Exam 3 Flashcards by Zach Bell

presents as a recurrent headache that is severe enough to interfere with daily functioning, can be with or without aura, can be triggered by changes in behavior/environment/diet/hormone levels, these headaches occurring 15+ days per month for a 3-month period or longer classified as chronic, two or more of the following are present (pain interrupts or worsens with physical activity, unilateral pain, pulsating pain, moderate-to-severe intensity)

migraines

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type of headache, pain usually reported to be mild to moderate in severity, non-pulsating, bilateral, described as band like tightness or pressure around the head, two or more of the following are present and are not aggravated by routine physical activity (bilateral pain, non-pulsating, mild or moderate intensity, no nausea/vomiting, either photophobia or phonophobia not both)

tension headaches

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type of headache, severe/intermittent/short in duration type pain, typically occur at night but attacks may occur multiple times per day, described as explosive/excruciating, at least one or more of the following (lacrimation, nasal congestion/rhinorrhea, eyelid edema, forehead or facial sweating/flushing, sensation of fullness in the ear, miosis and/or ptosis (droopy eyelid), sense of restlessness or agitation

cluster headaches

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theory of pathophysiology for migraine, suggested that intracerebral vasoconstriction has led to neural ischemia followed by reflex extracranial vasodilation and pain, not a likely mechanism due to lack of evidence

vascular hypothesis

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theory of pathophysiology for migraine, depressed neuronal electrical activity spreads across the brain producing transitory neural dysfunction, pathogenesis of migraine most likely due to an imbalance in modulation of nociception (detection of painful stimuli) and blood vessel tone by serotonergic and noradrenergic neurons

neuronal hypothesis

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highest prevalence in women 18-44 years old, more common in women throughout the age groups likely to be due to hormonal differences

migraine risk factors

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more common in women, environmental factors as opposed to genetic predisposition play a central role in development of this type of headache

tension risk factors

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more frequent in men, onset most common between 20-40 years, genetic predisposition is apparent though affected individuals often also present with additional risk factors like history of tobacco use, caffeine intake, alcohol abuse

cluster risk factors

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defined as transient focal neurologic symptoms that can occur prior to or during a migraine, typically present as wavy lines or spots within the field of vision but can also present as scotoma (blind spot/area of reduced vision in the visual field)

aura

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behavioral: emotional let down, fatigue, sleep excess or deficit, stress, vigorous physical activity
environmental: flickering lights, high altitude, loud noises, strong smells like perfumes, tobacco smoke, weather changes
food: alcohol, caffeine intake/withdrawal, chocolate, citrus fruits, bananas, figs, raisins, avocados, dairy products, fermented pickled products, missing meals, MSG, Asian food, seasoned salt, nitrites in processed meats, saccharin/aspartame, tyramine
medications: cimetidine, estrogen or OCs, indomethacin, nifedipine, nitrates, reserpine, theophylline, withdrawal due to overuse of analgesics/benzodiazepines/decongestants/ergotamine

potential triggers of headache

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why is it important to start pharmacologic abortive treatment early for acute headache?

poor drug absorption accompanying migraine attacks/enteric statis so larger doses of oral medications may be necessary for pain relief

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limit exposure to triggers, resting in dark quiet area, behavioral interventions (relaxation therapy, cognitive behavioral therapy, stress management training), alcohol in moderation, limiting tobacco use

nonpharmacologic management of headaches

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when might a longer elimination half-life be beneficial when treating with a triptan?

during a long lasting migraine attack

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is rimegepant (Nurtec ODT) abortive or prophylactic?

both

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is ubrogepant (Ubrelvy) abortive or prophylactic?

abortive

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is zavegapent (Zavzpret) abortive or prophylactic?

abortive

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MOA: high affinity, highly selective 5-HT1F receptor agonist, selective targeting of this receptor is hypothesized to decrease stimulation of trigeminal system and treat migraine pain without causing vasoconstriction

lasmiditan (Reyvow)

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MOA: selective agonist for serotonin (5HT1B and 5HT1D receptors) in cranial arteries, causes vasoconstriction and reduces sterile inflammation correlating with relief of migraine

triptans

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what is the difference between Reyvow and triptans?

