Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Pharmacology I > LAST DECK OF PHARM 1 > Flashcards

LAST DECK OF PHARM 1 Flashcards

1
Q

Patient with volume overload, who needs progressively higher doses of loop diuretics, usually has:

A

Loop Resistance

Tx with Chlorothiazide or Metolazone

Metolazone works at GFR <20ml/min
Retains efficacy at supa low GFRs!

Work on collecting duct:

  • Amiolioride (K)
  • Triamterne (K)
  • Spirnolactone (Ald)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do you fix Loop Resistance?

A
  • If on oral, use parenteral/IV.
  • Increase dose (limited).
  • Utilize continuous infusion loop diuretics.
  • Use a different loop, or add a thiazide diuretic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Causes of Loop Resistance

A
  • High sodium intake.
  • Reduced number of working nephrons from ATN.
  • Heavy proteinuria.
  • Renal compensation - water and salt reabsorbed at DCT.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What electrolytes are not as easily removed in Renal Replacement Therapy?

A

RRT - hemodialysis pulls off excess electrolytes to restore a normal balance.

Phosphorous and Magnesium
-High levels in trauma, rhabdomyolysis, tumor lysis syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why do you avoid calcium when doing RRT on a trauma patient, rhabdomyolysis patient, or tumor lysis syndrome?

A

High levels of phosphorous in blood.

Calcium and phosphorous can precipitate in the blood when at high conc. and form crystals causing further injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why do RRT patients develop hypocalcemia?

A

To keep blood from clotting, they use citrate anticoag., which binds to calcium in blood.

Prevents calcium from activating clotting factors. When put back into patients, prevents their blood from clotting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Kidney failure

Stages?
Causes?
Risks?
Patho? :)

A

CKD caused by diabetes, HTN, GN.

Stage 1 >90
Stage 2 60-89
Stage 3 30-59
Stage 4 15-29
Stage 5 <15 = Kidney Failure

Risks include DM, HTN, smoking, obesity, proteinuria.

Pathophys of CKD:
Progressive neuropathy leads to loss of nephron mass, glomerular capillary HTN, and proteinuria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Renal Osteodystrophy

A

Renal osteodystrophy is a bone disease that occurs when your kidneys fail to maintain proper levels of calcium and phosphorus in the blood.

It’s common in people with kidney disease and affects most dialysis patients.

  • Decreased renal fxc
  • Increased phosphate levels, which bind Ca and precipitate.
  • Hypocalcemia leads to increase in PTH.
  • More Ca and Phos reabsorbed, which MAKES THE PROBLEM WORSE.
  • Low Vitamin D levels also increase PTH secretion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CKD Related Mineral & Bone Disorders (3)

A

Parathyroid Hyperplasia: Result from renal osteodystrophy. Leads to resistance to calcium and vitamin D therapy.

Osteitis fibrosa cystica: High bone turnover disease. Leads to fibrosis of bone marrow and decreased erythropoiesis.

Osteomalacia: softening of bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

S/S CKD

A
  • Uremic symptoms cause fatigue, weakness, confusion, SOB
  • Peripheral neuropathies
  • Edema
  • Change in urine, foaming of urine
  • Abdominal distension from ascites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hemodialysis

A

Will have a fistula that connects artery and vein in arm. Allows for blood to be taken out of artery, goes through filtrate system, and is put back into the body through the vein.

4 hrs, 3x a week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Peritoneal Dialysis

A

Putting dialysate solution into the peritoneal space. Passive diffusion, blood transmits waste into the peritoneal space.

In several hours, take the waste out through a drain. Takes 20-30mins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management of CKD Diet

A

Limit protein to 0.8 g/kg/day
Limit sodium intake to <2g/day
Stop smoking
Start exercising

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you tx a diabetic with CKD?

A

ACEI or ARB to prevent progression, titrate the drug until GFR drops or you have a significant elevation in serum K occur.

Metformin for diabetes, continued until GFR <30ml/min or SCr >1.5 in males or 1.4 in females.

Stop the drug or it can accumulate at higher levels and form fatal lactic acidosis. :(

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do you treat a patient with CKD and HTN?

A
  • ACEI or ARB = 1st line in DM
  • Thiazide diuretics if not sufficient to control BP.
  • Manage BP - 140/90 to decrease albumin excretion, 130/80 if possible.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do you treat anemia in CKD?

A

Decreased production of erythropoietin from interstitial fibroblasts, which are damaged. Develop normochromic, normocytic anemia.

Tx: Erythropoiesis stimulating agents (ESA) and iron supplementation.

Need to take both for ESA to be effective.

Monitor: oxyhemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Target Hemoglobin in Anemia Tx:

A

Pt w/ hemoglobin b/w 9-10, ESA should be considered.
D/C ESA when Hgb is above 10 (11 in RRT pts).

If you continue treating above 13g/dL of hemoglobin = increased mortality, due to thrombosis.

Dose ESA w/ iron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the Erythropoiesis Stimulating Agents?

