Physio Exam 3 Renal 10-11

Front 1

Metabolic acidosis
Primary disorder
pH
Compensatory response
Predicted compensation
Limits of compensation

Back 1

decrease in HCO3
decrease
decrease in pCO2
Change in pCO2=1.0 to 1.5x in the plasma HCO3 concentration
10mmHg

Front 2

High anion gap

Back 2

High anion gap: Metabolic alkalosis. Metabolic acidosis: ketoacidosis, renal failure, methanol, ethylene glycol, salicylate, lactic acidosis..

Front 3

Acid Gain (high anion gap) except HCL specific mechanism

Back 3

-Incomplete fat oxidation (ketoacids
-Incomplete carbohydrate oxidation (lactic acid
-Gain of exogenous acid or toxins

Front 4

Incomplete fat oxidation (ketoacids) exnamples would be

Back 4

Diabetes, starvation

Front 5

Incomplete carbohydrate oxidation (lactic acid) examples

Back 5

Shock, sepsis, seizures

Front 6

Gain of exogenous acid or toxin examples

Back 6

1) Hydrochloric acid: NH4CI, arginine chloride, lysine chloride
2)Toxic alcohols: methanol, ethylene glycol, Salicylate

Front 7

Normal protein metabolism

Back 7

renal failure

Front 8

Bicarbonate Loss
(Normal Anion Gap) leading to metabolic acidosis can occur in

Back 8

Gastrointestinal HCO3 loss and Renal HCO3 loss

Front 9

Example of

Gastrointestinal HCO3- loss

Back 9

Diarrhea: loss of pancreatic, biliary, or intestinal secretions

Front 10

Example of renal HCO3 loss

Back 10

Proximal and distal renal tubular acidosis

Front 11

High Anion Gap in summary can be caused by

Back 11

Uremia
Ketoacidosis
Lactic acidosis
Salicylate toxicity
Methanol toxicity
Ethylene glycol toxicity
MUDPILES

Front 12

Incomplete metabolism of Fat, no insulin, glucagon goes up and breaks up fat. Occurs in diabetes, starvation and prolongued alcohol intake

Back 12

Ketosis

Front 13

Mitochondria defect or O2 delivery to to mitochondria appropiately, incomplete carbohydrate metabolism

Back 13

Lactic Acidosis

Front 14

Protein metabolism problems. Renal failure, accumulation of sulfate and phosphate and urea cant be excreted. This happens in patients on dyalisys, HCO3 added to compesate

Back 14

Uremia

Front 15

Formic acid formation is titrated by HCO3 and gives severe acidosis, leading to blindness

Back 15

Methanol toxicity

Front 16

Metabolism of ethylene glycol to oxalic acid and glycolic acid leading to precipitation of Ca2+

Back 16

Ethylene glycil toxicity

Front 17

How to treat Ethylene Glycol intoxication?

Back 17

give patient ethanol, which competes with ethylene glycol and do a dyalisis

Front 18

How can we know if a patient has uremia or not?

Back 18

creatine levels would be normal

Front 19

How can we know is not ketoacidosis?

Back 19

glucose levels would be normal, high glucose indicated ketoacidosis

Front 20

Normal Anion Gap aka

Back 20

Hypercholeremic acidosis because gap is normal. When this happens dont look for any of the acids tha cause high gap, instead this is caused by loss of HCO3. Seldom gained in Cl.

Front 21

In normal anion gap where can the HCO3 be lost?

Back 21

Kidney, GI, resection of illeum, diarrhea. Volume contraction occurs and Cl reab is enhanced leading to hyperchloremia

Front 22

Metabolic Alkalosis
Primary Disorder
pH
Compensatory Response
Predicted Compensation
Limits of compensation

Back 22

HCO3 goes up
pH goes up
pCO2 goes up
pCO2 should rise by 0.5-1x the rise in plasma HCO3 concentration

Front 23

Metabolic Alkalosis can occur because

Back 23

Acid loss
Bicarbonate Gain
Volume Depletion and Secondary
Hyperaldosteronism

Volume Expansion and Mineralocorticoid Excess

Front 24

Renal acid loss examples

Back 24

Mineralocorticoid excess (primary or secondary)
Diuretics
Distal delivery of a poorly reabsorbable anion with sodium (e.g., carbenicillin

Front 25

GI acid loss examples

Back 25

Gastric fluid loss

Front 26

Intracellular hydrogen shift example

Back 26

Potassium deficiency

Front 27

Bicarbonate Gain example

Back 27

Milk-alkali syndrome, administration of bicarbonate, citrate, or lactate

Front 28

Volume Depletion and Secondary
Hyperaldosteronism
can occur when

Back 28

Gastrointestinal origin (Urine Cl-  20 mEq/L)


Renal origin
(Urine Cl- > 20 mEq/L

Front 29

Volume Expansion and Mineralocorticoid Excess can occur when

Back 29

Low renin states (Urine Cl- > 20 mEq/L)


High renin states (Urine Cl- > 20 mEq/L)

Front 30

Low renin states (Urine Cl- > 20 mEq/L) example

Back 30

Primary hyperaldosteronism, Cushing's syndrome, exogenous mineralocorticoid
administration

Front 31

High renin states (Urine Cl- > 20 mEq/L) can occur when

Back 31

Renal artery stenosis, renin-secreting tumor

Front 32

Respiratory acidosis
Primary disorder
pH
Compensatory response
Predicted compensation
limits of compensation

Back 32

pCO2 incease
pH decrease
HCO3 increase
Acute: Plasma HCO3 concentration should rise about 1 for each increament of 10 in PCO2
Chronic: Plasma HCO3- concentration should rise by about 4 mEq/L for each increment of 10 mm Hg in PCO2
Acute limit: 32
Chronic limit: 45

Front 33

Respiratory acidosis sites of action

Back 33

Inhibition of
respiratory center
Disorders of respiratory muscle, nerves, chest wall
Upper and lower airway obstruction

Front 34

Inhibition of
respiratory center
example

Back 34

Patients who will not
breathe due to
Drugs: Anesthetics, ethanol narcosis, opiates, sedatives

Central nervous system lesions
Brain stem/high spinal chord lesion

Front 35

Disorders of respiratory muscle, nerves, chest wall can occur in

Back 35

Myasthenia gravis, poliomyelitis, kyphoscoliosis

Front 36

Upper and lower airway obstruction can occur when

Back 36

Pulmonary fibrosis

COPD

Front 37

Respiratory alkalosis
primary disorder
pH
Compensatory Response
Predicted compensation
Limits of compensation

Back 37

pCO2 decrease
pH increase
HCO3 decrease
Acute: Plasma HCO3- concentration should fall by about 2 mEq/L for each decrement of 10 mm Hg in PCO2, but usually not to < 18 mEq/L.

Chronic; Plasma HCO3- concentration should fall by about 5 mEq/L for each decrement of 10 mm Hg in PCO2, but usually not to < 12 mEq/L.

Acute; 18-20
Chronic; 12-15

Front 38

Causes of respiratory mechanism

Back 38

-Stimulation of
respiratory centers
-Stimulation of
peripheral chemoreceptors
-Stimulation of
intrathoracic receptors.
In all of these 3 the ventilation goes up

Front 39

Stimulation of
respiratory centers can occur due to

Back 39

Salicylate intoxication
Psychogenic hyperventilation
Hepatic cirrhosis
Brain stem lesions
Encephalitis
Pregnancy
Sepsis

Front 40

Stimulation of
peripheral chemoreceptors can occur due to

Back 40

Hypoxemia
Hypotension

Front 41

Stimulation of
intrathoracic receptors examples

Back 41

Restrictive lung disease
Pulmonary embolus
Pneumonia
Pneumothorax

Front 42

Rules to diagnose ACID-BASE disorders

Back 42

look at handout.