My some review points and images before exam. - medicalspirit

[ArchivalUser]

low anion gap:
is caused by hypoalbuminemia. Albumin is a negatively charged protein and its loss from the serum results in the retention of other negatively charged ions such as chloride and bicarbonate. As bicarbonate and chloride anions are used to calculate the anion gap, there is a subsequent decrease in the gap.
In hypoalbuminaemia the anion gap is reduced from between 2.5 to 3 mmol/L per 1 g/dL decrease in serum albumin.[9] Common conditions that reduce serum albumin in the clinical setting are hemorrhage, nephrotic syndrome, intestinal obstruction and liver cirrhosis.
The anion gap is sometimes reduced in multiple myeloma, where there is an increase in plasma IgG (paraproteinaemia).
Corrections can be made for hypoalbuminemia to give an accurate anion gap.

[ArchivalUser]

High anion gap metabolic acidosis
The anion gap is affected by changes in unmeasured ions. A high anion gap indicates acidosis. e.g. In uncontrolled diabetes, there is an increase in ketoacids (i.e. an increase in unmeasured anions) and a resulting increase in the anion gap. In these conditions, bicarbonate concentrations decrease, in response to the need to buffer the increased presence of acids (as a result of the underlying condition). The bicarbonate is consumed by the unmeasured anion (via its action as a buffer) resulting in a high anion gap.
Lactic acidosis
Ketoacidosis
Diabetic ketoacidosis
Alcohol abuse
Toxins:
Ethylene glycol
Lactic acid
Uremia
Methanol
Propylene Glycol
Phenformin
Aspirin
Cyanide, coupled with elevated venous oxygenation
Iron
Isoniazid
Renal failure, causes high anion gap acidosis by decreased acid excretion and decreased HCO3− reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate accounts for the high anion gap.
Note: a useful mnemonic to remember this is MUDPILES (methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates). A newer mnemonic CUTE DIMPLES includes C for Cyanide and T for Toluene. Historically, the "P" in MUDPILES was for paraldehyde. As paraldehyde is no longer used medically, the "P" in the MUDPILES mnemonic currently refers to propylene glycol, a substance common in pharmaceutical injections such as diazepam or lorazepam. Accumulation of propylene glycol is converted into lactate and pyruvate, which causes lactic acidosis. GOLDMARK standing for glycols, oxoproline, L-lactic acidosis, D-lactic acidosis, methanol, aspirin, renal failure, and ketoacidosis is also used as a mnemonic for the causes of high anion gap in metabolic acidosis.

[ArchivalUser]

normal gap is ween 12- 16 meq/l


Gap= (Na+ K)- (Hco3 + Cl)

[ArchivalUser]

obstruction: so
Increase in Co2 arterial blood
Increase In HCo3
Decrease in Ph
i.e Respiratory acidosis

[ArchivalUser]

VEGF (vascular endothelial growth factor) &BFGF ( basic fibroblast growth factor): Botha re heparin binding and both promote angiogenesis BUT BFGF mra expression does not increase after exercise.

* VEGF mra expression INCREASE after exercise.

[ArchivalUser]

*hydrogen ions that are exchanged for sodium are generated by carbonic anhydrase in the renal tubule epithelium causing increased production of bicarbonate. The increased bicarbonate and the excreted hydrogen combine to generate a metabolic alkalosis.

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Primary Hyperaldosteronism has many causes, including adrenal hyperplasia and adrenal carcinoma. When it occurs due to a solitary aldosterone-secreting adrenal adenoma (a type of benign tumor) known as Conn's syndrome.

Conn's syndrome is an Aldosterone-Producing Adenoma (APA).

* Layer affected is outer most layer of adrenal gland = Glomurulosa which normally produces Aldosterone.
* Pt. have:
1. Hypertention due to NA+ retension
2. Metabolic Alka losis= increased bicarbonate and the excreted hydrogen combine to generate a metabolic alkalosis.
3. high pH of the blood makes calcium less available to tissues and causes symptoms of hypocalcemia (low calcium levels).

[ArchivalUser]

* Secondary hyperaldosteronism is often related to decreased cardiac output which is associated with elevated renin levels.

Aldosterone enhances exchange of sodium for potassium in the kidney so increased aldosteronism will lead to hypernatremia and hypokalemia. Once the potassium has been significantly reduced by aldosterone, a sodium/hydrogen pump in the nephron becomes more active leading to increased excretion of hydrogen ions and further exacerbating the hypernatremia. The hydrogen ions that are exchanged for sodium are generated by carbonic anhydrase in the renal tubule epithelium causing increased production of bicarbonate. The increased bicarbonate and the excreted hydrogen combine to generate a metabolic alkalosis. The high pH of the blood makes calcium less available to the tissues and causes symptoms of hypocalcemia (low calcium levels).
The sodium retention leads to plasma volume expansion and elevated blood pressure. The increased blood pressure will lead to increased glomerular filtration rate and cause a decrease in renin release from the granular cells of the juxtaglomerular apparatus in the kidney. If there is a primary hyperaldosteronism the decreased renin (and subsequent decreased angiotensin II) will not lead to a decrease in aldosterone levels (a very helpful clinical tool in diagnosis of primary hyperaldosteronism).
Aside from high blood pressure manifestations of muscle cramps (due to hyperexcitability of neurons secondary to hypocalcemia), muscle weakness (due to hypoexcitability of skeletal muscles secondary to hypokalemia), and headaches (due to hypokalemia or high blood pressure) may be seen.

[ArchivalUser]

Celiac disease: malabsorption of vitamin D so
1. Vitamin D deficiency lead to hypocalcemia
2. low level of ca2+ = increased PTH ( secondary parathyroidism)
3. increased PTH ( secondary parathyroidism) willl cause urinary excretion of Phosphorus
therefore - serum Phosphorus is decreased


So, in celiac deisease we have: Serum PTH increase and Calicium and phosphorus decrease.

[ArchivalUser]

http://highered.mcgraw-hill.com/sites/00...iz_1_.html


http://highered.mcgraw-hill.com/sites/00...iz_2_.html

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http://library.med.utah.edu/WebPath/CVHTML/CV072.html