A 
Epoetin alfa (Epogen, Procrit)
Darbepoetin alfa (Aranesp)

Black box warning:

  • Increased risk of death, MI, stroke, VTE (sludging of blood, leads to clotting off).
  • Increased risk of cancer.

Dose 3-4x a week.

ADR: HTN and vascular access thrombosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do you monitor in CKD patient receiving ESA?

A

Monitor iron status.
Also, make sure you have adequate intake of B12 and folate - can be diminished by RRT.

Oral intake of iron alone may be insufficient for CKD patients, because their absorption is decreased to 10% (100% in those who are healthy).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Iron Preparations

A

Oral. Different doses of elemental iron in each.

  • Ferrous sulfate
  • Ferrous gluconate
  • Ferrous fumarate

IV

  • Iron Dextran
  • Sodium ferric gluconate
  • Iron sucrose (most commonly used)
  • Ferumoxytol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ADR of Iron Preps

A

Constipation, nausea, abdominal cramping, black discoloration of stool

TELL PATIENT THEIR STOOL WILL BE BLACK.

Allergic reactions: Hypotension, headaches, and dizziness. Can be fixed by lowering the infusion rate!
TEST Q!

Can also develop arthralgia and arthritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do you select an iron prep?

A
  • Oral therapy if possible. Has less side effects.
  • RRT patients are more likely to need IV prep.

Monitor:

  • Iron status every 3 months while on ESA.
  • Monthly, when titrating dose.

-Hgb, measure every 3 months, but monthly in RRT. When alterring, monitor weekly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Treatment goals for CKD Related Mineral & Bone Disorders

A
  • Normalize biochemical parameters.
  • Prevent dentrimental consequences.

Limit Ca * P product to <55
Less chance of crystal formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Nonpharmacologic therapy for CKD Related Mineral & Bone Disorders

A

Limit dietary phosphate intake <800mg per day.

Avoid cola, nuts, beer.

Dialysis won’t pull phosphate out.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What drugs treat CKD related mineral and bone disorder?

A

Phosphate binders:

  • Calcium carbonate
  • Calcium Acetate
  • Sevelamer Carbonate
  • Lanthanum Carbonate
  • Aluminum Hydroxide

Bind to phosphate ingested through GI tract and prevent it from being absorbed.

  • Used for hypocalcemia in early CKD.
  • Calcium Carbonate: Give prior to meals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why is Aluminum Hydroxide limited use in B&M disorders in CKD?

A

Aluminum will accumulate and can cause toxicity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Sevelamer Carbonate

A

Phosphate binder

  • Nonabsorbable hydrogel
  • Lowers LDL, raises HDL
  • Nice side effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

ADR phosphate binders

A
  • N/V, diarrhea, constipation
  • Hypercalcemia with calcium based products

Drug to drug interactions

  • Calcium salts can bind to iron, zinc, and FQ.
  • Take one hour before or 3 hours after.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Vitamin D Therapy

A

Ergocalciferol and cholecalciferol must be converted by the kidney to active form.

Calcitriol is an active form - stimulates absorption of calcium.
Leads to hypercalcemia and hyperphosphatemia.

Paracalcitrol - actives PTH receptors, but does NOT increase calcium and phosphate absorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Cinacalcet (Sensipar)

A

Sensitizes PTH receptors to effects of calcium.

Reduces PTH concentrations.

Will have enough calcium and not have as much PTH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Manifestations of DIKD

A 
AB abnormalities
Electrolyte imbalance
Urine sediment
Proteinuria
Pyuria
Hematuria
Decreased GFR*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical manifestation, signs, and symptoms of DIKD

A
  • Decline in GFR
  • Rise in SCr and BUN

-Anorexia, malaise, vommiting, SOB, edema

  • Decreased urine output, with progression to HTN and volume overload.
  • Esp with NSAIDs, ACEI, and contrast induced nephropathy (CIN).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Signs of PCT injury

A

Metabolic acidosis with bicarbonaturia, glycosuria, hypophosphatemia, and hypokalemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Signs of DCT injury

A

Polyuria due to impaired urinary concentration, metabolic acidosis from impaired acidification and hyperkalemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What can cause ATN?

A 
Aminoglycosides
Radio contrast media
Cisplatin
Amphotericin B
Foscarnet
Pentamidine
Foscarnet
Osmotically active agents, like colloids and mannitol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What drugs can cause osmotic nephrosis?

A

Mannitol
Dextran
IV immunoglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What drugs can cause hemodynamically mediated kidney injury?

A

ACEI
ARBS
NSAIDs
Cephalosporins, tacrolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What drugs causes obstructive nephropathy?

A 
Acyclovir
Sulfonamides
Indinavir
Foscarnet
Methotrexate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What drugs cause nephrolithiasis?

A

Sulfonamides
Triamterene
Indinavir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What drugs causes glomerular disease?

A

Lithium
NSAIDs
Pamidronate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What drugs can cause acute allergic interstitial nephritis?

A 
PCNs
Cipro
NSAIDs
PPIs
Loops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What drugs can cause vasculitis or thrombosis?

