Additional Cards Flashcards
Why do babies have jaundice normally
UDP-glucoronosyltransferase 1A1 (UGT1A1) is the key enzyme for bilirubin conjugation. Babies have low levels of this
Testing/results for
Primary hyperaldosteronism
Secondary hyperaldosteronism
Adrenal Virilism
Cushings Syndrome
Primary Adrenal insufficiency (Addisions Disease)
Secondary Adrenal insufficiency
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 relation to multiple myeloma
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
Monoclonal vs Polyclonal
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.
Mechanism of PBC
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.
PBC complications
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
Why is there increase in ALP and GGT in PBC?
ALP and GGT normally found in bile duct cells and therefore when destroyed by immune attack, these enzymes are released into bloodstream
Copro 3 levels difference in HCP and VP
Copro 3 more elevated in HCP than VP
Copro and proto equally elevated in VP
