NURS 660 / NURS 660 Exam 4 (2026–2027 Update) Psychopharmacology & Advanced Mental Health Review | Complete Questions & Answers | Verified Solutions | Grade A – Maryville

NURS 660 / NURS 660 Exam 4 (2026–2027 Update) Psychopharmacology & Advanced Mental Health Review | Complete Questions & Answers | Verified Solutions | Grade A – Maryville Q. Which medication is contraindicated with liver impairment? ANSWERS Atomoxine (Straterra) Q. What is one of the birth defects associated with Litihum? ANSWERS Ebstein's anomaly Q. Which SSRI drug causes cardiovascular malformations in the first trimester of pregnancy? ANSWERS Paroxetine (Paxil) Q. Mechanism of action of a stimulant for ADHD Methylphenidate and amphetamine? ANSWERS increases the intrasynaptic levels of both dopamine and norepinephrine Q. What causes nicotine withdrawal symptoms? ANSWERS Nicotine alpha 4 beta 2 post synaptic receptors desensitizes receptors which leads to addiction. Re-sensitization of the nicotine receptors leads to withdrawal Q. A patient diagnosed with ADHD can't stay focused or solve work-related problems difficulty maintaining attention sustained and problem-solving. What area of the brain is involved? ANSWERS Dorsal lateral prefontal cortex (CTSC loop) Q. What part of the brain is associated with selective attention? ANSWERS Dorsal anterior singlunate Q. What part of the brain is associated with hyperactivity? ANSWERS Prefrontal motor cortex Q. What part of the brain is associated with impulsivity? ANSWERS Orbitofrontal cortex Q. Atomoxetine (Strattera) lacks abuse potential because of what ANSWERS increases dopamine in the dorsal prefrontal cortex and not in the nucleus accumbens Q. What fetal malformation does valproate cause? ANSWERS Spina bifida Q. What region of the brain is hypothesized to cause impulsivity? ANSWERS ventral striatum Q. What region of the brain controls compulsivity? ANSWERS Dorsal striatum Q. What is the MOA of atomoxetine (Strattera)? ANSWERS Selective Norepinephrine Reuptake Inhibitor: Boosts neurotransmitter norepinephrine/ noradrenaline and may also increase dopamine in profrontal cortex • Blocks norepinephrine reuptake pumps, also known as norepinephrine transporters • Q. Amaloid precursor protein is first cleaved by what enzyme ANSWERS Alpha-secretase Q. What does paroxetine do to Straterra in the body? ANSWERS increases the effect of the drug in the body Q. If a patient is taking paroxetine and starts Straterra what should change about the Straterra dose? ANSWERS The dose should be decreased Q. An Alzheimer's patient has been taking 4mg of rivastigmine what side effects might you anticipate and why? ANSWERS GI side effects; inhibits peripheral uptake of ACH and butyrycholine Q. Which neurotransmitters lead to eurphoria and abuse in a patient with marijuana abuse and ADHD. Pulsatile delivery of stimulants can cause a frequent and rapid delivery amplifying phasic firing of NE and DA. ANSWERS Phasic firing is associated with reward, euphoria, and abuse Q. What does alcohol do to the CYP 450 system? ANSWERS lowers the rate of drug metabolism Q. Which ADHD medication is tolerated better guanfacine or clonidine? ANSWERS Guanfacine, both are alpha 2a agonists Q. Why do some people with ADHD abuse cocaine? What MOA does cocaine affect the same as methylphenidate? ANSWERS they have the same key binding site for the serotonin 2a receptor Q. MOA of naltrexone how does it help people come OFF alcohol? ANSWERS by blocking mu receptors to induce euphoria Q. Someone comes to the office with friend or significant other how they perceive the person with ADHD as compared to others? How would you word his question? ANSWERS ask him to compare his behavior to other people his age Q. What would you treat first after someone is arrested for cocaine that has ADHD? Which problem do you address first substance or adhd? ANSWERS treat the substance abuse first Q. What ADHD prescription is transported into neurons via dopamine transporter? ANSWERS adderall Q. Symptoms of dementia? ANSWERS trouble remembering familiar things, not recognizing family members, & difficulty performing writing tasks Q. Pleasure center pathway of the brain with links to addiction? ANSWERS mesolimbic dopamine pathway Q. Pleasure center pathway of the brain? Links to addiction ANSWERS histaminergic mechanisms and increases dopamine binding to dopamine receptor Q. 17 y/o girl had ADHD can't complete