A

Hydralazine
Allopurinol for gout
Methamphetamines
Cyclosporine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What drugs can cause cholesterol emboli?

A

warfarin

thrombolytics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Aminoglycosides and ATN

A

Tobramycin
Gentamycin

ATN occurs in 10% of patients, 58% of those critcally ill. - Happens when there is cumulation of drug in proximal epithelial cells. Generates reactive oxygen species that damage the mitochondria.

Will have progressive increase in BUN and Cr.

Reversible if you discontinue therapy.

Risk factors

  • large total dose
  • prolonged therapy
  • trough >2mcg/mL
  • concurrent nephrotoxins with use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How do you prevent aminoglycoside damage to the kidney?

A

Careful patient selection, alternative antibiotic use if possible.

Limit concurrent nephrotoxic usage.

  • Pharmacokinetic monitoring to achieve certain troughs.
  • Once daily doses are used now, rather than 3x per day.

If ATN develops, discontinue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Radiographic contrast media and ATN

A

Presentation: 24-48hrs after administration of contrast. Oliguria.

Contrast will induce a 50% reduction in blood flow causing renal ischemia and direct cellular toxicity. Occurs with high osmolar agents.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How do you avoid contrast induced ATN?

A

Isotonic Crystalloids - Used to maintain normal blood volume prior to contrast exposure and continued 6-24 hours after exposure.

AVOID ATN by using smallest dose possible, non-iodonated contrast agent, or low isoosmolar agent.

Other preventative agents to use:

  • Sodium bicarbonate, but wasn’t very helpful.
  • N-acetylcysteine (Mucomyst) - benefits patients at high risk for contrast induced nephropathy. Also good for tylenol OD.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Cysplatin Nephrotoxicity

A

Used for solid tumors. Doses are limited by nephrotoxicity.

Impairs tubular reabsorption.
Decreased urinary concentration ability.

Leads to polyuria, decreased GFR, and electrolyte wasting.

Drug accumulates in proximal epithelial tubular cells causing necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How do you prevent cysplatin induced nephropathy?

A

Prevent by doing dose reduction and decreased frequency of admin.

Avoid concurrent nephrotoxins.

Vigorous hydration with NS can flush the kidneys.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the antidote used to chelate cisplatin in normal cells?

A

Amifostine (Ethyol)

Give 30mins before cisplatin to avoid kidney injury in high risk patients.

Need supportive care and hemodialysis to replace electrolytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Amphotericin B and ATN

A

Used for severe fungal infections.

Leads to renal tubular acidosis and wasting of K, Na, and Mg. Occurs days to weeks after initiation.

Causes direct tubular cell damage. Interacts with ergosterol in cell membrane to kill fungal cells, but damages our cells as well.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How do you prevent amphotericin B ATN?

A

Liposomal formations (AmBisome)

Embed the drug within the bilayer of the liposome med instead of your own cells. Expensive therapy.

Also need adequate hydration, longer infusion times, and can do electrolyte repalcement PRN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Intratubular obstruction

A

Direct precipitation of drug crystals, which causes obstruction, nephritis, and acute tubular necrosis.

Can cause preciptation of tissue degradation products like tumor lysis syndrome and rhabdomyolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How do you prevent tumor lysis syndrome from intratbular obstruction?

A

Can cause precipitation of uric acid crystals.

Avoid by staying hydrated and allopurinol (Zyloprim).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How does rhabdomyolysis cause intratubular obstruction?

A

Can cause precipitation of myoglobin.

Can be caused by by using HMG-CoA reductase inhibitors and CYP3A4 inhibitors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

AKI is a cause of drug precipitation - Why? What drugs?

A

it causes low urine volumes, low drug solubility, and volume depletion.

Can be caused by acyclovir, foscarnet (precipitations calcium), and methotrexate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Total Body Water

A

Intracellular compartment

  • Potassium
  • Organic and inorganic phosphates

Extracellular compartment

  • Sodium
  • Chloride
  • Bicarbonate

Balance maintained by Na-K-ATPase pump.

Osmolality equal in ICF and ECF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Isotonic fluids (0.9% NaCl)

A

No net shift in ICF and ECF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Hypertonic solutions

>0.9% NaCl

A

Decrease in ICF and increase in ECF.

Water shunts out of the cell, ICF, and into the intravascular space, ECF.

Good for cerebral edema to draw water out of the space pushing on the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Hypotonic solution

<0.9% NaCl

A

Increase in ICF and decrease in ECF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

D5W

A

Free water; doesn’t have solutes in it to keep it in intravascular space.

Will have 40% in the extracellular space and 60% in the intracellular fluid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

0.45% NaCl

A

Hypotonic solution, larger volume stays in extracellular space with some intracellular.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

0.9% NaCl

A

Isotonic; all of it stays in the extracelluar fluid. Same concentration as blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

3% NaCl

A

Will draw water out of the intracellular space and shuttle to extracellular fluid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Serum Sodium

A

tightly regulated; determines plasma osmolality and blood volume.