Reyvow does not cause vasoconstriction and targets a different serotonin receptor compared to triptans

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which dosage forms might be helpful for treating a migraine patient who is experiencing nausea?

nasal sprays, injections

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what options are available for treating an acute tension headache?

OTC analgesics like NSAIDs or acetaminophen, can use prescription strength NSAIDs or acetaminophen with an opioid analgesic if necessary

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this type of headache occurs when patients use ergotamines, triptans, opioids, or other combinations for longer than 10 days per month or nonspecific analgesics for more than 15 days per month

rebound/medication overuse headache

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why aren’t oral triptans the best choice for treatment of acute cluster headache treatment? what other triptan dosage forms are a better option?

delayed onset of action so injectable or intranasal triptans would be better

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what is the primary novel therapy for abortive treatment of cluster headache?

administration of high flow rate oxygen

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what options (besides triptans and oxygen) are available for treatment of cluster headaches?

octreotide (somatostatin analog that has short half life and may be administered SC with no vasoconstrictive effects) glucocorticoids provided IV and later tapered orally

what options are available for adjunctive therapy for migraine patient experiencing nausea?

antiemetics like metoclopramide and prochlorperazine

when is prophylactic treatment of migraines warranted?

if headaches are frequent/severe, significant disability occurs, pain-relieving medications are used frequently, adverse effects occur with acute therapies

which medications are mainstay of tension headache prophylaxis?

tricyclic antidepressants, muscle relaxants can also be used

which medications are mainstay of cluster headache prophylaxis?

lithium, verapamil

most triptans can be repeated after how many hours? how about naratriptan?

2 hours, naratriptan 4 hours

which CGRP is approved for cluster headache?

emgality

benign prostatic hypertrophy (BPH) is the most common benign neoplasm in men who are at least ______ years old

tissue in the prostate that produces prostatic secretions including prostate-specific antigen (PSA)

glandular tissue

tissue in the prostate that can contract around the urethra and bladder outlet when stimulated, enlarged in BPH

stromal tissue

_________ (testosterone/estrogen) stimulates glandular tissue growth but do not have a direct effect on stromal tissue

testosterone

________ (testosterone/estrogen) may stimulate stromal tissue growth

estrogen

voiding symptoms including urinary frequency, nocturia, urgency with or without incontinence

irritative

voiding symptoms including urinary hesitancy, decreased force of urinary stream, straining to void, intermittency (urinary stream that stops and starts)

obstructive

what type of factor refers to anatomic obstruction of the bladder neck caused by an enlarged prostate (as the gland grows around the urethra the prostate occludes the urethral lumen) and this factor is obstructive or irritative?

static factors, obstructive

what type of factor refers to excessive stimulation of alpha 1A adrenergic receptors in the smooth muscle of the prostate, urethra, and bladder neck which results in smooth muscle contraction and reduces the caliber of the urethral lumen, and this factor is obstructive or irritative?

dynamic factors, obstructive

what type of factor refers to bladder detrusor muscle hypertrophy in response to prolonged bladder outlet obstruction, detrusor muscle fibers undergo hypertrophy so that the bladder can generate higher pressure to overcome bladder outlet obstruction, hypertrophic ladder muscle becomes irritable contracting abnormally in response to small amounts of urine in the bladder, and this factor is obstructive or irritative?

detrusor factors, irritative

how much is drug treatment expected to decrease the AUA symptom score by?

30-50% or 3 or more points

what is appropriate treatment for a BPH patient with mild symptoms?

watchful waiting

what is appropriate treatment for a BPH patient with moderate to severe symptoms (no BPH complications), any size prostate?

alpha 1 adrenergic antagonist

what is appropriate treatment for a BPH patient with moderate to severe symptoms (no BPH complications), any size prostate, with irritative voiding symptoms?

anticholinergic agent/mirabegron + alpha 1 adrenergic antagonist

what is appropriate treatment for a BPH patient with moderate to severe symptoms (no BPH complications), any size prostate, with erectile dysfunction?

tadalafil OR tadalafil + alpha 1 adrenergic antagonist

what is appropriate treatment for a BPH patient with moderate to severe symptoms (no BPH complications), prostate greater than 30 grams? what if they also have irritative voiding symptoms?

