serum creatinine levels (NOT blood)

increased serum Cr = inadequate GFR = impaired renal funciton

1. Acute renal failure

2. Chronic renal failure

3. Nephritic/nephrotic syndromes

4. Tubulointerstitial nephropathy

5. Obstructive nephropathy

- ischemia (2nd to pre-renal failure)

- trauma to the tubular structure

- extratubular obstruction

- acute glomerulonephritis

- pyelonephritis

1. Ischemic: secondary to surgery, severe hypovolemia, trauma, burns

2. Nephrotoxic: toxic agents that cause renal vasoconstriction and/or direct in lar obstruction

3. Tubular obstruction: myoglobin, uric acid, immunoglobulins (IgA)

Two types of glomerular disorders:

(Name)...cause...

Nephritic Syndromes: caused by diseases that produce an inflammatory response and damage the capillary wall

Nephrotic Syndromes: caused by disorders that damage the glomerular capillary membrane, increasing permeability, causing massive loss of protein into the urine.

Nephrotic syndrome involves increased permeability of the glomerulus membrane, protein (albumin) moves out of the blood and into the filtrate/urine, causing the intravascular fluid to become hypotonic. Water flows out of the hypotonic intravascular fluid into the tissues (edema). The liver increases serum proteins (since they were lost in the urine), which increses the producting of lipids.

nephrotic syndrome

thrombotic complications due to loss of proteins, including coagulant and anticoagulant factors

bacterial infection

abcess formation

RBC casts are associated with...

WBC casts are associated with...

Boad, waxy casts are associated with...

RBC casts = glomeularnephritis

WBC casts = tubular interstitial diseases (acute tubular necrosis, pyelonephritis)

Broad, waxy = chronic renal failure

methicillin

sulfonamide

furosemide

- damage medullary interstitial cells

 - inhibit prostaglandin synthesis, which contribute to tubular flow

Nothing specific...

Cells (WBC or RBC) in the urine of normal morphology signify lower urinary tract disease.

Cells with abnormal morphology signify renal disease.

Casts ALWAYS signify glomerular or tubular disease

funtional (normal) mechanisms...

transient increase due to heavy exercise, fever, or orthostatic proteinuria

the specific gravity

- varies with [solutes]

- index of hydration status and functional ability of kidneys to concentrate/dilute urine normal

range: 1.010-1.025

dilute urine due to decreased ADH

specific gravity decreases

75% decrease in renal function

*implication for dialysis

what substance is formed in the liver as a by-product of protein metabolist and is eliminated by kidneys?

What physiological function is it a marker of?

What is it influenced by?

What ratio is important?

BUN (blood urea nitrogen)

marker of...GFR

renal function influenced by...protein intake, hydration status, etc.

important ratio...BUN:Cr

**BUN:Cr ratio <20:1 = intrinsic renal failure **BUN:Cr ratio >20:1 = pre-renal failure

1. tubular reabsorption
2. tubular secretion

filtrate of protein-free plasma

filtrate one it has gone thru the tubules

1. arterial pressure--renal autoregulation
2. afferent arteriolar constriction--decreases GFR
3. efferent arteriolar constriction--increases GFR (overtime decreases)

The pressures opposing filtration are (2) 

blood colloid osmotic pressure and capsalar hydrostatic pressure

CO2 increases in repiratory                      

CO2 decreases in respiratory                     

acidosis

alkalosis

HCO3 increases result in                       

HCO3 decreses result in                      

alkalosis

acidosis

increases

retain

decreases

decrease (increse secretion)

decreased aldosterone

decreased catecholamines

decreased insulin

decreased distal flow rate

increased [H+]

effect on K+?

increased K+

hyperkalemia

increased aldosterone

increased catecholamines

increased insulin

increased distal flow rate

decreased [H+]

effect on K+?

decreased K+

hypokalemia

respiratory acidosis:

CO2         

H+          

pH          

metabolic response:

kidneys                HCO3

CO2 increases

H+ increases

pH decreases

kidneys reabsorb HCO3

respiratory aklalosis:

CO2         

H+          

pH          

metabolic response:

kidneys                HCO3

CO2 decreases

H+ decreases

pH increases

Kidneys excrete HCO3

metabolic alkalosis:

HCO3         

H+          

pH          

respiratory response:

lungs                CO2

HCO3 increases

H+ decreases

pH increases

lungs retain CO2 to buffer

metabolic acidosis:

HCO3         

H+          

pH          

respiratory response:

lungs                CO2

HCO3 decreases

H+ increases

pH decreases

lungs expel/remove CO2 to buffer

what is the most common cause of respiratory acidosis?

give 3 examples

decreased respiration

examples:

1. obstruction
2. damage to the lungs or chest wall
3. problem with the muscle of respiration or their neural input

[H+] decreases

[HCO3] increases

how does aldosterone effect Na+, K+, and H+?