Kidney regulates water extration via hypothalamaus.

Also affected by glucose and BUN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Arginine Vasopressin (AVP)

A

Also known as ADH.

Released from pituitary when increased response in osmolality. Too high solute content (dehydrated), will release AVP.

Inserts aquaporin channels into tubular lumen for water to be reabsorbed.

Increases thirst.

Stimulates RAAS, which increase BP and amount of water retention.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Hypertonic Hyponatremia

A
  • Excess effective osmoles
  • Dilute sodium in blood
  • Seen with glucose > 500.
  • Glucose switches osmolality to ECF.

Every increase in glucose, drops the serum sodium. Can be caused by other osmotic agents like mannnitol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Hypovolemic Hypotonic Hyponatremia

A

Due to excessive fluid loss, from diarrhea, vomiting, and diuretics.

Stimulates release of AVP. High urine osmolality, because AVP concentrates it.

Common with thiazides.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Euvolemic Hypotonic Hyponatremia

A

Normal amount of ECF Na, increases TBW and ECF volume.

Most often caused by SIADH (syndrome of inapropriate ADH secretion).

  • Small cell lung, pancreatic cancer
  • Pulmonary disease, TB, PNA, ARDS
  • Polydipsia
  • Head trauma, stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Drug induced causes of SIADH

A

Nicotine, tricyclic antidepressants, opioids, haloperidol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Increased sensitivity to ADH

A

acetaminopehn, carbamazepine, Iamotrigine, NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

MIXED of increased ADH release and sensitivity to ADH

A

Methylenedioxymethamphetamine
ACEI
SSRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Hypervolemic Hypotonic Hyponatremia

A

Volume overload
Kidney sodium and water excretion are impaired.

See sodium retention, volume expansion, and edema.

Seen in cirrhosis, CHF and nephrotic syndrome.

  • Acute
  • Chronic (>48hrs)

S/S depend on magnitude.

Mild: Nausea, malaise
Mod: Headache, lethargy, disorientation
Sever: Seizures, coma, brainstem herniation

74
Q

Hyponatremia lab tests

A

Serum sodium <135mEq/L
Plasma osmolality and urine sodium

Serum glucose, lipids, kidney and thyroid function tests help determine cause.

75
Q

Cerebral edema

A

Related to speed and degree of change in serum osmolality. Brain takes 48hrs to compensate.

Low serum osmolality causes inward shift of fluid to CNS which puts pressure on brainstem and can lead to herniation.

76
Q

Why is it bad to correct hyponatremia too quickly?

A

Correction of hyponatremia too quickly can lead to neuro consequences.

Water rushes out of the brain and there’s an ICF contraction. Acute decrease in brain cell volume leads to osmotic demyelination (central pontine myelinolysis).

77
Q

osmotic demyelination syndrome

A

Can cause hyperreflexia, para or quadriparesis, parkinsonism, pseudobulbar palsy, locked-in syndrome, and death 1-7 days after treatment.

78
Q

Tx of Hyponatremia

A
  • Treat underlying cause

- Balance risk of hyponatremia vs. osmotic demyelination syndrome

79
Q

How do you correct hypovolemic hyponatremia?

A

NS = main therapy

80
Q

How do you collect euvolemic/hypervolemic hyponatremia?

A
  • Manage with water restriction
  • Demeclocycine
  • AVP receptor antagonists
  • or NS + loop diuretic

Concentrated NaCl can manage symptoms of severe hyponatremia.

81
Q

How do you treat acute or severely symptomatic hypotonic hyponatremia?

A

3% NaCl or 0.9% NaCl

Target 120mEq/L (5% increase)

Compare urinary sodium to corrective fluid. 0.9% can sometimes worsen hyponatremia in patients with SIADH.

Loops used to prevent fluid overload.

82
Q

How do you treat severely symptomatic hypotonic hyponatremia?

A

NaCl at 0.9% is higher than what the patient has (150mEq/L).

Need normal saline to correct them.

83
Q

How do you treat hypervolemic hyponatremia patients?

A

May need loop diuretics and hypertonic saline (3% NaCl), which is more concentrated.

84
Q

What’s the main rule when calculating sodium chloride infusion?

A

Do NOT correct faster than 12 mEq/L in the first 24hrs!!!!!!

Goal is to achieve 125-130mEq/L. :)

TBW = 0.6L/kg in men, 0.5L/kg in women.

85
Q

66Y/O female presents to ED with vertigo and disorientation. She started carbamazepine 10 days ago. Serum Na is 108mEq/L. What do you do?

A
  1. Stop carbamazepine
  2. Desired serum sodium? 120mEq/L
  3. Determine how much 3% NaCl to infuse (math).

What if we wanted to infuse 0.9% NaCl?
…More math…

86
Q

How do you treat non-emergent hypovolemic hypotonic hyponatremia?

A

Use 0.9% NaCl - limits the risk of correcting too quickly, especially if a nurse hangs it at the wrong rate ;)

Helps replenish both volume and sodium.

