Renal F&e

Front 1

ADH-antidiuretic hormone.

Back 1

From hypothalamus, stored in post. pituitary.
Responds to changes in serum osmolality.
Alters renal tubule permeability to water.

Front 2

Aldosterone-adrenal hormone.

Back 2

Part of renin-angiotensin-aldosterone triad.
Conserves Na+, which retains water.
promotes sodium ion and water reabsorption in the distal tubule and collecting duct where Na+ is exchanged for potassium (K+) and hydrogen ions by a specific cellular pump (water follows salt)

Front 3

Renin release

Back 3

released when there is a fall in intravascular volume e.g. haemorrhage and dehydration.

Front 4

carbonic acid:bicarbonate ratio

Back 4

20:1

Front 5

Four main buffer systems in the body

Back 5

Bicarbionate-carbonic acid system
Phosphate system
Protein system
Hemoglobin system

Front 6

Cause of changes in respirations

Back 6

Change in respirations d/t action of H+ on medulla

Front 7

Control of Sodium Resorption

Back 7

Decreased blood volume and/or cardiac output, decreased extracellular sodium, increased extracellular potassium, and physical stress

Front 8

Drugs that impair water excretion

Back 8

chlorpropamide (Diabinese), morphine, barbiturates, isoproerenol (Isuprel)

Front 9

Aldactone

Back 9

Spironolactone (Blackstone) used if etiology overproduction of aldosterone

Front 10

Potassium

Back 10

98% Intracellular
Important in maintaining volume within the cell
Necessary for transmission of nerve impulses and muscle contraction
Important in control of hydrogen ion concentration
When potassium moves out of the cell, sodium and hydrogen move in

Front 11

Potassium & Kidney

Back 11

Decreased excretion in response to increase in H ion excretion
With alkalosis, increase reabsorbtion of H ion, excrete more K ions in exchange
Increased aldosterone causes increased potassium excretion
When sodium low – aldosterone causes the kidney to save
When potassium high – aldosterone causes kidney to excrete

Front 12

Potassium & metabolic alkalosis,

Back 12

Potassium loss causes metabolic alkalosis, and a metabolic alkalosis causes a low potassium

Front 13

Hypokalemia causes

Back 13

Loss through urinary tract
High sodium intake, excessive bicarbonate administration
Treatment with diuretics (not potassium sparing)
Adrenal cortical steroid hormones will cause increase in potassium excretion
Vomiting, gastric suctioning, intestional fistulas, diarrhea

Front 14

Hypokalemia & Cardiovascular system

Back 14

Postural hypotension, weak irregular pulse, Dyrsrhythmias, ECG changes, Myocardial damage, Cardiac arrest, Heart block

Front 15

Hypokalemia & Kidneys

Back 15

Decreases capacity to concentrate waste, Water loss, Thirst, Kidney damage

Front 16

Hypokalemia & Muscles

Back 16

Weakness, Paresthesis, leads to flaccid paralysis, weakness of respiratory muscles which leads to Respiratory arrest (probable cause of death in hypokalemia)

Front 17

Hypokalemia & Gastrointestinal tract

Back 17

Anorexia, Nausea, vomiting, Abdominal distension  decreased bowel sounds, paralytic ileus
From weakness of smooth muscles in digestive tract

Front 18

Hyperkalemia - causes

Back 18

Excess intake – greater than kidney’s ability to excrete
Decreased loss
Potassium sparing diuretics
Renal failure
Adrenal insufficiency
Shift of potassium out of cells
Trauma, crushing injuries, metabolic acidosis

Front 19

Hyperkalemia - effects

Back 19

CNS
Numbness, tingling, anxiety
Cardiovascular
Conduction disturbance, bradycardia, heart block, cardiac arrest
Renal
Oliguria anuria
GI
Nausea, vomiting, diarrhea, colic
Muscles
Early: irritability
Late: Weakness  flaccid paralysis

Front 20

Most Frequent Causes of Edema

Back 20

The most frequent causes of generalized edema are congestive heart failure, cirrhosis, and nephrotic syndrome