What would hyperaldoseronism lead to?

aldosterone causes the reabsorption of Na+,

and secretion of K+ and H+

hyperaldosteronism can lead to increased acid secretion, thus alkalosis

hypokalemia can lead to metabolic                   

name 2 things that can cause hypokalemia

alkalosis

hypokalemia causes K+ to leave the cells in exchange for H+ (K+ out, H+ in).  Pulling H+ out of the serum leaves behind a more basic environment.

diuretics and hyperaldosteronism can cause hypokalemia

in metabolic alkalosis:

CO2 is             

HCO3 is            

pH is            

in metabolic alkalosis:

CO2 is HIGH (increased)

HCO3 is HIGH (increased)

pH is HIGH

in metabolic acidosis:

CO2 is             

HCO3 is            

pH is            

in metabolic acidosis:

CO2 is LOW (decreased)*

HCO3 is LOW (decreased)

pH is LOW

metabolic acidosis due to bicarbonate loss can be due to:

CLUE:  metabolic acidosis due to acid loss means that there is a normal anion gap

the main causes of metabolic acidosis due to acid loss are:

CLUE:  metabolic acidosis due to acid loss means that there is an elevated anion gap

MUDPILES

Methanol

Uremia

Diabetic ketoacidosis

Paraldehyde

Iron or IZH

Lactic acid

Ethylene glycol

Salicylates

if non-anion gap metabolic acidosis is present and the kindeys are funcitoning normally, how will the kidneys compensate?

how to you measure this response?

What would the likely cause of the acidosis be?

the kidneys will compensate by trying to secrete the excess acid in the form of NH4+

Urine anion gap measures the [Na+] + [K+] - [Cl-]

If the urine anion gap is very negative (meaning a lot of NH4 present), the cause of acidosis is diarrhea

Type 1:  distal nephron, impaired H+ secretion, causes basic urine and kidney stones

Type 2:  proximal nephron, impaired HCO3 reabsorption

Type 4:  hypoaldosteronism, decreased H+ secretion, hyperkalemia, hyponatremia

adrenal insuffiency

decreased renin secretion (renal failure, diabetic neuropathy)

decreased angiotensin (ACE-I)

NORMAL:  pH:  7.4          CO2:  40            HCO3:  24

1:            pH:  7.3          CO2:  49            HCO3: 23

2:            pH:  7.39        CO2:  42            HCO3: 30

state: respiratory or metabolic?  acidosis or alkalosis?

what is #1 and what is #2?

what is a possible cause?

NORMAL:  pH:  7.4          CO2:  40            HCO3:  24

1:            pH:  7.3          CO2:  49            HCO3: 23

2:            pH:  7.39        CO2:  42            HCO3: 30

state:  respiratory acidosis

#1:  uncompinsated acidosis

#2:  compensated acidosis

cause:  decreased venitlation (COPD)

NORMAL:  pH:  7.4          CO2:  40            HCO3:  24

1:            pH:  7.32        CO2:  41            HCO3: 18

2:            pH:  7.37        CO2:  23            HCO3: 21

state: respiratory or metabolic?  acidosis or alkalosis?

what is #1 and what is #2?

what is a possible cause?

NORMAL:  pH:  7.4          CO2:  40            HCO3:  24

1:            pH:  7.32        CO2:  41            HCO3: 18

2:            pH:  7.37        CO2:  23            HCO3: 21

state:  metabolic acidosis

#1:  uncompinsated acidosis

#2:  compensated acidosis

cause:  depends on anion gap...MUDPILES or diarrhea/renal failure

NORMAL:  pH:  7.4          CO2:  40            HCO3:  24

1:            pH:  7.48        CO2:  28            HCO3: 24

2:            pH:  7.41        CO2:  36            HCO3: 20

state: respiratory or metabolic?  acidosis or alkalosis?

what is #1 and what is #2?

what is a possible cause?

NORMAL:  pH:  7.4          CO2:  40            HCO3:  24

1:            pH:  7.48        CO2:  28            HCO3: 24

2:            pH:  7.41        CO2:  36            HCO3: 20

state:  respiratory alkalosis

#1:  uncompinsated alkalosis

#2:  compensated alkalosis

cause:  hyperventilation

NORMAL:  pH:  7.4          CO2:  40         HCO3:  24

1:            pH:  7.75        CO2:  40         HCO3: 33

2:            pH:  7.55        CO2:  44         HCO3: 27

state: respiratory or metabolic?  acidosis or alkalosis?

what is #1 and what is #2?

what is a possible cause?