87
Q

If you have a patient with euvolemic hypertonic hypernatremia, what is the most likely culprit and how do you treat it?

A

Caused by SIADH.

  • Restrict water to 1000- 1200ml/day
  • Correct underlying cause.
  • D/C offending drugs.

Sodium chloride tablets and loop diuretics can be used to increase sodium intake and augment amount of kidney water retention.

88
Q

How do you combat oversecretion of ADH in SIADH?

A

Demeclocycline (tetracycline derivative)

Inhibits tubular AVP activity.
Induces DI.
Takes 3-6 days to work; bad for patients with liver disease or compromised fluid intake. Can cause AKI or renal tubular toxicity.

Don’t give to kids under 8 or pregnant woman.

89
Q

If demecloclycine didn’t work to manage SIADH hyponatremia (or it was a more severe hyponatremia), what could you give”?

A

V-2 antagonists (Vaptans)

Decrease water reabsoprtion in the kidneys. Aquaretics.

Conivaptan - IV only
Tolvaptan - available for home use, PO

Metabolized by CYP3A4
CI: Not good if patient isn’t producing urine.

Used for chronic correction, not acute.

90
Q

How do you treat a non-emergent hypervolemic hypotonic hyponatremia?

A

Need to have a negative water balance while minimizing changes to the intracellular volume.

Correct the underlying cause, limit fluid intake, limit sodium intake.

Need to improve cardiac contractility in CHF, via digoxin.

ACEI or ARB can reduce afterload.

91
Q

Hypernatremia

A

Occurs from renal or extra-renal fluid loss.

Can be caused by hypertonic fluids, excess sodium ingestion.

Water loss is from insensible losses - expired breath or sweat.

  • DI can have decreased release of AVP (central) or less kidney response (nephrogenic).
  • Causes large volumes of excreted and dilute urine.
92
Q

What causes hypovolemic hypernatremia?

A

Renal loss of water, diuretic use, post-op diuresis

93
Q

What causes euvolemic hypernatremia?

A

Diabetes insipidus - excreting water, primary polydipsia

94
Q

What causes hypervolemic hypernatremia?

A

Sodium overload from sodium bicarbonate, salt tablets, concentrated tube feedings, and sodium containing medications.

95
Q

(Hypernatremia) Central causes of DI

A

Ethanol ingestion, which decreases ADH/AVP secretion.

Neurosurgery, head trauma, CNS malignancy.

96
Q

(Hypernatremia) Nephrogenic causes of DI

A

Lithium, amphotericin B, demeclocycline, vaptans

Make AVP work less effectively in their mechanisms.

97
Q

Clinical presentation of Hypernatremia

A

In hypernatremia, ICF => ECF. Will have polyuria.

Decreased neuronal cell volume leads to weakness, lethargy, restlessness, irritability, confusion.

Acute onset is more symptomatic than chronic.

98
Q

Treatment goals of hypernatremia

A

Correct sodium to 145mEq/L

Rapid correction can lead to cerebral edema.

Restrict sodium and fluids to prevent recurrence.

99
Q

How do you treat hypovolemic hypernatremia?

A

0.9% NaCl until the volume is restored, then 0.45% NaCl (more hypotonic) or D5W.

Correction should not exceed 10-12mEq/L a day.`

100
Q

How do you treat a central diabetes insipidus; hypernatremia?

A

Replace AVP with desmopressin.

Has poor oral bioavailability; given as a nasal spray.
“Sniffin desmopressin” lol.

Adjust dose to achieve adequate urinary concentrations during sleep to prevent nocturia.

Goal:

  • Urine 1.5-2L per day
  • Serum Na 147-142

RISK of water intoxication and excess water retention!!!!

101
Q

How do you treat a nephrogenic diabetes insipidus; hypernatremia?

A
  • D/C causative agent
  • Correct electrolyte disturbances.
  • Induce mild ECF defecit to cut urine volume by 50%. Defecit wll cut urine volume by 50%.

Indomethacin (Indocin) which increases AVP activity.

102
Q

How do you treat sodium overload?

A

Limit intake
Loop diuretics to excrete sodium
D5W (free water)

103
Q

Physiology of Erections

A

Penis has 2 corpus cavernosum. Flaccid state has balanced venous and arterial flow.

During erections

  • increased arterial flow
  • decreased venous outflow
104
Q

What enhances arterial flow to the corpus cavernosum?

A

Enhanced by acetylcholine mediated vasodilation, cGMP, cAMP, and vasoactive intestinal polypeptide.

Nitric oxide is stimulated/released in epithelial cells.

cGMP decreases calcium in smooth muscle, leading to vasodilation = more blood flow to penis.

Acetylcholine or prostaglandin E enhance cAMP.

105
Q

Where does psychogenic stimuli to penis come from?

A
  • Sacral nerve reflex arc; nerve impulse is carried down the spinal cord to the peripheral cholinergic nerves.
  • Hypothalamus integrates external stimuli, uses dopamine (pro-erection)

-A2 receptors - when stimulated, can INHIBIT erections.