assignments or pay attention to what area of the cortex regulates this? ANSWERS anterior cingulate cortex Q. Modafinil what does it treat? ANSWERS narcolepsy and depression Q. Medication that is an NMDA receptor Antagonist ANSWERS Memantine Q. Women present with ETOH disorder multiple drinks daily children have been removed wants to stop cold turkey but had w/d symptoms is she a good candidate for reduced drinking as a goal? ANSWERS No. Reduced-risk drinking as a goal is controversial. However, some patients will not agree to abstinence as a goal. For these patients, it can still be beneficial to work with them to reduce their drinking. Q. What are the biomarkers indicative of Alzheimer's disease? Which is elevated and which is decreased? ANSWERS Decreased cerebrospinal fluid (CSF) levels of amyloid beta and increased CSF levels of tau protein Q. An athlete has natural HIGH what part of the brain is stimulated? Dopamine increase where? ANSWERS Amygdala mesolimbic pathway Q. What is the treatment for a Vicodin OD? ANSWERS Narcan Q. What does alcohol do in the ventral tegmental part of the brain? ANSWERS causes release of endogenous opioids, inhibits glutamate release, enhances GABA release by blocking presynaptic GABAb receptors Q. What two neurotransmitters are affected by alcohol? What is increased what is decreased? ANSWERS GABA and Glutamate. Increase GABA and decreases glutamate. Q. What role does the amygdala play in substance abuse? ANSWERS Communicates to the VTA when cues related to drugs of abuse are present. Q. Which a lipoprotein Genotype that predicts a faster progression of mild cognitive impairment to Alzheimer's to dementia? ANSWERS APEO4 Q. Someone wants to quit smoking what receptors reinforce these effects why you can't stop? What area of the brain is the alpha postsynaptic receptor? ANSWERS Alpha 4 beta 2 postsynaptic receptors in the VTA. Q. Someone tried MDMDA at a party. What is the key binding site for this hallucinogen? ANSWERS serotonin 2a Q. Child on stimulant what is black box warning for pediatric population? ANSWERS cardiovascular; ECG prior to starting therapy with Ritalin (methylphenidate). Q. The most common adverse side effect of Donepezil? ANSWERS GI side effects Q. The core symptoms of ADHD are linked to what area of the brain? ANSWERS prefrontal cortex Q. Selective attention is due to what area of the PFC malfunctioning? ANSWERS dorsal ACC (anterior cingulate cortex) Q. sustained attention and problem solving linked to what area of the brain? D ANSWERS LPFC hyperactivity is linked to what area of the brain? prefrontal motor cortex what test assessing sustained attention? N-back test where is sustained attention modulated in brain? CSTC loop in the DLPFC insufficient activation in the DLPFC can cause inattention "sustaiNed attention- N back" what test assesses selective attention? Stroop test "Selective, Stroop, Cingulate" where in the brain is selective attention modulated? the CSTC loop, Dorsal anterior cingulate cortex issues with sustained attention are: difficulty completing tasks disorganization trouble sustaining mental effort issues with selective attention are: difficulty with detail carless mistakes not listening losing things being distracted forgetting things what part of the brain modulates impulsitivity? orbitofrontal cortex what symptoms of impulsitivity are observed? talking excessively blurting things out not waiting ones turn interrupting what part of the brain modulates hyperactivity? prefrontal cortex what are some key observations in the prefrontal cortex as it relates to ADHD? orbitofrontal cortex (OFC)-- impulsivity and hyperactivity DLPFC/DaCC-- sustained/selective attention issues how do NE and DA amounts manifest in relation to fatigue/anxiety? too little NE and DA = fatigue too much = anxiety what two receptors in the PRC are thought to be involved with ADHD treatment? alpha 2 a D1 how does ADHD affect NE and DA levels? NE levels low, signal reduced DA levels low, noise increased results in: fidget and inattention how should you treat NE and DA in adhd? increase NE Increase DA what receptors does NE stimulate in the postsynapse? alpha 2 a; even better effect when beta1 receptors also stimulated what effect does DA have on receptors and what does this cause? decreases the noise and prevents inappropriate connections from taking place through stimulating D1 receptors what effect does NE have on