NURS 6501: Final Exam:
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Question 1
Which of the following is classified as a connective tissue disease?
Group of answer choices
- Systemic lupus erythematosus
- Granulomatosis with polyangiitis
- Psoriasis
- Osteoarthritis
- Systemic lupus erythematosus (SLE) is an autoimmune disease that affects connective tissues, leading to inflammation in multiple organs, including the skin, joints, kidneys, and more.
- Granulomatosis with polyangiitis (GPA) is a type of vasculitis (inflammation of blood vessels), not primarily a connective tissue disease.
- Psoriasis is an autoimmune condition primarily affecting the skin (a keratinocyte disorder, not connective tissue).
- Osteoarthritis is a degenerative joint disease, primarily affecting cartilage (a connective tissue), but it is not classified as a systemic connective tissue disease like SLE.
- Formal operational stage
- Concrete operational stage
- Preoperational stage
- Sensorimotor stage
- Symbolic thought (using words, images, and pretend play to represent objects).
- Make-believe play (engaging in imaginative and fantasy activities).
- Egocentrism (difficulty seeing others' perspectives).
- Sensorimotor stage (0–2 years): Infants learn through sensory experiences and motor actions (no symbolic thought yet).
- Concrete operational stage (7–11 years): Children develop logical thinking about concrete events but struggle with abstract concepts.
- Formal operational stage (12+ years): Abstract and hypothetical thinking emerges.
- Stepwise deterioration in cognitive function
- Presence of neurofibrillary tangles and amyloid plaques
- Early development of hallucinations and parkinsonian features
- Insidious onset with slow, progressive cognitive decline
- Stepwise deterioration: Cognitive decline occurs in a staircase-like pattern, with sudden worsening after vascular events (e.g., strokes) followed by periods of stability.
- Neurofibrillary tangles and amyloid plaques: These are hallmarks of Alzheimer’s disease, not vascular dementia.
- Hallucinations and parkinsonian features: These are more typical of Lewy body dementia.
- Insidious onset with slow, progressive decline: This describes Alzheimer’s disease, not the abrupt changes seen in vascular dementia.
- Ribosome
- Reverse transcriptase
- Protease
- Integrase
- Reverse transcriptase – Converts viral RNA into DNA (a process called reverse transcription).
- Ribosome: Host cell machinery for protein synthesis, not viral enzyme.
- Protease: Cleaves viral polyproteins into functional proteins during maturation.
- Integrase: Inserts viral DNA into the host genome (works after reverse transcription).
- Increased white blood cells
- Trichomonads
- Clue cells
- Pseudohyphae
- Pseudohyphae (elongated, branching filamentous structures)
- Budding yeast cells
- Increased white blood cells (WBCs): More suggestive of bacterial vaginosis or trichomoniasis, though mild inflammation can occur in candidiasis.
- Trichomonads: Motile, flagellated protozoa seen in trichomoniasis, not candidiasis.
- Clue cells: Epithelial cells coated with Gardnerella vaginalis bacteria, diagnostic for bacterial vaginosis, not yeast infections.
- A rational fear that leads to avoidance of certain situations
- An occasional feeling of nervousness that arises in response to stressful events and resolves quickly
- A temporary increase in stress levels during significant life changes, such as starting a new job
- Intense, frequent, and irrational episodes where thoughts become erratic and the mind races uncontrollably
- Irrational and uncontrollable anxiety (not just rational fear or situational stress).
- Persistent symptoms (not occasional or short-lived).
- Cognitive effects (racing thoughts, difficulty concentrating, catastrophizing).
- Rational fear leading to avoidance: More aligned with specific phobias (a subset of anxiety disorders), but not the broad definition of pathological anxiety.
- Occasional nervousness resolving quickly: Normal stress response, not an anxiety disorder.
- Temporary stress during life changes: Adjustment disorder or normal stress, not chronic anxiety.
- Associated with fever and jaw claudication
- Gradual onset over several days
- Severe, often described as the worst headache of one’s life
- Intermittent and unilateral, typically in the temporal area
- Sudden, explosive ("thunderclap") headache—patients often describe it as "the worst headache of my life."
- Peak intensity within seconds to minutes (not gradual onset).
- Associated symptoms: Neck stiffness (meningismus), nausea/vomiting, photophobia, or loss of consciousness.
- Fever and jaw claudication: Seen in temporal arteritis (giant cell arteritis), not SAH.
- Gradual onset over days: Suggests tension-type headache or migraine, not SAH.
- Intermittent and unilateral temporal pain: Classic for migraine or cluster headache, not SAH.
- Generalized anxiety disorder
- Agoraphobia
- Social anxiety disorder
- Panic disorder
- Fear/anxiety about two or more of the following:
- Public transportation
- Open spaces (e.g., parking lots, bridges)
- Enclosed spaces (e.g., stores, theaters)
- Crowds or standing in line
- Being outside the home alone
- Avoidance of these situations due to fear of panic-like symptoms or inability to escape.