106
Q

What drug can cause erectile dysfunction, why?

A

Clonidine
Acts on A2 receptors
Inhibits erection

107
Q

What causes detumescense?

Detumescense: fancy word for penis deflation lol

A

Mediated by NE

Contracts the vascular smooth muscle, which decreases that arterial flow. Allows venous outflow (drainage) to increase.

108
Q

Testosterone

A

Decreases after 40Y/O

Important to stimulate libido.

109
Q

5-alpha reductase

A

Enzyme
Converts testosterone to DHT
Enlarges size of prostate

Small amounts can convert to estradiol, which causes gynecomastia in men.

110
Q

What medications cause ED?

A

Anticholinergics:

  • Antihistamines
  • Anti-parkinsonian drugs
  • TCA’s
  • Phenothiazines

Dopamine antagonists:

  • Phenothiazines
  • Metoclopramide

Blocking Ach receptors makes it difficult to achieve erection.

111
Q

How do you avoid antihistamines caused by ED?

A

Use a second generation antihistamines; don’t penetrate the BB barrier.

112
Q

What antidepressant medication has lowest incidence of ED?

A

Buproprion

113
Q

Why do dopamine antagonists cause ED?

A

The blockade of dopamine increases prolactin levels, which decreases the production of testosterone.

114
Q

What medications supress testosterone mediated libido stimulation?

A
  • Estrogens
  • Anti-androgens
  • Digoxin
  • Spirnolactone
  • Ketoconazole
  • Cimetidine
115
Q

What CNS depressants suppress the perception of external psychogenic stimuli?

A
  • Benzodiazepines
  • Opiates
  • Large doses of ethanol
  • Anticonvulsants

Suppressed perception of psychogenic stimuli.

116
Q

What agents decrease penile blood flow?

A
  • Diuretics
  • Beta antagonists
  • Central sympatholytics (Clonidine, Methyldopa)
117
Q

Vacuum Erection Device

A

Negative pressure in the cylinder draws arterial blood into the corpus cavernosa.

Onset 3-20mins.

60-80% satisfaction, but aren’t discreet.

Good for patients who can’t use PDE-5 inhibitors or other agents.

118
Q

Phosphodiesterase Inhibitors MOA

A

Sildenafil (Viagra)
Vardenafil (Levitra)
Tadalafil (Cialis)
Avanafil (Stendra) *new

Non-hydrolyzable analogs of cGMP

Sexual stimulation to patient releases nitric oxide from nerves, which stimulates increased levels of cGMP to produce erection. By giving PDE-5 inhibitor, you inhibit breakdown of cGMP, which leads to higher levels to have an erection.

119
Q

Which PDE inhibitor has a long half-life?

A
  • Tadalafil has the longest half-life and duration of action
  • Can last through the weekend

-Make sure you tell patient drugs take 30-60mins for onset to work.

120
Q

PDE inhibitors: Place in Therapy?

A

First line therapy, especially for younger patients.

They’re discreet.

50-80% effective.
Poor responders usually have comorbid conditions.

121
Q

Therapeutic failures of PDE inhibitors

A

Educate the patient on food interactions (ex: Can’t have a fatty meal and take Viagra, so would prescribe Cialis which you can have a fatty meal with).

Patient should try 5-8 doses, before saying its a failure.

Titrate up dose as needed.

Tell patient to avoid XS alcohol.

122
Q

When are PDE inhibitors contraindicated?

A

Avoid in healthy patients, sickle cell, leukemia, multiple myeloma, or other therapies.

Risk for priapism goes up with these drugs!

123
Q

PDE-6

A

Founds in rods and cones of eye.

When inhibited, can see blurry vision and cyanopsia (blue vision)

Seen in sildenafil (worse), followed by vardenafil, avanafil, and tadalafil (least).

124
Q

PDE-11

A

Located on striated muscles.

When inhibited, leads to myalgias. Seen in Tadalafil.

125
Q

What PDE inhibitor causes myalgias?

A

Tadalafil

126
Q

What PDE inhibitor causes cyanopsia?

A

Sildenafil

127
Q

What PDE inhibitors have a slower onset when consumed with food?

A

Sildenafil
Vardenafil

Slowed onset if they’re taken within two hours of food. Will then have a 1-2 hour onset.

128
Q

Tadalafil

A

Has the slowest onset

Longest duration of action (36hrs)

129
Q

PDE5 are metabolized by?

A

CYP3A4

130
Q

What PDE inhibitors need to be renally adjusted?

A

Sildenafil

Tadalafil

131
Q

Most common ADR of PDE inhibitors?

A

The vasodilation can cause facial flushing, headache, dyspepsia, nasal congestion, and dizziness.

Patient’s BP will have 8-10mmHg drop in systolic BP. Usually asymptomatic.

132
Q

Who do you NEVER ever prescribe PDE inhibitors to?

A

People on nitrates and antihypertensives

Don’t use on high risk cardiac patients.

