Pathophysiology

Exxageration of cortisol actions. Altered fat metabolism (fat deposition), muscle weakness, extremeties are thin (protein breakdown). Osteoporosis might develop (destruction of proteins).
Low potassium levels, hypertension (sodium retention -> fluid volume increase)
Inflammatory and immune response is inhibited

Diagnosis of hypercortisolism and test the cause of the cortisol hypersecretion

Treatment is to remove or correct cause of it

Blood levels (aldosterone and ACTH) can be measured.

24h urine test can measure excretion of metabolic end products of adrenal hormones

Suppression and stimulation tests (asess HPA feedback system) and can help diagnose ACTH secreting tumors

Parathyroid hormone, produced by the parathyroid glands

Regulate calcium and phosphorus concentration in blood.

Calcium receptor in parathyroid acts rapidly to calcium levels. When calcium in plasma is high PTH is inhibited and Ca is deposited in bone. When Ca is low, PTH is secreted and calcium resorbed from bone

PTH promotes release of Ca from bone
Promotes activation of vitamin D by the kidneys (enhance intestinal absorptiom and stimulate konservation in kidneys)
Promotes phosphage excretion in kidneys

PTH deficiency resulting in hypocalcemia

Congenital absence of parathyroid glands (or aquired), neck injury, cancer. May have autoimmune origin.

Graves disease, hashimoto disease, heavy metal damage, tumors, are risk factors

Decrease in plasma calcium -> excitability of muscles -> muscle cramps and spasms, tingling of hand and feet.
Prolonged QT-interval (arryhtmias), hypotension

Chronic could cause anxiety and personality changes, and defecective teeth

Low plasma calcium levels and high plasma phosphate levels (or low plasma PTH)

Hypersecretion of PTH

Primary disorder caused by hyperplasia (increased tisue mass/proliferation), tumors

or secondary by chronic renal failure/malabsorption of Ca

hypercalcemia and increase in calcium in urine (hypercalciuria). Potential of kidney stones.

Chronic bone resorption produces demineralization (PTH too high -> release Ca from bone) -> fractions and bone lesions

Often asymptomatic too

Hyperplasia of parathyroid glands and renal failure - increased PTH levels due to decreased plasma calcium and activated vitamin D levels. -> Decrease of Ca receptors lead to more resistant feedback regulation -> Ca accumulates further (PTH gets secreted) -> calcification of vessels/tissue, abnormalities in bone

Classiefied as a vitamin but functions as a hormone

Acts to sustain normal calcium and phosphorus levels be increaseing absorption from intestine.
Also necessary for normal bone formation

UV-irradiation on skin or from diet

In the kidneys. Activation enhanced by PTH.

Ca and P absorption in intestine increases, and reabsorption of calcium and magnesium in kidney (and increased elimination of phosphorus)

A hormone which lowers the blood calcium levels (anatagonist of PTH)

Secreted in thyroid, it inhibits release of calcium from bones into extracellular fluid (inhibits osteoclast (degradation of bones) activity).
Reduces renal reabsorption of calcium and phosphate

Increased blood calcium stimulates Calcitonin release

Overall role in mineral homeostasis is uncertain

Hormone producesd by fibroblasts in renal interstitium(lumen). Regulates production of RBC in bone marrow

Synthesis of erythropoietin is stimulated by tissue hypoxia (may be due to anemia, high altitudes, impaired oxygenation due to cardiac or pulmonary disease).
Lack of Erythropoietin can also be seen in chronic kidney deseases (inability of kidney to produce it)

Urine test: collect and anazlyze urine from 24h
Glomerular Riltration Rate (GFR): Collect timed samples of blood and urine and measure Creatine e.g.
Blood test: Test for waste-products usually removed by kidney (K+, Posphate, creatinin)
 

Filter the blood, reabsorb substances needed for constancy of body fluids, and excrete metabolic waste

Normal urine: 95% water, metabolic wast, no plasma protein, blood cells or glucose

Proteinurea: excess protein in urine -> abnormal filtration of albumin (Protein) in glomeruli or defec in reabsorption in tubules 
Urine specific gravity /(osmolarity): provides indication of hydration status and functional bility of kidney. Decreased renal function -> decreased specific gravity (loss of concentrating ability)

Creatinin (wast product of muscle metabolism)is measured because it is freely filtedred in glomeruli (no reabsorption in tubules or secretion from blood to tubules).

Comparison of blood and urine creatinin levels.

Clearance rate=Urine concentration*urine volume/plasma concentration
Clearance: amount of creatine cleared by kidney in 1 min

Kidney removes wastes and maiintains electroylte and PH balance.

K1, posphate, blood urea nitrogen (BUN: end product of protein metabolism) or creatin increase in renal failure, pH, Ca2+ and HCO3- decrease in failure.

Endoscopy, imaging technique (Ultrasound, MR,....) or in other/special cases biopsy

Inflammation process that involves glomerular structures.

Acute Postinfectious: after infection due to immune antibodies and antigens
Rapidly progressive: progresses rabidly and involves proliferation of glomerularl cells
Chronic: slowly progressing, characterized by small/hardened kidneys

Infection from bacterias or viral agents such as hepatitis or other parasites

Infection due to deposition of immune antibodies and antigens. Characterized by enlargement of glomerulus. leukocytes, neutrophils and monocites cause hypercellularity (presence of larg number of cells), swelling of endothelial cells. Swelling damages capillary lumen.
May be interstitial edema and inflammation, and tubules often contain RBC.

Sodium and water retention -> edema and hypertension

Decreased urine output,  proteinuria (proteins in urine) and hematuria (blood in urine) due to increased capillary permeability. 
Cola-colored urine due to degraded RBC's in urine