NORMAL:  pH:  7.4          CO2:  40         HCO3:  24

1:            pH:  7.75        CO2:  40         HCO3: 33

2:            pH:  7.55        CO2:  44         HCO3: 27

state:  metabolic alkalosis

#1:  uncompinsated alkalosis

#2:  compensated alkalosis

cause:  hyperaldosteronism, hypokalemia, diuretics, vomiting

"stones, bones and moans"...

weakness, N/V, constipation, anorexia

mental status alteration

bone pain, osteitis, fibrosa

short QT

cause?

PTHrP

Parathyroid related protein

chronic renal failure is a common cause of                

why?

seconday hyperparathyroidism

decreased vit D metabolism leads to decreaed Ca+, which causes the parathyroid to secrete PTH

Vit D is activated to calcitrol in the kidney.  If kidney don´t do their job, no activated vit D= no Ca abs in small intestines = hypocalcemia.

Most common causes are hyperparathyroidism, bone metastesis, excess vit D.  Causes decrease in neuromuscular excitability.

electrolyte imbalance?

decr neuromuscular exitability & cardiac dysrhythmias

seen in diabetic ketoacidosis (why?)

electrolyte disorder?

hypokalemia

diabetic ketoacidosis:  shift of K+ from ECF to ICF due to increased insulin

Assoc with cell detruction (like tumor & chemo). 

electrolyte disorder?

what other electrolyte disorder can this cause?

hyperphosphatemia

hyperphosphatemia can cause hypocalcemia

related to inadequate intestinal absorption, bone formation, hypoparathyroidism, vit D deficiency. Causes decr in membrane excitability

electrolyte disorder?

Associated with DM.

*Signs/sx similar to which other electrolyte imbalance?

hypomagnesemia

S/S similar to hypocalcemia

Could be due to decr renal excretion.  ECG changes: acute T wave, wide QRS, ST depression

acidosis (why?)

hyperkalemia

acidosis:  shift of K+ from ICF to ECF in exchange for H+

Assoc w/ vit D def, alcoholism, malabsorption syndromes.

*When do symtoms become evident?*

hypophosphatemia

*symptoms become evident with severe depletion*

PTH:  stimulates renal secretion of phosphorus and Ca+ absorption from the GI (due to Vit D activation)

Calcitriol:  stimulates phosphorus absorption, stimulates Ca+ release from bones, absorption from GI, and increases tubular reabsorption of Ca+

calcitriol:

what is it?

where is it synthesized?

what activates it?

what stimulates its release?

what is it major action?

what is its effect on bone and GI?

calcitriol:

what is it? vit D3

where is it synthesized? cells of the proximal tubule of the nephron (kidney)

what activates it?  PTH

what stimulates its release?  increased plamsa Ca+, PTH

what is it major action? increase Ca+ and phosphate conc.

what is its effect on bone and GI?  GI:  enhances absorption of Ca, phosphate, Mg

Bone:  provides the proper balance of Ca and phospate to support mineralization

PTH is stimulate by...effects..

Calicitonin is stimulated by...effects

Vit D is stimulated by...effects

PTH: stimulated by low Ca, increased Ca+ by stimulating Vit D and bone resorption

Calcitonin:  stimulated by high Ca, decreases Ca+ by promoting bone formation

Vit D (calcitriole):  stimulated by low Ca and by low PHOS, promotes increase in serum Ca by increasing GI absorbtion, promotes increase in PHOS from bone and GI absorbtion

excess glucocoticosteroids =

excess mineralocorticoids =

hypofunction of adrenal cortex =

excess glucocoticosteroids = Cushing's disease/syndrome

excess mineralocorticoids = Conn's (primary)

hypofunction of adrenal cortex = Addison's disease

mineralcorticoid =

glucocorticoid =

androgen =

catecholemines =

*what part are these all from?

Adrenal Cortex (80%)

steroid hormones

mineralcorticoid = aldosterone

glucocorticoid = cortisol

androgen = DHEA

Adrenal Medulla (20%) 

catecholemines = EPI and NE

hypothalamus

↓

CRH

↓

Ant. pituitary

↓

ACTH

↓

Adrenal cortex

↓

cortisol

this hormone has catabolic effect on bone/muscle/adipose tissue, inhibits GH, increases glucose (gluconeogenesis), increases SNS, and controls immune/inflammatory response

cortisol

has circadian rhythm...peak just before waking and lowest 11pm-1am

DHEA (androgen)

secondary sex cx in females