133
Q

What ADR does Sildenafil have, specifically?

A

PDE-6 effects (Sildenafil)

  • photophobia
  • blurred vision
  • loss of blue-green color discrimination

Reversible, if you switch to a different agent.

134
Q

What is a severe ADR of PDE inhibitors that you have to warn your patients of?

A

Nonarteritic anterior ischemic optic neuropathy (NAION)

Sudden, unilateral painless blindness that may be irreversible.

Due to drop in blood flow to the optic nerve.

Tell patient to stop taking medication right away if it happens.

135
Q

What ADR does Tadalafil have, specifically?

A

Produces back and limb muscle pain, bc of PDE-11 effects.

136
Q

What ADR does Vardenafil have, specifically?

A

QTc prolongation

137
Q

Priapism

A

Not seen frequently with PDE inhibitors, but can be seen with higher doses and other pro-erectogenic drugs.

138
Q

Do not use nitrates when on phosphodiesterase inhibitors. Why?

A

Synergistic effects with cGMP can cause severe hypotension.

No nitrates for 24 hours after use of PDE inhibitors (or 48hrs after tadalafil).

If you have to treat angina, use other agents.

139
Q

If hypotension occurs from PDE inhibitors, how do you treat?

A

Trendelenburg position and fluids

140
Q

Alprostadil, prostaglandin E1

A

If patient can’t take PDE inhibitor, you can use a prostaglandin E1, called Alprostadil.

  • Caverject, Edex - intracavernous injection. Patient administer themselves.
  • MUSE - medicated urethral system for erection; intraurethral insert.

MOA: Stimulate adenylyl cyclase to increase cAMP and decrease intracellular Ca, allowing smooth muscle to relax for blow to flow in.

141
Q

Why is Alprostadil good for diabetics?

A

The drug is not nitric oxide dependent, so good for patients with impaired nitric oxide pathway.

  • diabetic nephropathy
  • prostatectomy
  • failed PDE inhibitor treatment
142
Q

Intracavernosal injections

A
  • More efficacious than the intraurethral insert, but is more painful to give.
  • Excellent bioavailability.
  • Preferred over other agents
  • Less risk of priapism.
  • Mean duration of action: 12-44 minutes

Psychogenic ED needs a lower dose than a vasculogenic ED.

No tolerance can develop to this therapy.

143
Q

How do you inject Alprostadil?

A
  • Inject into one cavernosa (one side).
  • Duration greater than 1 hour is not expected
  • Metabolized quick in cavernosa; limited systemic effects

Administer 5-10mins prior o intercourse. Use aseptic technique.

144
Q

Alprostadil ADR

A

May have local tissue damage with injection, but improves with better technique as they get used to it.

Cavernosal plaques or fibrotic areas that can occur. Don’t use injections until they’re resolved.

  • Local burning discomfort or pain
  • Priapism
145
Q

Intraurethral injection ADR

A

Risk for urethral strictures and difficulty voiding.

146
Q

Penile prostheses ADR

A

Inflatable prosthetics that are surgically implanted.

Most common ADR is infection.

147
Q

Prostate epithelial glandular tissue

A

Produces secretions

Stimulated by androgens (DHT, testosterone)

148
Q

Prostate stromal tissue

A

smooth muscle

embedded with alpha 1 adrenergic receptors

149
Q

Prostate capsule

A

fibrous connective tissue

contains adrenergic receptors

150
Q

BPH summary

A

Testosterone converted by 5-alpha reductase to DHT; causes prostate enlargement, acne, and hair growth.

Some testosterone is converted to estrogen by aromatase, whcih leads to stromal growth.

151
Q

Static factors

A

Prostate blocks urinary flow, usually due to androgen stimulating the epithelial tissue or estrogen stimulating the stromal tissue.

152
Q

Dynamic factors

A

Excessive a-adrenergic tone on stromal tissue, bladder neck, or posterior urethra.

Triggered during stress or pain.

153
Q

What medications can cause symptoms of BPH?

A
  • Testosterone replacement, bc the new testosterone substrate is converted to DHT.
  • Adrenergic agonists, like pseudoephedrine, ephedrine, phenylephedrine
  • Anticholinergics, which decrease the detrusor muscle contraction. Can have urine retained when not fully contracted.
154
Q

Prostatic smooth muscle relaxers

A

A1 adrenergic antagonists, usually used as a first-line therapy for BPH.

Do not decrease size of prostate, but reduce the adrenergic effects.

155
Q

Reducing testosterone stimulatory effects

A

5-alpha reductase inhibitors, which decrease the amount of DHT that affects the prostate.

156
Q

Agents relaxing bladder and detrusor muscle:

A

Antimuscarinics

Reduces irritable voiding symptoms

157
Q

What is the first line treatment for BPH?

A

Alpha 1 antagonists

158
Q

What treatment is preferred for cardiovascular patients with BPH or a severely enlarged prostate?

A

5-alpha reductase inhibitors

159
Q

How do you treat a patient with ED and BPH?