- Generalized anxiety disorder (GAD): Excessive worry about many everyday things, not situational avoidance.
- Social anxiety disorder: Fear of social scrutiny (e.g., embarrassment), not open spaces or crowds per se.
- Panic disorder: Recurrent panic attacks may lead to agoraphobia, but the question describes avoidance behaviors (not just panic attacks).
- Retrovirus
- Double-stranded DNA virus
- Double-stranded RNA virus
- Single-stranded RNA virus
- Virus type: HSV is a double-stranded DNA virus (family Herpesviridae).
- Transmission: Sexual contact or direct mucosal/skin exposure.
- Symptoms:
- Clusters of painful vesicles that ulcerate and crust over.
- May include prodromal tingling, itching, or burning.
- Recurrent outbreaks possible due to viral latency in nerve ganglia.
- Retrovirus (e.g., HIV): Causes systemic immunosuppression, not localized vesicular lesions.
- Double-stranded RNA virus (e.g., rotavirus): Primarily causes gastroenteritis.
- Single-stranded RNA virus (e.g., HCV, influenza): Not associated with genital vesicular rashes.
- Social anxiety disorder
- Generalized anxiety disorder
- Major depressive disorder
- Separation anxiety disorder
- Excessive fear/anxiety about separation from attachment figures (parents, caregivers).
- Physical symptoms (headaches, stomachaches, nausea) in anticipation of separation.
- Avoidance behaviors (refusing to go to school, clinginess).
- Duration: Symptoms persist for ≥ 4 weeks in children.
- Social anxiety disorder: Fear revolves around social scrutiny (e.g., embarrassment in class), not separation.
- Generalized anxiety disorder (GAD): Excessive worry about multiple topics (e.g., grades, friendships), not just separation.
- Major depressive disorder: Would include symptoms like anhedonia, low mood, or fatigue—not just situation-specific anxiety.
- Pregnancy
- Diabetes
- Oral contraceptives
- Menopause
- Pregnancy – Increased estrogen levels raise glycogen in vaginal secretions, promoting yeast growth.
- Diabetes (poorly controlled) – High glucose levels in vaginal secretions feed yeast.
- Oral contraceptives – Higher estrogen levels alter the vaginal environment.
- Antibiotic use – Disrupts normal vaginal flora (e.g., lactobacilli).
- Immunosuppression (e.g., HIV, corticosteroids).
- Postmenopausal women have lower estrogen levels, leading to a thinner, less glycogen-rich vaginal epithelium, which is less favorable for Candida overgrowth.
- Vaginal atrophy in menopause increases susceptibility to bacterial vaginosis or atrophic vaginitis, not typically candidiasis.
- Syncope
- Migraine aura
- Seizure
- Hypertension
- Syncope – Brief loss of consciousness due to cerebral hypoperfusion (can resemble TIA if accompanied by transient weakness).
- Migraine aura – Reversible neurologic symptoms (e.g., visual changes, paresthesias) that may mimic TIA.
- Seizure – Postictal Todd’s paralysis can appear like a TIA.
- Hypoglycemia – Can cause focal neurologic deficits.
- Peripheral vestibular disorders (e.g., BPPV) – May mimic vertebrobasilar TIA.
- While hypertension is a risk factor for stroke/TIA, it does not directly cause transient focal neurologic deficits.
- Severe hypertension may lead to hypertensive encephalopathy (global confusion, headache), but this is a diffuse process, not focal like TIA.
- Histrionic personality disorder
- Antisocial personality disorder
- Avoidant personality disorder
- Paranoid personality disorder
- Cluster A (Odd/Eccentric):
- Paranoid, Schizoid, Schizotypal
- Cluster B (Dramatic/Emotional/Erratic):
- Antisocial, Borderline, Histrionic, Narcissistic
- Cluster C (Anxious/Fearful):
- Avoidant, Dependent, Obsessive-Compulsive
- Social inhibition due to fear of rejection/criticism.
- Feelings of inadequacy and hypersensitivity to negative evaluation.
- Avoids interpersonal interactions despite a desire for connection (unlike Schizoid PD).
- Histrionic (Cluster B): Excessive emotionality and attention-seeking.
- Antisocial (Cluster B): Disregard for others’ rights, impulsivity, deceitfulness.
- Paranoid (Cluster A): Distrust and suspicion of others’ motives.
- Chlamydia trachomatis
- Ureaplasma urealyticum
- Mycoplasma genitalium
- Neisseria gonorrhoeae
- Neisseria gonorrhoeae – A Gram-negative diplococcus that is intracellular (often seen inside neutrophils).
- Chlamydia trachomatis: Causes non-gonococcal urethritis (NGU) with mucoid/purulent discharge, but no organisms are seen on Gram stain (obligate intracellular, requires PCR/NAAT).