receptors and what does this cause? increases the incoming signal and allows for increase connections between prefrontal networks through stimulation of alpha 2A receptors what effect do slow dose stimulants have? amplify tonic NE and DA signals block NET in PFC block DAT in nucleus accumbens why do slow dose stimulants have less abuse potential? they dont occupy DAT too quickly or extensively, which is thought to reduce abuse potential what is salience provoked phasic firing? - bursts of DA release this can reinforce learning and reward conditioning which can lead to motivation to pursue rewarding experiences (education, career development) Can also lead to drug abuse.... how do pulsatile stimulants affect NE and DA? rapid increase in both can lead to feelings of euphoria and abuse ex: methylphenidate and amphetamine what is a big factor in if stimulants are abused? route and dose what stimulant is a competitive inhibitor of DAT and NET? amphetamine are both methylphenidate and amphetamine taken into the DA terminal? no, only amphetamine this is bc amphetamine and VMAT what happens when amphetamine is taken in to the terminal? can go into the vesicle and displace DA; this can lead to a fast release of DA which causes euphoric (and abuse causing) what is the MOA of methylphenidate on DA neurons? works on DAT similarly to SSRI (blocks reuptake of DA into terminal) this leads to more DA availability -- not taken into the terminal itself what is the MOA of methylphenidate on NE neurons? works on NET adverse effects of stimulants (methylphenidate, amphetamine) generalized anxiety adverse affects of atomoxetine (strattera?) dysuria, erectile dysfunction, decreased libido, liver damage (rare) adverse effect of wellbutrin/ bupropion sweating adverse effects of desipramine (norpramin) increased BP and HR, orthostatic hypotension, prolonged QT interval what are some adverse effects of stimulants in the pediatric and adolescent population should be aware of? - serious cardiovascular events/sudden death - mania, aggression - growth suppression - seizures - peripheral vasculopathy (raynauds) - blurred vision - tics what are examples of NET inhibitors for adhd? atomoxetine (strattera) buproprion (wellbutrin) venlafaxine (effexor) duloxetine (cymbalta) desvenlafaxine (prystiq) milnacipran (savella) desipramine nortriptyline what ADHD medication doesnt have abuse potential? atomoxetine (strattera) what drug class is atomoxetine? NE reuptake inhibitor How does Atomoxetine (Strattera) work? causes NE and DA levels to increase in PFC relative lack of NETs in nucleus accumbens prevents atomoxetine from increasing DA and NE levels in the brain area, thus reducing abuse potential increases attention, decreases hyperactivity what ADHD medication can cause liver injury? strattera if a patient develops jaundice and evidence of liver injury while taking strattera, what should you do? stop the med and dont restart it what med metabolism pathway dose strattera work? CYP2D6 keep in mind when rx with paroxetine, fluoxetine, quinidine what causes guanfacine to absorb quicker? high-fat meals is guanfacine or clonidine more alpha 2a selective? guanfacine, which also means it has less side effects Guanfacine (Intuniv) α2A-adrenergic agonist prescribed for the treatment of ADHD. Guanfacine is believed to improve attention and memory by stimulating α2A-adrenergic receptors in the prefrontal cortex. once daily dosing Clonidine (Catapres) Alpha-2 agonist (centrally acting) also inihibts imidolazine receptors Decreases sympathetic outflow Used for primary htn, migraine, ADHD, alcohol withdrawal Can cause sedation, dry mouth, rebound htn Do not d/c abruptly Contraindicated w/ anticoagulants Do not use w/ prazosin, MAOIs, TCAs, CNS depressants Twice daily dosing w/ larger dose at bedtime what type of adhd symptoms might atomoxetine not work well with? inattentive in addition to ADHD, modafinil might help what? substance use disorder 2 alpha 2 adrenergic agonists are? clonidine guanfacine what is the pathology of alzheimers? -Extracellular amyloid plaque build up - Intracellular formation of neurofibrilary tangles (made up of Tau protein) what is the pathology of dementia with lewy bodies? alpha synuclein what type of disorder is related to prion pathology? cruetzfeldt jacobs what are the clinical features of alzheimers? memory defict aphasia apraxia (inability to performed learned behavior) agnosia what are the clinical features of dementia with lewy bodies? memory issues, fluctuating attention extrapyramidal psychosis Frontotemporal Dementia Frontal and temporal regions degenerate, resulting in badly impaired emotional stability, decision-making and language use Huntington's disease Genetic disorder that causes progressive deterioration of brain cells. caused by a dominant allele. symptoms do not appear until about the age of 30. chorea (involuntary muscle movements) executive dysfunction Creutzfeldt-Jakob disease Chronic, progressive, fatal disease of the central nervous system caused by a prion. ataxia (seems like drunk) myoclonus what are normal memory changes with aging? reduced speed of processing Signs of Alzheimer's Disease •Memory loss affecting job skills or other activities •Difficulty performing familiar tasks •Problems with language •Disorientation regarding time or place •Impaired judgment •Problems with abstract thinking •Misplacing objects •Changes in mood or behavior •Changes in personality •Loss of initiative Processing of amyloid precursor protein enzyme B-secretase APP to form 2 peptides and through further process can form plaques what two key brain characteristics are present in alzheimers disease? beta-amyloid plaques neurofibrillary tangles which amyloid protein is soluble? a-APP what is the strongest risk factor for alzheimers? age what two enzymes terminate acetylcholine? ACheE, BuChe Rivistigmine (Exelon) twice daily with meals AChe, BuChe GI side effects NO HEPATOTOXICITY no drug to drug interactions bc not metabolized by CYP450 available in a transdermal patch what dementia medication must be taken 4x daily? tacrine Tacrine (Cognex) * Cholinesterase Inhibitors * 1st to be approved by FDA. * Treats mild to moderate AD. * Improves functioning and slows progression. * NO longer used for Dementia due to HIGH frequency of side effects: elevated liver levels gastrointestinal effects liver toxicity Donezepil (Aricept) cholinesterase inhibitor once daily AChE only Galantamine once-daily, extended release AChE only what medications would you use for mild-mod dementia/alzheimers? what classification are all these medications? donepezil, galantamine, rivastigamine cholinesterase inhibitors what medication would you give for moderate to severe alzheimers? memantine NMDA receptor agonist How do cholinesterase inhibitors work? The make acetylcholine more available by inhibiting enzymes from breaking it down. acetylcholine helps neurons communicate How does Memantine (Namenda) work? blocks excessive extrasynaptic activity of N-methyl-D-aspartate (NMDA) it is non-competitive, and low affinity binds to magnesium site when it is open blocks the downstream release of glutamate by acting as a "plug" at the NMDA receptor site How does Donepezil (Aricept) work? It increases acetylcholine concentrations at receptor sites and inhibits acetylcholinesterase present in both central and peripheral nervous system in the CNS, acetylcholine can help with cognition in the gut/perihperal, causes GI side effects has a very long half life (once daily administration) How does rivastigmine work? inhibits AChE and BuChe RENALLY excreted How does Galantamine treat Alzheimer's disease? allosterically potentiating ligand that modulates nicotinic receptors to increase acetylcholine release as well as acetylcholine inhibitor what part of the brain circuit is responsible for impulsivity and reward? ventral striatum what part of the brain circuit is responsible for compulsivity and motor response? dorsal striatum what neurotransmitter is essential to the reward circuit? dopamine What pathway is responsible for the reward response? mesolimbic - VTA to NA what is the action of alcohol in the VTA? what receptors does it act on? acts on mu receptors- releases endogenous opioids acts on VSCCs- inhibits glutamate release enhances GABA release how does acute alcohol use affect medications? increases liver enzymes, which increases rate of metabolism how does chronic use of alcohol effect medications? causes liver damage which impairs metabolism How does naltrexone work? By blocking opioid receptors this blocks the reward of drinking dont use in liver patients How does acamprosate work? works on GABA and glutamate pathway and is very effective in maintaining abstinence in dependent drinkers even in severe cases dont use in renal patients How does Disulfiram (Antabuse) work? if