A

PDE inhibitor, first line

May not be as effective for BPH, but treats both.

160
Q

How do you treat a patient with mostly irritative symptoms from BPH?

A

Anticholinergic drugs added to other therapies

Make sure they don’t have a high post void residual - otherwise, meds will cause urinary retention.

161
Q

Alpha-1 Adrenergic Antagonists

FIRST Generation

A

Phenoxybenzamine

  • Not used often
  • Cause tachycardia and arrythmias
162
Q

Alpha-1 Adrenergic Antagonists

SECOND Generation

A

Prazosin
Terazosin
Doxazosin
Alfuzosin (more used for BPH)

Don’t have alpha-2 antagonism… problematic.

Main ADR:

  • First dose syncope
  • Orthostatic hypotension
  • Dizziness

Start low, titrate up over several weeks. Dose at bedtime, so they won’t experience syncope or hypotension during the day.

Monitor BP, might have synergy with antihypertensives

163
Q

Alpha-1 Adrenergic Antagonists

THIRD Generation

A

Tamsulosin
Silodosin

Uroselective for alpha-1A adrenergic receptor, which is found in prostate.

Have fewer side effects than first generation. Probably used the most. :)

164
Q

Why do we refrain from using Prazosin for BPH?

A

Has a lot of CV effects, not recommended

165
Q

Why is Alfuzosin recommended for BPH?

A

Has lowest incidence of systemic side effects; no dose titration needed.

166
Q

How do you take Tamsulosin?

A
  • Needs to be taken on an empty stomach.
  • Avoid in patients with SULFA allergies.

Silodosin not used, bc of the dug interactions and organ impairment.

167
Q

If a patient has ED, but you are treating his BPH - Why do you need to be careful?

A

PDE inhibitors for ED can have synergistic drops in BP when prescribed with alpha-1 adrenergic antagonists for BPH.

Less likely to see if you use tadalafil and tamsulosin.

168
Q

5-Alpha Reductase Inhibitors

A

Finasteride
Dutasteride

Act on type 2, 5-alpha reductase in prostate to stop conversion of testosterone to DHT. Useful to reduce large prostate size.

May lead to sexual dysfunction, decreases prostate excretions, ED from reduced nitric oxide pathway, and decreased libido.

Pregnancy Category X - Women should not even handle these pills bc of the effects on potential fetus.

169
Q

When do you prescribe 5-Alpha Reductase Inhibitors for BPH?

A

Good for patients who can’t tolerate A1-antagonists. Reduce prostate size by 25%.

CONS:
Slower onset
Higher incidence of sexual side effects
Second line for sexually active males.

170
Q

BPH + ED = PDEI

A

May counteract effects of alpha-1 antagonists and 5-a reductase inhibitors.

Use Tadalafil most frequently

171
Q

When BPH isn’t responsive to treatment, what do you do?

A

Prostatectomy

172
Q

What medications cause urethral hyperactivity?

A

TCAs

Alpha-agonists

173
Q

What medications decrease bladder contractility?

A

Anticholinergics
TCAs
CCBs
Antipsychotics

174
Q

What’s the first line therapy for urinary incontinence?

A

Non-pharmacologic therapy

Behavioral intervention
Toilet scheduling regimen
Pelvic floor rehab

175
Q

How do you treat urge urinary incontinence?

A

Anticholinergics - enhance bladder storage

  • oxybutinin - used a lot
  • tolterodine- used a lot
  • tropsium
  • solifenacin
  • darifenacin
  • fesoterodine

ADR: anticholinergic reaction - dry mouth, decreased secretions, cutaneous flushing, blurry vision, hyperthermia

Don’t use with urinary retention, gastric retention, myasthenia gravis.

Can cause mental status change in elderly.

176
Q

When do you avoid tolterodine?

A

Don’t give to patients with a creatinine clearance under 10ml/min.

Reduce the dose if patient is on CYP3A4 inhibitors.

177
Q

What’s a risk with using oxybutynin for urge incontinence?

A

May have orthostatic hypotension from alpha blockade.

Comes in XL formulation, first line because it minimizes the side effects (less dry mouth).

Do NOT crush or chew, bc it will break the XR formulation.

178
Q

Tropsium

A

Second generation anticholinergic for urge incontinence.

Poor bioavailabilty, have to take on an empty stomach

Don’t give to a renally impaired patient.

179
Q

Botulinum toxin A

A

Potent neurotoxin that paralyzes smooth and striated muscle. Inject into detrusor muscle, to prevent release of Ach.

ADR include hematuria, UTI, retention, dysuria.

Use if failed the other therapies.

180
Q

How do you treat urethral underactivity?

A

Increase urethral closure with estrogens, which increase proliferation of urethral epithelium.

Alpha receptor agonists

181
Q

What alpha receptor antagonist was removed from the market for stroke risk? Was originally used to treat urethral underactivity.

A

Phenylpropanolamine

182
Q

Cymbalta

A

Selective NE reuptake inhibitor. Used to increase urethral tone.

Clinical Pharmacology I (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions