Renal 8 Flashcards
Effects of Angiotensin 2
Increased Cardiac output
Increased Na+ Reabsorbtion
Thirst
Increased vasopressin secretion
Increased peripheral vasoconstriction
Stimulus: Low blood pressure
Thirst is controlled by
Hypothalamus
What are the sources of increasing thirst
Increased blood osmolarity
Decreased blood volume
Decreased blood pressure
Dry mouth
Behavioural mechnaisms for salt intake
increased aldosterone
increased angiotensin 2
Avoidance behaviours
Helps prevent dehydration
CV system responds
To blood volume and blood pressure
Renal responds to
Blood volume and blood osmolarity
increase osmolarity and increase blood volume
When eating salty popcorn. Ingesting more salt than water. Ingestion of hypertonic saline
How do kidneys resolve increase osmolarity and increased blood volume
By excreting hyperosmotic urine
Increased volume and no change in osmolarity
If salt and water are ingestes equally to isotonic solution
Increase volume and decreased osmolarity
Simply drinking pure water
Kidneys cannot excrete pure water
No volume increased osmolarity
Kidneys created concentrated urine
Thirst is triggered
Eating salt without drinking water, increases ECF osmolarity
No change in volume decreased osmolarity
if you are sweating. can lead to hypokalemia or hyponatremia
Decrease volume Increased osmolarity
Dehydration. due to excessive excersie or sweating or diarrhea
Can result in inadequate perfusion (decreased blood volume) and cell dysfunction
You want to increase water intake
Decrease volume no chnage osmolarity
Hemorrhage
Need blood transfusion
Decrease volume Decrease dehydration
May be due to incomplete dehydration
Dehydration is due to
Decreased blood pressure and increased osmolarity
Dehydration is restored by
- Conserving fluid to prevent additional loss
- Trigger cardiovascular reflexes to incrase blood pressure
- Stimulate thirst so normal fluid volume and osmolarity can be restored
ANP release in stimulated by
Increased blood volume
Renin - angiotensin is stimulated by
Decreased blood volume
Increase in osmolarity
Inhibits aldosterone release
What senses dehydration in CVVCC
Cartoid and aortic baroreceptors
how does CVCC respond to dehydration
Heart rate goes up as SA node controls shifts from parasympathetic to sympathetic.
2. Force of ventricular contraction increases from sympathetic stimulation
3. Sympathetic input to arterioles increases peripheral resistance (Vasoconstriction)
4. Sympathetic vasoconstriction of afferent arterioles in kidney decreses GFR, coserving fluid
5. Increased sympathetic activity at granular cells increases renin seretion
Direcr responses of Low blood pressure
Decreases blood pressure directly decreases GFR
Paracrine feedback at macula densa cells causees granular cells to release renin
Granular cells respond to decreased blood pressure by releasing renin
Decreased blood pressure, and increased osmolarity and increased ang 2 stimulate vasopressin and the thirst centers at hypothalamus
ANG 2 reinforces CV response
Results of blood pressure mechanisms
- Rapid attmept by the CVCC to maintain blood pressure
- Restoration of volume by water conservation and fluis intake
- Restoration of normal osmolarity by decreased na+ reabsorbtion and increased water reabsorbtion and intake
pH of solution
Is a measurement of H+ Concentration
pH of 7
Neutral
A Change of 1 pH represents
10 fold change in H+ concentration
Normal pH
in ECF is 7.38-7.42
pH chnages can
Denature proteins
low pH
Acidosis (CNS depression, cofusion and coma)
High pH
Alkalosis (Hykerexcitability)
Sustained respiratory muscle contracttion
Body is exposed
To more acid than base
The largest source of acid is
Production of CO2 from aerobic metabolism
pH homeostasis depends on 3 mechanisms
- Buffers (First line of defence)
- Vnetilation (handles 75% of disturnamces)
- Renal regulation of H+ and HCO3 (lowest)
Intracellular buffers
Hemoglobin
Major extracellular buffer
HCO3 itself
Which of the following occurs during dehydration
Decreased aldosterone release
Increased vasopressin release
Increased ANG II released
Increased Sympathetic
Decreased ANC
Buffer systems include
Proteins, phosphate ions and HCO3 -
Intracellular buffer
Hemoglobin
most important extracellular buffer system
Bicarbonate
Increased CO2
Equilibrium shifts to right
It creates one hydrogen and one bicarbonate
Increased hydrogen
Bicarbonate acts as a buffer creating carbonic acid. Function within a narrow range.
Increased in CO2
Hypoventilation (Right Shift)
Decrease CO2
Hyperventilation (Left shift)
Rate of breathing increases when
Decreases plasma H+ and increased plasma CO2
Kidneys respond to disturbances
Slowly
Directly
Indirectly
how do you do it directly
By altering excretion or reabsorbtion of H+
How do you do it indirectly
By changing the rate at which HCO3- buffer is reabsorbed or secreted
Hydrogen is not
Filteres
The proximal tubule
secretes H+ and reabsorbs HCO3-
Glutamine
Metabolizes to ammonium and HCO3
The distal nephron
Controls acid secretion and initial portion of the collecting duct
Type A intercalated cells
During acidosis
There is excess hydrogen and co2
Goal is to secrete hydrogen
Also result in hyperkalemis
Type B interclated cells
During Alkalosis
HCO3 and K+ is secreted
Hypokalemia
Acidosis
More acidic
Types of Acid/base disturbances
Respiratory
Metabolic
Collecting duct
Plays a significant role in the fine regulation of acid base balance
Alkalosis
More basic
Respiratory acidosis
Increased CO2 and H+
Occurs in Alveloar hypoventilation results in CO2 retention and elevated plasma CO2
What causes acidosis
Pulmonary fibrosis
Skeletal muscle disorders
Muscle dystrophy
How is respiratory acidosis fixed
Must occur via Renal mechanisms
Respiratory alkalosis
Decreased CO2 Decreased H+
Less commON
Result of hyperventilation
Metabolic acidosis
Excessive acid intake
Excessive metabolic production of hydrogen
Can be due to ketoacidosis
Excessive Bicarbonate loss (Diarrhea)
Metabolic Alkalosis
Excessive vomiting of acidic stomach contents or excessive ingestion of bicarbonate ccontaining antacids