5 alpha reductase inhibitor OR 5 alpha reductase inhibitor + alpha 1 adrenergic antagonist, if irritative voiding symptoms may add anticholinergic agent or mirabegron

what is appropriate treatment for a BPH patient with severe symptoms (no BPH complications)?

5 alpha reductase inhibitor + alpha 1 adrenergic antagonist

what is appropriate treatment for a BPH patient with severe symptoms and BPH complications?

surgery

mild AUA symptom score

0-7

moderate AUA symptoms score

8-19

severe AUA symptoms score

more than 20

androgens, alpha adrenergic agonists, anticholinergic agents, caffeine, anticonvulsants, diuretics, antidepressants (SSRIs), opiates, sedatives

medications that can cause/worsen BPH voiding symptoms

refers to preferential inhibition of alpha 1A receptors which comprise 70% of alpha 1 receptors in the prostatic stroma, prostatic urethra, bladder neck, these alpha adrenergic antagonists have the potential to produce less hypotension than other alpha 1 adrenergic antagonists because they have a lower likelihood of antagonizing alpha 1B adrenergic receptors in peripheral vasculature

uroselective agents - alfuzosin, tamsulosin, silodosin

which 5 alpha reductase inhibitor is selective for Type II isoenzyme and which is non-selective inhibitor of both Type I and II? are they therapeutically interchangeable?

finasteride is selective for Type II, dutasteride is non-selective, no difference in clinical efficacy, therapeutically equivalent

which BPH agents relax smooth muscle?

alpha antagonists and tadalafil

which BPH agents reduce size of enlarged prostate?

5 alpha reductase inhibitors

which BPH agents are useful in patients with enlarged prostates?

alpha antagonists, 5 alpha reductase inhibitors, anticholinergics, tadalafil

which BPH agents have efficacy in relieving irritative voiding symptoms?

anticholinergics, mirabegron

which BPH agents reduce frequency of BPH related complications?

5 alpha reductase inhibitors

which BPH agents decrease PSA?

5 alpha reductase inhibitors

out of all of the BPH agents, which does not have cardiovascular adverse effects?

5 alpha reductase inhibitors

which BPH agents require adjustment for renal failure?

anticholinergics (use with caution), tadalafil, mirabegron

which BPH agents require adjustment for hepatic failure?

5 alpha reductase inhibitors (caution because metabolized extensively in liver), anticholinergics (use with caution), tadalafil, mirabegron

floppy iris syndrome and orthostatic hypotension are common ADRs for which BPH agents?

alpha adrenergic antagonists

sexual dysfunction is a common ADR of which BPH agents?

5 alpha reductase inhibitors

xerostomia (dry mouth) is a common ADR of which BPH agents?

anticholinergics

hearing loss, hypotension, priapism, visual disturbances are common ADRs of which BPH agents?

tadalafil

angioedema, cardiovascular effects, urinary retention are common ADRs of which BPH agents?

mirabegron

why are 5 alpha reductase inhibitors teratogenic?

exposure to these agents is contraindicated in pregnancy because the drugs may cause feminization of a male fetus so must wear gloves when handling

this BPH agent should be reserved for patients with both BPH and erectile dysfunction or those with LUTS (lower urinary tract symptoms) that are not responsive to alpha adrenergic antagonists, relaxation of smooth muscle of the urethra/prostate/bladder neck, relaxation of the detrusor muscle, relaxation of vascular smooth muscle

tadalafil

this BPH agent is indicated when a patient has bothersome irritative voiding symptoms despite treatment with an alpha adrenergic antagonist, typically added to alpha adrenergic antagonist

anticholinergic

beta 3 adrenergic agonist that causes release of NE which stimulates beta 3 adrenergic receptors reducing irritative voiding symptoms, not FDA approved for BPH but can be helpful as alternative therapy, typically added to an alpha adrenergic antagonist

mirabegron

this type of ED includes abnormalities in the vascular, hormonal , or neurologic systems of may be medication induced, factors associated with this include chronic medical conditions (HTN, diabetes, BPH, renal failure), surgical procedures, smoking, excessive alcohol, obesity, poor overall health, trauma, medications (antihypertensives, CNS depressants, lipid meds, antidepressants/antipsychotics, anticonvulsants, GI agents, antiandrogens, hormones, recreational drugs)

organic dysfunction

this type of ED occurs if a patient does not respond to psychological arousal, common causes include performance anxiety, strained relationships, lack of sexual arousability, psychiatric disorders like depression or schizophrenia

psychogenic dysfunction

these are contraindicated in people with sickle cell disease and history of priapism, should be used with caution in those taking oral anticoagulants/have bleeding disorders, generally these are more acceptable to older patients in stable relationships/infrequent sexual encounters

vacuum devices

prostaglandin E1 analog that produces an erection by stimulating adenyl cyclase leading to increased cAMP, smooth muscle relaxation, rapid arterial flow, and increased penile rigidity, available as an injection or suppository, use with caution in patients with sickle cell disease, those taking anticoagulants, bleeding disorders, increased risk of priapism and bleeding

alprostadil

these agents selectively inhibit PDE5 which is responsible for degradation of cGMP, smooth muscle is induced leading to an erection, only effective in the presence of sexual stimulation to drive the NO/cGMP system, facilitators not initiators

PDE inhibitors (tadalafil, sildenafil, vardenafil, avanafil)

PDE5 inhibitors are _______ (acceptable/contraindicated) in patients taking organic nitrates

contraindicated, PDE5 inhibitors can lead to hypotension and patients taking nitrates are at highest risk of significant drop in blood pressure if taken together

when is testosterone the initial treatment of choice for ED?

in patients with low serum testosterone levels since it corrects decreased libido, fatigue, muscle loss, sleep disturbances, depressed mood

what medical conditions are contraindications to testosterone therapy?

prostate cancer, erythrocytosis, uncontrolled HF, sleep apnea

how long should patients be treated with testosterone supplementation before initiating additional ED therapy?

3 months

which types of insulin are rapid acting (bolus)?

lispro, aspart, glulisine

which types of insulin are long acting (basal)?

glargine, detemir, degludec, humulin

autoimmune disease in which the insulin producing beta cells of the pancreas are destroyed leaving the individual insulin deficient

type 1 diabetes

form of autoimmune diabetes hallmarked by a milder autoimmune process and slower progression of beta cell failure as compared with type 1, adult age at onset, presence of islet autoantibodies, insulin dependence

latent autoimmune diabetes in adults (LADA)

usually slow and progressive in its development, risk factors include first degree family history, overweight/obese, habitual physical inactivity, race/ethnicity, previously identified A1c between 5.7-6.4%, HTN, low HDL or high triglycerides, history of gestational diabetes, history of cardiovascular disease

type 2 diabetes

glucose is stored here ad glycogen, glycogenolysis converts stored glycogen back to glucose, glucose is primarily supplied to the brain by stores of glycogen here during fasting, during exercise most glucose is supplied through gluconeogenesis that happens here stimulated by epi and NE

liver

insulin and glucagon are produced here, beta cells produces insulin and amylin whereas alpha cells produce glucagon, main function of insulin is to decrease blood glucose and elevated BG is necessary for insulin release above basal levels

pancreas

what fasting plasma glucose results are consistent with a diagnosis of diabetes?

greater than or equal to 126 mg/dL

what postprandial plasma glucose results are consistent with a diagnosis of diabetes?

greater than or equal to 200 mg/dL with symptoms of diabetes like polydipsia, polyuria, unexplained weight loss

what A1c results are consistent with a diagnosis of diabetes?

greater than or equal to 6.5%

what fast plasma glucose results are consistent with a diagnosis of prediabetes?

100-125 mg/dL

this occurs when there is a lack of insulin peripheral tissues cannot take up and store glucose, causes body to think it is starving and ketones are produced as byproducts of free fatty acid metabolism in the liver, excessive amounts of ketones formed leads to body getting rid of them through urine leading to dehydration, patients prone to this should test for ketones during stressful events like acute illness, women with preexisting diabetes before pregnancy or with gestational diabetes should be prescribed ketone strips and educated on prevention/detection

diabetic ketoacidosis

what types of insulin are used in a pump? can either T1DM or T2DM patients use an insulin pump?

regular or rapid acting (rapid more common), insulin pumps may be used to lower blood glucose in any type of diabetes but patients must be on multiple daily insulin injections so patients with type 1 are always candidates and type 2 are sometimes candidates

use of this device may improve blood glucose levels, reduce wide fluctuations in BG levels, and allow individuals to have more flexibility in timing and content of meals/exercise schedules for improved quality of life

insulin pumps

causes of this include delayed or inadequate amounts of food intake (especially carbs), excessive doses of sulfonylureas/insulin, exercising when insulin doses are reaching peak effect, inadequately adjusted drug therapy in patients with impaired renal or hepatic function

hypoglycemia

when is glucagon indicated and how is it administered?

patients with hypoglycemia experiencing a loss of consciousness should be given glucagon, IM or SC, patient should be rolled on side since common ADR is vomiting

what electrolytes need to be replaced in DKA? what is used for fluid replacement? what type of insulin is preferred?

potassium, normal saline for fluid replacement, regular insulin

life threatening condition similar to DKA that also arises from inadequate insulin but occurs primarily in older patients with type 2 diabetes, lacks the ketonemia and acidosis, key diagnostic criteria for this are plasma glucose levels greater than 600 mg/dL, arterial pH greater than 7.3, serum bicarbonate greater than 15 mEq/L, minimal ketonemia/ketonuria

HHS

critically ill patients should be started on what route of administration of insulin? what about patients that are not critically ill?

IV, scheduled SC

patients should monitor their BG levels more frequently on these days because it is common for this to increase BG levels, should check glucose and urine for ketones every 4 hours, should continue to take medications, should maintain normal caloric/carb intake, drink fluid to avoid dehydration

sick days

when nutrients enter the stomach and intestines, this hormone is released which stimulates insulin secretion, this effect is mediated by GLP-1 and GIP

incretin

kidneys hold onto glucose rather than letting glucose be dumped into the urine to help correct hyperglycemia, glucose filtered by the kidneys is completely reabsorbed when BG values are normal but once BG levels get higher than 180 mg/dL glucose begins to be spilled into excreted urine, this transporter reabsorbs majority of filtered glucose in proximal tubule, when these transporters are inhibited there will be an increase in excretion of glucose by the kidney which lowers glucose concentrations in the plasma

SGLT2

what is the oral drug of first choice in a type 2 diabetes patient without cardiovascular disease, HF, liver or kidney disease, or the need for weight loss?

metformin

what is first line therapy for type 2 diabetes patients with ASCVD or indicators of high CVD risk? what if they are still above A1c goal after this?

GLP-1 with proven CVD benefit or SGLT2i, then add other agent if not at goal

what is first line therapy for type 2 diabetes patients with HF?

SGLT2i

what is first line therapy for type 2 diabetes patients with CKD?

SGLT2i or GLP-1 with proven CKD benefit, if not at A1c goal add other agent

agents with efficacy for weight loss in type 2 diabetes patients

semaglutide, tirzepatide, dulaglutide, liraglutide, SGLT2i

agents with efficacy for achievement and maintenance of glycemic goals in type 2 diabetes patients

dulaglutide, semaglutide, tirzepatide, insulin, metformin, pioglitazone, SGLT2i, sulfonylurea, DPP-4i

initiation of basal insulin

start 10 units per day OR 0.1-0.2 units/kg per day

titration of basal insulin

increase by 2 units every 3 days to reach FPG goal without hypoglycemia

initiation of bolus insulin

4 units per day or 10% of basal insulin dose

titration of bolus insulin

increase dose by 1-2 units or 10-15% twice weekly

which agents have benefits in MASH patients?

GLP-1, dual GLP-1/GIP, pioglitazone

which agents have benefits in MACE patients?

metformin, SGLT2i, GLP-1, pioglitazone

which agents have benefit in HF patients?

SGLT2i

Exam 3 Flashcards

(117 cards)