Front 21

Nephrotic Syndrome

Back 21

Pathophysiology: increased glomerular permeability to plasma protein; massive urinary protein loss
Hyperalbuminuria; hypoalbuminemia
Edema, ascites, hypovolemia
Increased ADH & aldosterone*

Front 22

Primary Nephrotic Syndrome

Back 22

Minimal Change Nephrotic Syndrome (MCNS) – Most common
Membranous Nephropathy – thickening causes the glomeruli to become “leaky”
Glomerulonephritis – inflammation of glomeruli and nephrons
Focal segmental glomerulosclerosis – small scars form on the glomeruli

Front 23

Secondary Nephrotic Syndrome

Back 23

Damage to glomeruli from complications of:
Diabetes
About 20 years after onset of DM (20-40% of patients with DM)
Microalbuminuria is an earliest sign of diabetic nephropathy presenting ~ 10 years after onset of disease
SLE (systemic lupus erythematosus)
amyloidosis
Glomerular damage leading to nephrotic syndrome
a rare side-effect from certain medications and toxins
Ex. mercury.

Front 24

anasarca

Back 24

generalized edema

Front 25

Early S&S Nephrotic syndrome

Back 25

frothy urine due to protein (patients notice)
The first sign in children is usually swelling of the face
periorbital edema common presentation  followed by swelling of the entire body
Adults can present with edema of dependent parts
Facial swelling or anasarca can be the presenting symptom.
deep vein thrombosis

Front 26

Defining Characteristics of Nephrosis

Back 26

Edema*+periorbital, Proteinuria* >3+,  serum albumin*, Weight gain, Ascites, Pleural effusion
 serum cholesterol*, BP normal or slightly increased, Lethargic & Irritable, Easily fatigued, Anorexia
Diarrhea, Poor GI absorption, Difficulty breathing Pallor,  Urine: dark, frothy

Front 27

Goals of Treatment` Nephrotic Syndrome

Back 27

Reduce urinary protein loss
Reduce fluid retention
Prevent infection
Minimize complications (specially those of therapy)

Front 28

Nephrotic Syndrome Treatment (Dependent on pathology)

Back 28

High doses of corticosteroids- first line of treatment; 2 mg/kg
Response occurs in 10-20 days, 90% respond within 3 weeks
First response is a sudden increase in urine with a large loss of water weight (may stop diuretics at this time)
Taper off over several weeks – too fast may cause relapse, or other complications depending on length of therapy
Then stop if child/patient asymptomatic
Teach parents/patient to monitor for relapse
Urine dipstick for protein
2/3 will relapse

Front 29

high dose steroid long term effects

Back 29

Hirsutism
Growth retardation
Bone dimineralization; catarct
HTN, infection, hyperglycemia

Front 30

Nephrotic Syndrome Treatment complications

Back 30

consequences of severe proteinuria are the main clinical problem: brittle hair and nails, alopecia, stunted growth, demineralization of bone peritonitis
opportunistic infections are prevalent (varicella risk very important)peritonitis
opportunistic infections are prevalent (varicella risk very important)

Front 31

Nephrotic Syndrome
Activity

Back 31

Bedrest during edema phase, select play activity accordingly
Increase activity as edema subsides
Recreational & diversional activities
Focus on developmental task needs
Resume activities with discretion after edema and proteinuria resolved

Front 32

Effects of acidosis on the body

Back 32

Major effect is depression of the CNS
Signs/Sx include distressed respirations, anxiety, disorientation, confusion, body weakness ( coma)

Front 33

Effects of alkalosis on the body

Back 33

Over excitability of the nervous system
In both CNS and PNS (see 1st here)
Muscles will go into state of tetany as result of over stim
Tingling sensation in fingers in toes (early indicator), palpitation, perspiration, tetany, heart arrhythmias

Front 34

Anion Gap

Back 34

Normal is 10-14 mEq
Anion gap = Na+ - (HCO3- + Cl-)
When anion gap elevated, acidosis likely caused by organic acids (lactate and ketoacids)

Front 35

epogen

Back 35

stimulates production of RBC's Tx for anemia

Front 36

earliest sign of renal tubule damage

Back 36

Decr. serum glucose