Additional Cards

UDP-glucoronosyltransferase 1A1 (UGT1A1) is the key enzyme for bilirubin conjugation. Babies have low levels of this

Primary hyperaldosteronism (adrenal gland) 1. Increase aldosterone 2.Decrease PRA (aldo:renin) >20 3. Decrease K 4. Increase Na Secondary hyperaldosteronism (Renin mediated) - occurs in chronic liver conditions, diuretic medications Adrenal Virilism 1. Karotyping - determine sex 2. Abdominal ultrasound - observe for vagina, cervix and urethra 3. Accumulation of 17-hydroxyprogesterone Cushings Syndrome 1. Late night salivary test (high cortisol) 2. 24hr urine free cortisol (high cortisol) 3. Dexomethasone suppression test (Low and High) Primary Adrenal insufficiency (Addisions Disease) 1. Decreased Na 2.Increased K 3. High BUN 4.Low HCO3- 5. Hyperpigmentation Secondary Adrenal insufficiency NONE of the following: Decreased Na Increased K High BUN Low HCO3- Hyperpigmentation Due to the near normal secretion of aldosterone However to differeniate the two Addisions disease and secondary, must do ACTH and CRH stimulation tests: ACTH: In both cases show no rise in cortisol levels CRH: Primary: Major increase in ACTH but No increase in cortisol Secondary and tertiary: deficient increase in cortisol and ABSENT increase in ACTH (Secondary) or delayed/exaggerated increase in ACTH (Tertiary)

CRP is a surrogate marker of IL-6 activity. IL-6 is referred to as the plasma cell growth factor Therefore, the more CRP = more IL-6 = more plasma cell growth = myeloma indicator IL-6 signaling pathway in MM cells overall promotes an inflammatory microenvironment in the bone which results in bone loss IL-6 enhances osteoclast differentiation

polyclonal antibodies, which are produced by multiple immune cells monoclonal antibodies are generated by identical immune cells which are clones of a single parent cell. This means that the antibody recognizes only a single epitope of an antigen and is extremely specific.

T cells attack the cells that line the bile ducts in the liver and as the cells are damaged they start letting bile out of the bile duct via leaks in their tight junctions and into interstital space where it can get into the blood and liver cells causing chronic inflammation and symptoms of choleostasis due to the distrubance in bile flow. Begins with chronic inflammation which progresses to cirrhosis as more cells are destyoed by the immune attack.

Symptoms are related to the leakage of bile and inflammation caused at liver tissue. Jaundice (due to leaking of conjugated bilirunin from bile) Leakage of cholestrol into blood (bile contains mostly cholestrol) which can despot in the skin overtime causing xanthomas Itchy skin (pruritus) due to accumulation of bile salts in the skin (present in bile) Joint pain

ALP and GGT normally found in bile duct cells and therefore when destroyed by immune attack, these enzymes are released into bloodstream

Copro 3 more elevated in HCP than VP Copro and proto equally elevated in VP