JGA

Juxtaglomerular apparatus

[distal tubule,basically the thick ascending tubule]

Vasopressin

inc blood pressure

-secreted by pituitary gland

-helps retain water

inc BP 

-triggered by [K+] vol depletion 

-brings in Na+

-proiduced in glomerulous by adrenal gland

-increases K+ secretion

-Atrial Natriuretic Peptide 

-Promotes salt and water excretion

-lowers BP

Urea

Ethanol

Na+

Hyperkalemia is ________

Hypokalemia is ___________

1. Metabolic Acidosis

2. Metabolic Alkalosis

1. combination with bicarbonate to minimize free H+

2. excreting this acid by kidney (NEEDS AMMONIUM)

[kidney excretes the H+ and returns HCO3- to blood]

1. carbonate in bones

2. HPO4,2- and protein anions in cell

3. H+ combos with bicarbonate in extracellular fluid

1. CARBONIC ACID

2. HYDROGEN AND 

3.BICARBONATE

1. pROXIMAL TUBULE=NH4+  SUBSTITUTES A H+ AT Na+/H+ EXCHANGER TO LEAVE CELL

2. cOLLECTING DUCTS= NH3 I LIPID SOLUBLE AND CAN PASSIVELY DIFFUCE INTO LUMEN TO COMBINE WITH H+ TO FORM AMMONIUM

INC ACID PRODUCTION

IMPAIRED RENAL EXCRETION

ACID SECRETION

AS AMMONIUM

TYPES OF ACUTE RENAL FAILURE

iNTRINSIC RENAL DISEASE

pRERENAL DISEASE

postrenal disease

iNTRINSIC RENAL DISEASE: DIS PROGRESS W/ DEC # OF FUNC NEPHRONS[damaged struct]

pRERENAL DISEASE: DECLINED RENAL PERFUSION

[blood flow]

postrenal: obstruction of urine outflow from kidney

TOXINS CLEARED BY GFR _________

nITROGEN WASTE_____________

1. uREMIC MOLECULES

2. aZOTEMIA

UREMIA

[TOXICITY DUE TO ACUTE RENAL FAIL]

-PERICARDITIS(INFLAMED PERICARDIUM)

-HYPERKALEMIA

-EDEMA

-BONE DISEASE

-ANEMIA

ACUTE RENAL FAILURE IS PLASMA CREATINE CONC OF AT LEAST _________

OR INC OF GREATER THAN __________OVER BASELINE VALUE OF SCr OR CALCULATED CREATININE CLEARANCE

FALL IN URINE OF LESS THAN__________ML PER DAY

1. 0.5 mg/dL

2. 50%

3. <400 ml/day

Prostatic Disease

or 

Anti-cholinergic drugs

With PRERENAL DISEASE IV fluids will_____________ GFR

With Acute TUBULAR NECROSIS(ATN) pt will have ___________________

increase GFR to baseline(Na+ retention is response, and inc AVP)

Continued decrease(w/ ATN AVP and Na+ retention is impaired)

Causes:cancer,prostatic hypertrophy,blood clots

ARF

ACUTE RENAL FAILURE

-major cause of intrinsic ARF

-Causes by anticancer and antibiotics

-2 types=post ishcemic and toxic

-urine contains EPITHELIAL CASTS

[indicating tubular necrosis]

-ISCHEMIA REDUCES ALREADY LOW PO2 IN MEDULLA CAUSING HYPOXIA & NECROSIS

-500,00 pts w/ end stage renal disease(20% die)

-32$ billion in medicare costs to treat

-casues:diabetic nephropathy,chronic glomerular diseases, polycistic kidney dis,hypertensive nephrosclerosis

STAGE 5 = LESS THAN 15 ML/MIN GFR. DIALYSIS OR TRANSPLANT NEEDED

STAGE 1 &2 = NO SYMPTOMS

STAGE 3&4 COMPLICATIONS START

initiating mechanisms= 

Progressive mechanisms=

initiating mechanisms= specific to underlying etiology

Progressive mechanisms= hyperfiltration and hypertrophy of the remaining viable nephrons

GLOMERULONEPHRITIS

[INITIATING MECHANISM]

-DAMAGE TO GLOMERULUS

-sx: proteinuria,low albumin, high cholesterol,high triglyceride,edema

-damaged epithelium, glomerular basement membranes gone (cant filter by charge anymore and allows albumin in urine)

POLYCYSTIC KIDNEY DISEASE

[INITIATING MECHANISM]

-Genetic disorder cysts in kidneys

-50% of people w/ it progress to end stage renal disease

-4th leading cause of RF

HYPERTENSION

[PROGRESSIVE MECHANISM]

-due to dec GFR 

-80% of cases due to inadequate Na+ secretion

***CHRONIC RENAL FAILURE HTN is ultimately linked to dec GFR and inability to maintain electrolyte balance

-elevated intraglomerular pressure

-glomerular hypertrophy

-proteinuria

-Cant stop secretion of PTH due torenal failure. Renal failure causes us not to make calcitriol

-CALCITRIOL stops/regulate PTH secretion

OSTEITIS FIBROSA CYSTICA

METASTIC CALCIFICATIONS

Tx:

-maintain normal plasma conc.of phosphate[diet,calcium based binders]

-inhibit PTH[high dose calcitriol]

OSTEITIS FIBROSA CYSTICA

METASTIC CALCIFICATIONS

OSTEITIS FIBROSA CYSTICA:skeletal demineralization, bone cysts, spontaneous fractures

METASTIC CALCIFICATIONS: Ca2+ phosphate precipitates out of plasma and settles in arteries,soft tissue, and viscera

Capillary [peritubuluar] network is _________pressure

Afferent and efferent arterioles are _______resistance

Glomerular capillary network is _______pressure

Capillary [peritubuluar] network is ___low______pressure

Afferent and efferent arterioles are __high_____resistance

Glomerular capillary network is ___high____pressure

Where filtrate forms=___________

Where blood filtrate converted to urine=___________

Where filtrate forms=___Glomerulus________

Where blood filtrate converted to urine=__Tubules____

[tubule meets glomerulus at BOWMANS CAPSULE]

PODOCYTES FILTER BY_________

GLOMERULAR BASEMENT MEMBRANE FILTER BY______

SIZE AND CHARGE

CHARGE

-protects kideny from hi P

-Autoreflex = stretch dependent

[in vascular smoothe muscle]

-response to vol loss or dec BP

-depends on SNS

(renin/angiotensin)

-recovery of fluidand solutes here

-Na+ and glucose reabsorbtion here

-acid-base balance

-regulation of Ca2+ & HPO4,2-

-reg factors ang II,norepi,GFR act on PT

DESCENDING LIMB =

ASCENDING LIMB= 

DESCENDING LIMB = PERMEABLE TO WATER BUT NOT IONS

ASCENDING LIMB= PERMEABLE TO IONS BUT NOT WATER

[MAKES INTERSTITIAL FLUID CONCENTRATED W/ COUNTERCURRENT MECHANISM]

Na+ pushed into interstitial space by atpase

some Na+ reabsorbed into capillary and water reabsorbed from thin descending limb

DISTAL CONVOLUTED TUBULE

-starts at macula densa

-fine control of water and salt excretion

-potently excretes Na+ in presence of loop diuretic

DISTAL TUBULE

[Na+ Cl- CO-TRANSPORTER]

-collects filtrate

intercalated cells make 1/3 

-ANP,AVP and aldosterone under hormonal control

-found in collecting tubule(make 1/3)

-secrete H+ or HCO3-

-reabsorb K+

solute completely cleared by kidney

freely filtered at glomerulus

not reabsorbed, secreted,synthesized, or metabolized by kidney

achieves stable plasma conc

plasma concentration of creatinine(tells GFR)

Cr conc=men normal at 0.8 to 1.3 mg/dL (women 0.6-1.0)

women GFR =95 +/- 20ml/min

men GFR =120 +/- 25ml/min 

PROTEIN IS FOUND IN

POTASSIUM IN

Na+ IN

PROTEIN IS FOUND IN= PLASMA

POTASSIUM IN= CELLS

Na+ IN = INTERSTITIAL FLUID

Osmolality determines_________

Osmotic pressure determines_________

Osmolality determines___# of solutes______

Osmotic pressure determines__fluid distribut___

-hypernatremia

inc plasma osmolality

inc ECF vol

dec ICF vol

inc urine Na+ excretion

-hyponatremia

dec plasma osmolality

inc ECF vol

inc ICF vol

inc urine Na+ excretion

no change in osmolality or plasma sodium

inc extracellular fluid volume

no change in intracellular fluid vol

inc urine Na+ excretion

Osmoreceptors are found where?