someone drinks, causes build up of acetyldehyde in system which causes very unpleasant effects of alcohol what is an important consideration when prescribing naltrexone? patient must be completely free of opioids can be given IM what effect do hallucinogenics have on 5ht2a receptors? agonism How does nicotine work? It Directly Stimulate Dopaminergic Neurons heading to the Nucleus Accumbens. long term stimulation of receptors leads to desensitization- where no longer react to nicotine as receptors resensitize, they initiate craving and withdrawal receptors will upregulate to compensate, which can increase cravings further What SSRI should be avoided in pregnancy? Paxil - cardiac and congenital abnormalities what 3 medications carry risk of congenital malformation to fetus? lithium, carbamazepine, valproate what medication carries risk of neurotube defects? valproate if you are going to taper off paroxetine (paxil) what must you remember? taper slowly if a patient is taking paxil while pregnant, what additional test should be ordered? ultrasound to monitor for fetal malformations what factors could affect drug absoprtion and distribution in the elderly? increased total body fat, decreased lea muscle, decreased total body water, decreased GI motility what might affect drug metabolism in the elderly? decreased hepatic mass, decreased hepatic flow - results in reduced first-pass metabolism what factors might impair elimination of medications in the elderly? decreased cardiac output, decreased flow to kidneys, decreased renal clearance - increased elimination half life what second-generation antipsychotic has the most efficacy for treating aggression in to the elderly? risperidone What are the 4 ADHD symptoms and their associated brain regions? - Inattention, selective: dorsal anterior Singulet - inattention, sustained: dorsolateral PFC - hyperactive: prefrontal motor cortex - impulsive: orbitofrontal cortex what loop or brain circuit is responsible for hyperactivity and impulsivity? CSTC what symptoms of ADHD does too little NE and DA cause? distraction, forgetful, fatigue what types of symptoms does too much NE and DA cause? mania, psychosis what is the mechanism of action for amphetamine? - Competitively inhibit dopamine transporter - Works on VMAT o Taken up into dopamine terminal o Packaged into vesicles o Displaces dopamine into terminals - DIRECT release what is the mechanism of action of methylphenidate? Blocks dopamine and norepinephrine transporter Does not get taken up by transports - No direct release, just more availability what med class might help most with hyperactivity, but not as much with inattention? alpha 2 a agonist clonidine, guanfacine clinidine has more side effects (sedation, hypotension, dry mouth" what twp types of dementia have TAU pathophysiology? alzheimers, frontotemporal what is the pathology of lewy body demenita? Alpha-synuclien what type of dementia is prion related? cruetzfeldt jacobs what are the signs and symptoms of alzheimers? Memory deficit Aphasia Apraxia Agnosia Dementia with Lewy Bodies (DLB) signs and symptoms dementia involving visual hallucinations, cognitive fluctuations, and atypical movements Memory deficit Fluctuating attention Extrapyramidal signs Psychosis (hallucinations) **Rapid eye movement/sleep issues*** Frontotemporal Dementia Frontal and temporal regions degenerate, resulting in badly impaired emotional stability, decision-making and language use Memory deficit Speech/language disorders Disinhibition **Hyperorality*** Huntington's disease symptoms Genetic disorder that causes progressive deterioration of brain cells. caused by a dominant allele. symptoms do not appear until about the age of 30. Memory deficit Executive dysfunction Chorea Creutzfeldt-Jakob disease symptoms Fatal infection; neurological symptoms include trembling Memory deficit Ataxia Myoclonus Language disturbance What breaks down acetylcholine? acetylcholinesterase BuCHE what alzheimers medication causes the most GI upset? Rivastigmine Peripheral blockade why do dementia medications cause GI issues? Cholinergic activity- parasympathetic what part of the brain is responsible for reward? amygdala what part of the brain is responsible for memory? hippocampus what part of the bottom-up mechanism is responsible for for impulsivity and reward pathways? ventral striatum what part of the bottom-up mechanism is responsible for for compulsivity and motor? dorsal striatum what part of the brain is top-down and what does it do? PFC, disinhibition what pathwa does dopamine cause reinforcement and reward? mesolimbic VTA-- nucleaus accumbens How does the ETOH affect VTA stimulate dopamine release? 