypercalcemia
MOA: increased cAMP in osteoclasts interferes with the membrane
transport of phosphate and calcium decreased osteoclast-induced bone
reabsorption
decreased Ca2+ and phosphate in plasma
increased Ca2+ excretion in urine large decrease in plasma Ca2+
(convenient for hypercalcemia; in osteoporosis, adding a thiazide diuretic
retains calcium)
Does not promote new bone growth
Salmon calcitonin has ~100x affinity for CT receptor as human calcitonin
Most patients develop resistance to CT within 24 hours (tachyphylaxis)
ADRs: Rhinitis, hypersensitivity to salmon calcitonin
Teriparatide: Peptide fragment of PTH
MOA: osteoclast activation (briefly)attraction and activation of osteoblasts (for longer periods of
time) increased bone formation
1-34 PTH and estrogens synergize their ability to increment bone mass
Contrarily, 1-34 PTH effect is lowered by bisphosphonates
Denosumab: Human monoclonal antibody to RANK ligand (RANKL) on osteoblast surface
MOA: Prevents RANKL binding to RANK in pre-osteoclasts and inhibits maturation to osteoclasts
Reduces survival of osteoclastsdecr. osteoclast population decr. bone resorption
ADRs: Hypocalcemia, infections, dermatologic reactions
2.

Rh factor: Mom is Rh (15% of white women) but dad is Rh +, so baby is Rh +, IgG from mom
can pass placenta and cause hemolysis in baby
55. A woman who is blood type A, Rh-negative has delivered a baby whose blood type is O, Rh-positive.
This baby may suffer from hemolytic disease of the newborn if the mother produced anti-Rh(D) antibodies.
3. Does ABO/blood type cause problems w/ pregnancy?
a. The patient and her husband are ABO compatible. Therefore, there is a higher risk of Rh
alloimmunization because fetal red blood cells last longer in the maternal circulation.
4. Eclampsia
a. Eclamptic convulsion, hypertension, proteinuria, nausea, vomiting,
headaches, cortical blindness, placental abruption.
b. This woman has classic features of eclampsia defined by
hypertension, edema, and proteinuria, typically with onset in the
third trimester. The addition of seizures defines eclampsia.
Primigravid women are at greater risk. Although the precise cause
of preeclampsia/eclampsia is unknown, placental ischemia is
believed to be the underlying mechanism. This is associated with
shallow placentation and incomplete conversion of decidual vessels
into high-volume channels required to perfuse the placenta
adequately.
5. Pre-eclampsia: Hypertension, proteinuria
a. HELLP: Hemolysis, Elevated Liver enzymes, Low Platelet count

6. With hyperparathyroidism, which test do you also need to run along w/ serum calcium, to get a better
picture of free calcium? (I think the answer is urine phosphorus?)
Parathyroid carcinoma, secreting high levels of PTH, is primary
hyperparathyroidism.
Most commonly caused by a parathyroid adenoma, but can be caused by a
parathyroid carcinoma.
Typically, hypercalcemia and elevated or normal PTH (PTH elevated relative to
calcium level).
Secondary hyperparathyroidism occurs when a patient has elevated PTH
secondary to low serum calcium levels.
Typically caused by kidney failure or not enough calcium in the diet.
Tertiary hyperparathyroidism:
Pt had secondary hyperparathyroidism, now has a kidney transplant and an
autonomous parathyroid gland
Pseudohyperparathyroidism: persistent hypercalcemia and
hypophosphatemia.
Due to ectopic secretion of parathyroid hormone(-like) polypeptides or other bone
resorbing substances by neoplasms that occur outside of the parathyroid gland.
7. Know which anti-lipid and anti-HTN drugs can cause hyperglycemia & how to fix it
8. Insulin types (rapid, long, etc.) how quickly are they absorbed, what is the point of doing rapid post
prandially and long-acting twice a day? (prevent post food spikes in blood sugar & mimic a normal
basal level of insulin)

Insulin directly acts to increase glucose uptake.

