501 exam 1

Tonicity
NS?

Gain of H2O:

Loss of Na+

patho:
Addison’s disease
Decreased aldosterone secretion
Diuretics
Vomiting
Diaphoresis
Wounds

patho:
SIADH
Heart failure
Polydipsia/Hyperglycemia
Excess intake (IV, PO) fluids

patho:
Excessive PO Na⁺ intake
Decreased water intake
Sodium retention

Gain of Na+

Cushing’s Syndrome
Hyperaldosteronism
Renal Failure

patho:
Diabetes Insipidus
Osmotic diuresis
Burns
Dehydration
Fever/infection
Diarrhea

Loss of H2O

Correct slowly (48 hours)
Prevent cerebral edema
Monitor Neuro

Treat cause
Lasix (due to poor KF)

Restore normal serum Na+ levels
Hypotonic IVF (0.225%)

Nutrition
Na+ restriction

Nutrition
Increase oral intake NaCl tabs

Treat cause
Decrease loop diuretics

Restore normal serum Na+ levels
Small volume hypertonic IVF (2%-3%) saline

K+ regulation

pressure exerted by proteins in the blood plasma or interstitial fluid.

force generated by the pressure of fluid within capillary on the capillary wall.

Sodium polystyrene sulfonate (Kayexalate) has been used as an oral or rectal therapy for

intercellular shifts of glucose is common for ___________.

β2-agonist(s) that has a stimulatory effect on Na+/K+ ATPase and the resultant intracellular shift of potassium

Calcium Gluconate/Calcium Chloride prevents the deleterious cardiac effects of severe __________.

clinical manifestation: 
Acute weight loss
Increased ADH secretion
Increased serum osmolarity
Decreased vascular volume

labs
Increased hematocrit
Increased BUN
(blood urea nitrogen)
Increased spec. gravity

S/S
Decreased urine output
Tachycardia
Postural hypotension
Elevated temperature

Manifestations
Acute, rapid weight gain
Peripheral edema
Increased interstitial fluid
U/O- polyuria
Increase vascular volume

Labs
Dilutional hyponatremia
Dilutional anemia
Hematocrit decreased
BUN decreased

s/s
Dependent edema
Generalized edema
Pulmonary edema
Jugular Vein Distention

causes:
Diabetes Insipidus
Osmotic diuresis
Burns
Dehydration
Fever/infection
Diarrhea

causes:
Decreased water intake
Sodium retention
Cushing’s Syndrome
Hyperaldosteronism
Renal Failure

HCO3- retention 
loss of K+ & H+

hypomagnesium
hypernatremia

causes
Diuretics
Alcoholism
GI
Laxative abuse
Hyperglycemia
DKA
HHNS
Gastric Suctioning
Massive Burns

what causes decreased aldosterone secretion?

Addison’s disease 
Tx

Hyperglycemia vs DKA

DI

SIADH

low Hydrostatic Pressure

Venous Obstruction

low Capillary Colloidal Pressure

Loss of plasma proteins

Production of plasma proteins

high Vascular Volume

Ischemia & cell death/necrosis

release of ______ results in efferent arteriole vasoconstriction.

Release of renin results in ______ arteriole vasoconstriction.

vasoconstriction of the efferent arteriole in the kidneys results in __________.

angiotensin II triggers _______ at the adrenal cortex

angiotensin II triggers Aldosterone in the _______

aldosterone produces
1
2
3

Na+ controls _______ fluid

1.6 to 2.6 mg/dL

135-145 mEq/L

3.5-5.0 mEq/L

7.35-7.45

35-45

22-26 mEq/L

anemia + hyperventiation

COPD + hypoventilation

diuresis + hypernatremia

hypokalemia
hypernatremia 
diuresis
hyperaldosterism

hyponatremia + edema

high SG
low u/o

low SG
high u/o

hypernatremia + polyruria

what cause increased ADH secretion

cushings syndrome

addison's disease

-zudin

blocking RNA strand

AZT

MAO:
inhibits human DNA

bone marrow suppression
CP450 
hepatotoxic

-gravir

Blocks integration of viral DNA

there is one opportunity for this HIV drug to be effective

attachment inhibitors

blocks HIV receptors so they cannot bind

RNA inhibitor

bind to RT

inhibits human DNA

steven johnson syndrome HIV

HIV
hyperglycemia

internalization

cuts up protein

PI MAO

INSTI MAO

RTIs MAO

entry inhibitors 
MAO

aldosterone vs ADH

Addisons vs Cushings

indications for neuromuscular blockers

blocks Ach --> nicotinic_M receptors

panuronium

polarizing neuromuscular blocker

agonist to nicotinic_M receptors

side effects of these drugs are that they trigger a histamne release, resulting in hypotension

Adverse effects
Headache
Reflex bradycardia
Reslessness and excitability

alpha 1 agonist

Alpha 2 adrenergic receptors

inhibits norepinephrine

Selectively activates alpha 2 receptors in CNS where autonomic regulation of C-V system occurs (brainstem)

stimulates sympathetic outflow to blood vessels and heart is reduced

BETA 1 Receptor

Stimulation results in:
increased heart rate, force, automaticity, conduction rates
lipolysis
renin release

positive inotropic 
positive chronotropic
postive dromostropic

Used during and following cardiac surgery, CHF, low CO states, shock
Given IV

Contraindications:
Angina, CAD, heart monitor

Adverse effects
Tachycardia
Chest pain, hypotension

Stimulation results in:
Bronchodilitation
Vasodilitation
Slight decrease in peripheral resistance
Relaxation of pregnant uterus
Glycogenolysis
Release of glucagon