1. Directly acts on opiate receptors causing release of endogenous opiates which releases dopamine 2. Acts on glutamate receptors; calcium channels, inhibits glutamate release, affects dopamine 3. Enhances GABA release, direct/indirect what are alcohols effects on GABA and glutamate? increases GABA, decreases glutamate if someone abruptly stops drinking, how does this affect GABA and glutamate? decrease GABA, increase glutamate (opposite of its normal effects) what receptor does nicotine bind to? where? alpha 4 beta 2 receptor VTA is amphetamine or methylphenidate transported into neurons via dopamine transporter? amphetamine What is the clinical significance of the difference in mechanism of action of methylphenidate vs. amphetamine? - At high doses, amphetamine can cause rapid release of dopamine into the synapse, which may be linked to euphoria what are two stimulants? amphetamine, methylphenidate Both regulate the activity of dopamine and norepinephrine what typeof modulator is methylphenidate? allosteric how does methylphenidate work? - Binds to dopamine and norepinephrine transporter o Allosteric modulator § Binds to neurotransmitter at a different site than the neurotransmitter binds o Stops the action of the transporter, which blocks the reuptake of the neurotransmitter o Not taken up into presynaptic neuron How does amphetamine work? Amphetamine makes synaptic vesicles containing dopamine "leaky," so dopamine pours into the cytoplasm. It also reverses the transporter, driving dopamine into the synapse - Blocks the transporters for dopamine and norepinephrine o Pseudo substrate and competitive inhibitor § Binds to same site as dopamine or neurotransmitter, and competes- this prevents reuptake o Transported into presynaptic nerve terminal o VMAT binding, which further blocks dopamine o High doses of amphetamine can cause displacement of stored dopamine and norepinephrine which can push into presynaptic terminal § Can cause "dumping" of dopamine and "euphoria" what system do stimulants suppress? limbic how do stimulants effect emotions? blunting what ADHD medication doesnt have negative impact on emotions? strattera Guanfacine alpha 2 agonist activates executive system Vyvanse (lisdexamfetamine) -Stimulant Tx for ADHD -SE: dry mouth, loss of appetite, insomnia, weight loss, dizziness, irritability, n/v/d -Black Box warning for abuse and dependence what patients should avoid adderall? - Avoid with heart disease, glaucoma, history of addiction Adderall amphetamine/dextroamphetamine - Activates and speeds up brain o Faster and higher rate of communication between neurons o Increases dopamine (reward system) § Increased risk of addiction - Monitor: BP, pulse, height/weight - Side effects: difficulty sleeping, weight loss, dry mouth - XR lasts 12 hours; IR 4-6 hours ADHD + DE/NA Dopamine: Reward, risk, impulsiveness Norepinephrine: Attention, arousal Biomarkers for Alzheimer's - Amyloid-beta accumulation - Neuronal degeneration/injury o Elevated CSF tau - Decreased fluorodeoxyglucose uptake - Atrophy in the hippocampus an temporoparietal regions what type of dementia are DELUSIONS common in? alzheimers what is a defining feature of dementia lewy body? visual hallucinations what type of dementia is at risk for developing extra pyramidal symptoms? DLBa MOA of Amantadine symmetrel: The mechanism of action in PD is poorly understood but animal studies suggest either that it induces release or decreases reuptake of dopamine. Screening labs vs. diagnostic screening = asymptomatic diagnostic = Symptoms -- seeking diagnosis Primary Prevention aimed at preventing illness and disease (usually in the history interview portion) strategies include: - healthy diet and exercise - ideal body weight - safe sexual practices - seatbelt use etc. Secondary Prevention Identifying disease at the earliest stage - biometrics - thorough musculoskeletal and cardiovascular exam - Screening tests (eg. duck walk for osgood schlatter, adam forward bend for scoliosis) *Aspirin is only recommended as secondary prevention* tertiary prevention actions taken to contain damage once a disease or disability has progressed beyond its