Exam 2 Additional Information (Week 3)

Question 1

What is an endogenous hormone

Answer 1

Antidiuretic Hormone
ADH
arginine vasopressin

Question 2

Where is ADH produced?

Answer 2

hypothalamus

Question 3

Where is ADH stored?

Answer 3

posterior pituitary

Question 4

What does ADH control?

Answer 4

osmoregulation

release stimulated by increased osmolality and hypovolemia

Question 5

Additional role of ADH

Answer 5

potent vasoconstrictor, but dilates renal afferent pulmonary and cerebral arterioles

Question 6

What are the three type of vasopressin receptors?

Answer 6

V1 -V3

Question 7

V1

Answer 7

mediates vasoconstriction

Question 8

V2

Answer 8

mediates water reabsorption in the renal collecting ductts

Question 9

V3

Answer 9

found in the CNS and stimulate modulation of corticotrophin secretion

Question 10

Multiple Uses of Vasopressin are

Answer 10

post cardiopulmonary bypass shock
refractory hypotension
reduce bleeding in von willebrand's disease
anti-diuresis in diabetes insipidus
treatment of enuresis

Question 11

Dosages of Vasopressin

Answer 11

low dose gtt 0.03-0.04unit/min up to 0.1unit/min

1-2units bolus

Question 12

Onset of vasopressin

Answer 12

1-5 minutes

Question 13

Peak of vasopressin

Answer 13

5 minutes

Question 14

DOA of vasopressin

Answer 14

10-30mins

Question 15

Complications of vasopressin are seen at

Answer 15

> 0.04units/min

Question 16

What are the complications of vasopressin?

Answer 16

GI ischemia
decreased CO
skin or digital necrosis

Question 17

Sodium nitroprusside is

Answer 17

a direct acting, nonselective peripheral vasodilator
relaxation of arterial and venous smooth muscle
lacks significant effects on nonvascular smooth muscle and cardiac muscle

Question 18

MOA of Sodium Nitroprusside

Answer 18

interacts with oxyhemoglobin and dissociates to form methemoglobin which releases NO and cyanide
NO activates guanylate cyclase (in the vascular muscle) thus increasing cGMP
cGMP inhibits calcium entry into vascular smooth muscle but increases uptake of Ca into SR
results in vasodilation via NO

Question 19

Metabolism of Sodium Nitroprusside

Answer 19

transfer of electron from the iron (Fe) of oxyhemoglobin to SNP yields metHgb and an unstable SNP radical
unstable SNP radical breaks down all 5 cyanide ions are released
one of these cyanide ions reacts with methgb to form cyanomethemoglobin (nontoxic)
remainder are metabolized in the liver and kidney-> converted to thiocynate

Question 20

SNP Toxicity

Answer 20

occurs d/t effects of high plasma concentrations of thiocyanate

Question 21

Cyanide toxicity

Answer 21

can occur at rates >2ug/kg/min for long periods
suspect when patient starts demonstrating resistance to hypotensive effects or previous responsive patient who is unresponsive (tachyphylaxis) at rates >2-10ug/kg/min
may precipate tissue anoxia, anaerobic metabolism and lactic acidosis

Question 22

Treatment of cyanide toxicity

Answer 22

immediate d/c of SNP
100% O2 administration despite normal oxygen saturation
sodium bicarbonate to correct metabolic acidosis
sodium thiosulfate 150mg/kg over 15 mins
sodium nitrate 5mg/kg if severe toxicity

Question 23

sodium thiosulfate acts

Answer 23

as a sulfur donor to convert cynaide to thiocyanate

Question 24

What does sodium nitrate do

Answer 24

converts hemoglobin to methgb which converts cyanide to cyanomethemoglobin

Question 25

Thiocyanate toxicity

Answer 25

rare as thiocyanate is cleared by kidney in 3-7 days

less toxic then cyanide

Question 26

Symptoms of thiocyanate toxicity

Answer 26

N/V tinnitus, fatigue, CNS hyperreflexia, confusion, psychosis, miosis seizure and coma

Question 27

Methemoglobemia

Answer 27

rare
should be considered as differential diagnosis in patients with impaired oxygenation despite adequate cardiac output and arterial oxygenation

Question 28

Dosages of SNP

Answer 28

0.3ug/kg/min - 10ug/kg/min
max dose: should not be infused for greater that 10 mintues
immediate onset
short duration of action
requires continous IV adminstration to maintain therapeutic effect
extremely potent- use of A-line

Question 29

SNP effects (CV)

Answer 29

direct venous and arterial vasodilation, decreased venous capacitance due to venous return
baroreceptor mediated reflex responses increase HR
decrease SBP, decrease PVR, increase contractility, causes intracoronary steal in areas of damage associated with MI, decreased diastolic BP -> decreased coronary perfusion

Question 30

SNP Effects (CNS)

Answer 30

increase CBF and ICP with modest decrease in MAP or with greater decrease in MAP can reduce cerebral BF (caution with carotid disease)

Question 31

SNP Effects (Pulmonary)

Answer 31

attenuation of hypoxic vasoconstrction

Question 32

SNP Effects (blood)

Answer 32

increase in intracellular GMP inhibit platelet aggregation and increase bleeding time

Question 33

Clinical Uses of SNP

Answer 33

controlled HTN (0.3-0.5 ug/kg/min do no exceed 2ug/kg/min)
HTN crisis- 1-2ug/kg gtt IV can be adminstered as bolus
Cardiac Disease- decreases LV afterload, benefits management of MR or AR, CHF and HF
consider coronary steal

Question 34

Pharmacokinetics of Enalapril (Prodrug and Duration of BP lowering effects

Answer 34

yes to prodrug (enalaprilat)
12-24 hours of lowered BP
enalaprilat- 6hrs

Question 35

Pharmacokinetics of Lisinopril

Prodrug and Duration of BP lowering effects

Answer 35

No prodrug

24 hours

Question 36

Pharmacokinetics of Ramipril

Prodrug and Duration of BP lowering effects

Answer 36

Yes, ramiprilat

24 hours

Question 37

Pharamcokinetics of Captopril

Prodrug and Duration of BP lowering effects

Answer 37

no

about 6 hours

Question 38

Pharmacokinetics of Benazepril

Prodrug and Duration of BP lowering effects

Answer 38

yes, benazeprilat

24 hours

Question 39

Pharmacokinetics of ARBS

Answer 39

highly protein bound
Majority not effected by renal dysfunction
Majority effected by hepatic dysfunction
Peaks in various hours after administration
Variable elimination 1/2 times