Used to treat
asthma, bronchospasm, COPD, CHF, CF

Nonselective adrenergic receptors

Produces both alpha and beta effects

Used to Tx
shock, asthma, CP resuscitation, heart blocks, simple glaucoma, adjunct to topical anesthesia, anaphylactic shock, GI hemorrhag

Given topically, IM, Sub Q, IV

Wide ranging effects depending upon receptor

Contraindications
Hypersensitivity
narrow-angle glaucoma
labor
coronary insufficiency

contraindicated w/ ventricular dysrhythmias, diabetes, Parkinson’s disease, & uncorrected hypovolemia

agonist for alpha and beta 1

Alpha-Adrenergic Blockers

non-selective adrenergic antagonists

Selective alpha 1 blockade

MAO: vasodilation
Tx: HTN
ADR: orthostatic hypotension

Beta Blockers

cardioselective

noncardioselective

cardioselective only at therapeutic levels, at higher does will exhibit noncardioselectivity

noncardioselective

Used for BP and HR control
Used more often than alpha blockers

May also have alpha blockade property even at therapeutic levels

how much do e have to give to illicit a response

max efficacy

receptor activation intensity

relative potency

what does the drug do at the site of acton

simple vs modified occupied theory

RN is only person whose actions are not routinely checked by others. A few exceptions

Threshold for detecting response is reached

largest effect that a drug can produce

Indicated by height of Dose-Response curve

bigger doses unable to elicit a further increase in response
All receptors bound by drug

relative potency vs affinity

potency is a difference in _______ whereas efficacy is a difference in _________.

*bigger doses unable to elicit a further increase in response
*All receptors bound by drug

does not account for relative potency or max efficacy

Reflected in drug’s maximal efficacy

Bind irreversibly to receptors

Continual exposure to agonist

down-regulation

Continual exposure to antagonist

up-regulation

Dose required to produce a defined effect in 50% of population

movement of drug from blood to sites of action

Drug molecules tend to accumulate on side where pH favors ionization

Blood flow to tissues

movement across cell membranes

Polar, ionized, protein-bound= No
lipid-soluble yes

Drug movement at the capillary bed

Blood Brain Barrier

chemical reactions --> metabolites

study of a single gene’s role in the client’s response to drugs

study of how genes affect a client’s response to drugs

absorption
first pass metobolism

Concentration gradient drives reabsorption of drug from lumen of tubule back into bloodstream

Must be lipid soluble to cross tubular and vessel cell membranes

Ionized and polar drugs remain in urine to be excreted

Fluid & molecules move through capillary pores into tubular urine

Time required to eliminate 50% of total amount of drug in body

An index of how rapidly a decline in drug occurs

Reflection of metabolism and excretion

The rate of drug eliminated depends on amount of drug present

_______ of drug determines dosing intervals

Thiazide diuretics

MAO
Na+ excretion at distal tubs
Decrease GFR
blocks H2O reabsorption

USE
Hypernatremia
Hyper/Hypokalemia

Tx
Edema
HF
preferred drug

Adverse Effects
Hypokalemia/hyperglycemia
Hyponatremia/dehydration
Orthostatic HTN

DDI
NSAIDS→ Reduced diuresis with what drugs?

High-ceiling (loop) diuretic

MAO
Na+ excretion at ascending loop of Henle

USE
Hypernatremia
Hyperkalemia
Hypokalemia
2nd-line HTN
Edema

diuretics indicated for renal impairment

diuretics contraindicated for Hyponatremia

diuretics w ADR: ototoxicity

NSAIDS = synergist to which diuretics

K+ Sparing diuretics

MAO
Aldosterone receptor antagonists
Prevent the re-absorption of Na+ @ the collecting duct

USE
Combo w/ thiazides & loops
Effects are delayed

Tx
Edema

Adverse effects
Hyperkalemia

diuretics that have Synergy w/
ACE inhibitors
ARBs

diuretics that are contraindicated with salt substitutes (KCl)

Osmotic diuretics, Mannitol, may have ADR w/ what type fluid imbalance?

Treat cause
Decrease loop diuretics

Tx 
when would you use Diuretics  (Lasix, HCTZ) w/ K+ sparing like Spironolactone?

Only therapeutic use of irreversible agent

Bone marrow depression, which leads to aplastic anemia and neutropenia, would also be ADR for which type of HIV drug

-vir-

-vir

lactic acidosis ADR w/ HIV drug_____.

—Resistance: virus mutates gene encoding the glycoprotein è alters shape so drug can no longer bind

Reserved for patients who have failed more standard HAART (RTIs and PIs)

only approved CCR5 antagonist

SIADH vs DI

the rate at which red blood cells sediment in a period of one hour.

It is a common hematology test, and is a non-specific measure of inflammation.

high ESR indicates what