HYPOTHALAMUS

In Organum Vasculosuum of laminus terminalis

[osmoregulation,influence AVP release and thirst]

-changes in water balance

-handling of sodium

inherited defects in V2 receptor or aquaporin-2 gene

  decrease in the ability of the kidney to concentrate the urine

-can be aquired from lithium therapy or hypercalcemia

AVP stimulates the production of renal _________

NSAIDs inhibit their synthesis

In Organum Vasculosuum of laminus terminalis

 [HYPOTHALAMUS]

____________does not stimulate AVP

plasma sodium conc(_____&______) are major determinants of AVP 

UREA

Mannitol&Glucose

ANG II  promotes reabsorption of H2O and Na+....ECF vol is expanded

but _______concentration is not changed.

[regulated primarily by AVP]

Macula Densa cells in DT

Afferent arterioles

Cardiopulmonary Baroreceptors

Aldosterone activates the _______________ in cytosol

which stimulates Na+ channel protein creation.

Mineral Corticoid receptors(MR)

[action in principle cells of cortical collecting ducts]

-STEROID HORMONE FREELY CROSS MEMBRANE OF CELL

-binds mineralcorticoid receptor too

-11BHSD converts Cortisol to cortisone(now cant bind MR)

[now Aldosterone can bind and make Na+ channels open]

-

-made in myocardial cells of atria(in ventricles during HF)

-vasodilator

-inc urinary Na+ and water excretion

-closes luminal Na+ channels in COLLECTING DUCT

-correction for hyponatremia

-permanant brain damage due to rapid shrinking of brain & damaged myelin sheath

-Hypothyroidism(decreases AVP release and dec GFR)

-SIADH(elevated AVP due to brain defects,or ectopic tumor in lungs pumpin too much AVP)

-Cortisol deficiency

-AFTER MAJOR SURGERY, MALIGNANCY, W/ NEUROLOGICAL DISEASE

-gradual reduction in [pNa] and most patients are asymptomatic

-associated conditions=ECTOPIC TUMORS(LUNG),PULMONARY DISEASE,DRUGS(ORAL HYPOGLYCEMIC AGENT/CHLORPROPAMIDE)

elevated AVP alone cannot casuehyponatremia in absence of water intak****

3 TESTS TO DIAGNOSE  hyponatremia

<280mOsm/kg Water

-Plasma Osmolality

-urine Osmolality

-Urine sodium conc

-[pNa]> 146 mEq/mL

-Thirst is ultimate protection

-Etiology: FEVER, RESP INFECTIONS, CENTRALOR NEPHROGENIC DIABETES INSIPIDUS, OSMOTIC DIURESIS DUE TO GLUCOSE,gi LOSS, HYPOTHALAMIC LESION

-WATER

-THIRST

DIABETES MELLITUS CAN CAUSE________

DUE TO PULLING WATER TO ecf

MORE THAN 3L/DAY

GIVE PT DDAVP

[CONTINUES TO CONCENTRATE URINE = CNS prob mOsm>500mOsm/kg]

kidney prob

[cant concentrate urine <300mOsm/kg]

DECREASED LUMENAL CHLORIDE 

AND 

AUTOREG OF BARORECEPTORS IN AFFERENT ARTERIOLE

nORMAL gfr MEN

 VS WOMEN

MEN 120+/-25

WOMEN 95+/-20

=[(140-AGE)XWEIGHT IN KG]/(SCrX72) 

(MULTIPLY BY0.85 FOR FEMALE Pt)