early stages - referral to PT for positive duck walk found to have osgood schlatter When to screen for colonoscopy ages 45-75 every 10 years When to do a PAP 21 -29 every 3 years 30-65 every 5 years with HPV co-testing When to do a mammogram biannually age 50-74 (age 40 if first degree relative) When to screen for lung cancer age 50-80 with 20 pack year smoking history (or quit within the last 15 years) When to screen for AAA ultrasound men 65-75 who have ever smoked (1 time screening) when to do a dexa scan 65+ or sooner if increased risk using a risk calculator ( low BMI, ETOH, cigarettes, steroids, hx of fractures in the last year) - once every two years When to start statins: age 40-75 with at least one CVD risk factor and 10% ASCVD risk factor when do patients qualify for bariatric surgery BMI40 (non-diabetics) BMI 35 (diabetics) What are drusen spots small, round, yellow-white spots on the outer retina, scattered and diffuse - Protein and fat deposits in eye (fundoscopic exam) yellow spots Papilledema swelling and inflammation of the optic nerve at the point of entrance into the eye through the optic disk (due to increased ICP --- most commonly from HTN*** - cloudy moon **Not a sharp disk macular degeneration central vision loss most common type of oral cancer squamous cell carcinoma (tongue) most common type of skin cancer basal cell carcinoma Asthma Treatment SABA are no longer 1st tier ICS/formoterol are first line (if using both use albuterol first then ICS) ICS = Budesonide - Rinse mouth after ICS - Severe asthma exacerbations = ORAL Steroids NEW treatment regiment ICS/SABA combination use as a rescue inhaler only Step 1/2 - ICS/formoterol as needed Step 3 - ICS/formoterol: Routine maintenance Step 4 - ICS/Formoterol: Medium dose maintenance Step 5 - ICS/formoterol and ADD on LAMA Is the Asthma controlled?? 1. daytime asthma symptoms more than 2x/wk? 2. Night time wakings with asthma. 3. SABA use for symptoms more than 2x/wk 4. Any activity limitation due to asthma well controlled = None of these partly controlled = 1-2 of these uncontrolled = 3-4 of these homeless people screen for HEP, TB, HIV *TB will show cavitation on an x-ray chest x-ray reporting consolidation = pneumonia physical exam findings: diminished lung sounds, tactile fremitus, dull percusion Cavitation emptiness inside a consolidation (gas bubbles = necrotic tissue) could be inside a nodule/mass What diagnosis would you consider for an IV drug user with fatigue, wt loss, fever? endocarditis, HIV/TB Stable Angina myocardial oxygen demand is greater than myocardial oxygen supply - provoked by exertion and relieved by rest and hnitro -typically lasting minutes prinzemetals angina coronary artery vasospasms - atypical pattern - wakes people up between midnight and 6am Unstable angina new onset, increase in frequency, intensity or duration - OR occurs at rest RED flags for GERD cough sore throat wt loss physical complaints/signs of gall bladder disease RUQ pain, (Fair, fat, forty, female, fertile- pregnancy, - can be caused by rapid weight loss - + murphy's sign Diverticulitis LLQ pain, point tenderness, bloating, diarrhea, constipation - population: ETOH, chronic constipation, 45, IBS Celiac disease constipation, diarrhea, wt loss, anemia/malabsorption - more CONSTANT, vague, -- doesnt come and go as much common causes of malabsorption PPI use, chronic pancreatitis Bacterial prostatitis fever, pain, bloody, pus - painful orgasm, rectal bleeding - more systemic symptoms - tender prostate treat with antibiotics for 4-6 weeks BPH difficulty peeing (sitting helps) no pain urinary retention Tests to use with knee instability Lachmans/anterior drawer: ACL (hold leg up under thigh, pull tibia forward Knee locking?? Meniscus Rheumatoid arthritis on an x-ray looks like: erosive soft tissue swelling, joint space narrowing and osteoporosis osteoarthritis on an x-ray spur growth, nodules, hypertrophic back pain and x-ray looks like spine is self-fusing` AKYLOSING SPONDOLITIS: HLA-B27 - treated by breaking back and inserting rods/screws Cushings vs Addisons cushings: increased cortisol, buffalo hump/abnormal hair - personality changes/mood swings - edema/swelling - diagnosed with early morning cortisol testing - delayed puberty - short, central wt gain Cushings vs ADDISONS Addisons = Decreased cortisol - anorexia, abd pain, wt loss - mood swings/ personality changes - muscle wasting, shrinking - autoimmune - ACTH levels (dexamethasone challenge test Risk factors for pancreatic cancer 40, wt gain, obesity, smoking, occupational chemical exposure, diabetes #1 cause of death worldwide Metastatic liver cancer Risks for liver cancer chronic hep, cirrhosis, ETOH, obesity, - increased risk for farmers due to mold on grains and corn Thalassemia Hemolytic anemia due to a defect in hemoglobin formation - decreased or absent production of hemogloboin, microcytic anemia, improper oxygen transportation and destruction of RBC - leads to mild or severe microcytic or hypochromic anemia - 2 types beta and alpha Hereditary Spherocytosis changed shape of RBC/Sphere, decreased life span - Spleenomegaly (splenectomy) - anemia - hyperbilirubinemia - increase folate consumption NSAIDS and any inflammatory bowel disease can cause: malabsorption Anemia of chronic disease treat with ERYTHROPOETIN - best treatment - usually have chronic kidney disease what to test for with an HIV positive patient HEP, STI --*PAP smear* what is the best treatment for cystic acne? ACUTANE - to limit scarring how do you treat acne rosacea doxycycline, glucocorticoids, retinoids * NOT benzyl peroxide* what vitamin is most often associated with neuropathies and parasthesias? B12 deficiency what med is preferred for HTN with the presence of osteoporosis calcium channel blockers (amlodipine) What are the common migraine triggers? NITRATE containing foods (hot dogs) MSG and tyramine foods hormone changes stress medications: vasodilators, oral contraceptives excessive/insufficient sleep smoking exposure to bright florescent lights fasting/skipping meals strong odors head trauma, weather changes motion sicknes cold stimulus lack of exercise Right sided heart failure 1. Jungular Vein Distention 2. Ascending Dependent Edema (pitting) 3. Weight Gain 4. Hepatomegaly (Liver Enlargement) 5. Ascites lethargic, nausea Left sided heart failure 1. Pnea, SOB 2. Crackles/rales 3. Oliguria 4. Frothy Sputum 5. Displaced Apical Pulse (Hypertrophy) - increased HR - orthopnea - cough - wt gain hyperthyroidism graves, POSTPARTUM, goiter, drugs, thyroid nodules - wt loss, nervousness, dyspnea, intolderance to heat, palpitations, tachycardia, restlessness - thyroid enlargement best screening in the office for alzheimers/dementia mini mental exam what tests confirms HIV? Western blot - elisa = screening -- if positive -- confirm with western blot Type 1 hypersensitivity IgE mediated hypersensitivity Ex: Allergies, drug allergies Type 2 hypersensitivity Cytotoxic ANTIBODY mediated cell destruction Ex: Autoimmune hemolytic anemia BLOOD TRANSFUSIONS Type 3 hypersensitivity immune complex mediated RA, lupus, erythematosus Type 4 hypersensitivity reaction T-cell dependent like contact dermatitis, TB, Leprosy, GVHD Allergic contact dermatitis Mid-systolic click with late systolic murmur mitral valve prolapse aortic stenosis murmur "mid-systolic ejection murmur best heard at the 2nd right intercostal space" - lub whoosh - radiates to carotid artery and apex - (sepsis) Syncope Angina Dyspnea aortic regurgitation early diastolic murmur (best heard over the apex) - rolling R after dub regurg = raptor = roaring - best heard on expiration with patient sitting forward - lub dub rrrr Mitral stenosis murmur Diastolic RUMBLE with opening snap. LOW frequency= Rumble mid diastolic murmur (between lub and dub) (no sound of silence) APEX = loudest here, use bell, patient lying in Left lateral position flushed cheeks Most common symptom of renal stenosis hypertension Hematuria and proteinuria = glomerular nephritis or injury Hep C testing HCV antibody = positive if ever exposed to HEP C HCV RNA = assess the viral load ( + = active infection, - = no active infection) If HCV antibody positive and RNA negative - infected but but cleared spontaneously or treated - antibody test may be false + Cauda equina syndrome damage to bundle of spinal nerves coming out of the bottom of spine (could be caused by large lumbar disc herniation) S/S: decreased bowel and bladder control - decreased sexual function - saddle anesthesia - 1 or both legs/knees weakness/paraplegia confirm with MRI ---- surgical decompression in 48 hours what medication should all patients with CHF be on SGLT-2 (flozins) canagiflozin, dapagliflozin, empagliflozin what meds to avoid with heart block? avoid blocking - calcium channel blockers and beta blockers BLOCKERS NO BLOCKING