Glucose in the beta cells activates the transcription of the proinsulin gene.
Proinsulin is packaged into secretory vesicles and converted to insulin by an
enzymatic reaction involving pro-protein convertase I and II.
Insulin is metabolized in the liver and the kidney.
Biguanides (Metformin) blocks hepatic gluconeogenesis (decreases hepatic
production of glucose) and increases insulin sensitivity.
Sulfonylureas (ex. glyburide) and miglitinides (ex. repaglinide) work on the
cell membrane to promote insulin secretion from pancreatic beta cells.
1. Sulfonylureas increase the bioavailability of insulin in the blood by binding
to a receptor that is a part of the ATP-dependent K that stimulates Ca2+ influx,
leading to insulin secretion.
Polarize the pancreatic beta cell stimulating Ca reuptake leading to increased
insulin secretion.
Enhancement of hepatic insulinase activity has been attributed to sulfonylureas at
higher concentrations, which contributes to the hypoglycemic effect of these
drugs.
The sulfonylureas are degraded by the hepatic P450 enzymes.
Sulfonylureas block insulin degradation by inhibition of hepatic insulinases.
2. The Meglitinide class of antidiabetic drug, e.g. Repaglinide, promote rapid
insulin secretion and rapid degradation.
Although they act through different receptors from sulfonylureas, they also act on ATPdependent potassium channels to promote release of insulin and rapid degradation.
Thiazolidinediones (glitizones) are PPAR gamma agonists which stimulate
glucose and lipid metabolism and increase insulin sensitivity.

4. The thiazolidinedione class of antidiabetic drugs act as ligands to activate

peroxisome proliferator activated receptor.
Thiazolidinediones (glitazonesPPARties are glitta zonesTZDs like to PPARty)
increase processing of Type 1 insulin receptors by rough endoplasmic reticulum.

It then acts on beta-oxidation and fatty acid metabolism.

Thiazolidinediones promote the action of insulin by activation of transcription
factors which are phophorylated by protein kinases which are activated by IRS-2.
Troglitazone (all TZDs) is only used if the patient is already diabetic.

3. Acarbose inhibits the enzymatic conversion of complex carbohydates to

hexoses, which decreases the demand on insulin secretion.
Acarbose and miglitol are direct antagonists of intestinal alpha-glucosidase in the
enzymatic conversion of dietary carbohydrates to glucose.
Glucose absorption/levels will be decreased and therefore, insulin secretion will be
inhibited.
5. The gut peptide, glucose insulinotropic peptide, exenatide, increases the
bioavailability of insulin by acting through a membrane receptor in the
pancreatic beta cell to stimulate insulin secretion.
This is a GLP-1 (incretin) analog.
GLP-1 agonists act centrally to increase satiety and energy metabolism.
6. The modified amylin peptide, pramlintide, is FDA-approved to treat Type 1
and Type 2 DM.
It acts by decreasing insulin resistance by blocking glucagon release from
the pancreatic alpha cells.
This amylin analog decreases glucagon release, prolongs gastric emptying times,
and reduces caloric intake through a centrally mediated mechanism.

The treatment of diabetic ketoacidosis includes:

Administer regular insulin as dictated by blood sugar levels.
Replace fluids and sodium loss with isotonic saline and later hypotonic
saline.
For severe acidosis, administer bicarbonate.
Administer potassium as needed.
o Potassium must be monitored carefully in DKA; as the insulin pulls the sugar
into the cell, it also lowers potassium.
Intestinal angiodysplasia, major bad outcome:
a. Anemia or hemorrhage
Fastest laxative: saline laxatives or bisacodyl
Mesalamine (what all a-salicylates turn into) works in all parts of lower GI
(requires azo-reductase for conversion to active form)

Aminosalicylates: Mode of Actions: Reduce leukotriene synthesis by inhibiting

lipoxygenase (LTB4 production)
Reduce (prostaglandin synthesis)
inhibition of superoxide formation
inhibition of the production of cytokines
Miscellaneous:
Docusate is a stool softener.
Dopamine stimulates adrenergic and dopaminergic receptors. It causes nausea and vomiting.

Loperamide prevents diarrhea.

Sucralfate is used for coating the stomach to decrease acid causing ulcers.
Sometimes metformin is used to prevent development of diabetes.
HMG CoA reductase inhibitors (statins) block the synthesis of cholesterol.

Infliximab & Adalimumab: Chimeric monoclonal antibody against tumor necrosis factor-alpha (TNF-a)
Thalidomide Accelerates degradation of mRNA for TNF-a
Physiologic Jaundice of the Newborn
Higher RBC volume with shorter life span
Decreased hepatic receptors for albumin albumin-bilirubin complexes
Decreased glucuronyltransferase in hepatocytes
Results in unconjugated (indirect) hyperbilirubinemia
At risk for kernicterus if bilirubin>20mg/dL
Treatment: UV phototherapy or phenobarbital administration