- Ureaplasma urealyticum & Mycoplasma genitalium: Also cause NGU but are too small to visualize on Gram stain (no cell wall).
- Long-standing hypertension
- Cerebral amyloid angiopathy
- Hemorrhagic transformation of an ischemic stroke
- Rupture of a cerebral aneurysm
- Location: The basal ganglia (especially the putamen) is the most common site of hypertensive hemorrhage.
- Risk Factors:
- Poorly controlled hypertension (major risk factor).
- No history of trauma/anticoagulants (rules out traumatic hemorrhage or coagulopathy-related bleeding).
- Absence of Alternative Causes:
- Cerebral amyloid angiopathy (CAA): Typically causes lobar hemorrhages (cortical/subcortical) in older adults, not deep structures like basal ganglia.
- Hemorrhagic transformation of ischemic stroke: Usually occurs days after ischemia, not as an initial presentation.
- Cerebral aneurysm rupture: Leads to subarachnoid hemorrhage (SAH), not intraparenchymal hemorrhage in the basal ganglia.
- Reduced testosterone levels leading to prostatic tissue scarring
- Increased smooth muscle relaxation in the bladder neck
- Increased cortisol levels causing prostate tissue shrinkage
- Hyperplasia and hypertrophy of prostatic tissue leading to urethral compression
- Hyperplasia (↑ cell number) and hypertrophy (↑ cell size) of prostatic stromal and epithelial cells in the transition zone of the prostate.
- This enlarges the prostate, compressing the prostatic urethra, leading to:
- Increased post-void residual volume (incomplete bladder emptying).
- Obstructive symptoms (weak stream, hesitancy, urinary retention).
- Reduced testosterone levels causing scarring: BPH is not caused by low testosterone; it’s linked to dihydrotestosterone (DHT) stimulation of prostate growth.
- Increased smooth muscle relaxation in the bladder neck: BPH involves increased smooth muscle tone (α1-adrenergic mediated), not relaxation.
- Increased cortisol causing prostate shrinkage: Cortisol does not shrink the prostate; BPH is driven by androgens (DHT) and aging.
- DHT (derived from testosterone via 5α-reductase) promotes prostate growth.
- α1-adrenergic receptors in the prostate increase smooth muscle tone, worsening obstruction.
- Amygdala
- Basal ganglia
- Hippocampus
- Cerebellum
- Hippocampus – A key structure for memory, emotion regulation, and stress response.
- Prolonged cortisol exposure leads to hippocampal atrophy (shrinking) via:
- Neuronal apoptosis (cell death).
- Reduced neurogenesis (decreased BDNF).
- Prolonged cortisol exposure leads to hippocampal atrophy (shrinking) via:
- Amygdala: While hyperactive in depression (contributing to fear/anxiety), it is less vulnerable to cortisol-induced atrophy.
- Basal ganglia: More associated with motor control/reward processing; atrophy here is linked to Parkinson’s, not depression.
- Cerebellum: Primarily involved in motor coordination; not a primary target in depression.
- Menstrual phase
- Luteal phase
- Ovulatory phase
- Follicular phase
- Occur during the luteal phase (the 1–2 weeks before menstruation).
- Resolve shortly after menstruation begins (menstrual phase).
- Follows ovulation (ovulatory phase).
- Dominated by progesterone (and some estrogen) secretion from the corpus luteum.
- In PMDD, sensitivity to hormonal fluctuations (especially progesterone metabolites) triggers:
- Mood swings, irritability, depression, anxiety.
- Physical symptoms (bloating, fatigue).
- Follicular phase (post-menstruation to ovulation): Generally asymptomatic in PMDD.
- Ovulatory phase (~day 14): Brief estrogen surge; not typically linked to PMDD symptoms.
- Menstrual phase (bleeding): Symptoms improve during/after menses.
- Elderly individuals
- Men who have sex with men
- Postmenopausal women
- Heterosexual teenagers
- Men who have sex with men (MSM), particularly those with multiple partners, HIV coinfection, or inconsistent condom use.
- Congenital syphilis has also risen sharply, but the question focuses on incidence (new cases), which is highest in MSM.
- Elderly individuals: Syphilis is uncommon in this group (though underdiagnosis occurs).
- Postmenopausal women: Very low incidence; hormonal changes reduce sexual activity/risk.
- Heterosexual teenagers: Gonorrhea/chlamydia are more prevalent; syphilis is rarer in this group.
- MSM account for ~50% of primary/secondary syphilis cases in the U.S.
- HIV coinfection further increases risk due to overlapping risk behaviors.
- Inflammatory response due to autoimmune disease
- Degeneration of joint cartilage
- Deposition of urate crystals
- Accumulation of calcium pyrophosphate crystals
- Urate crystal deposition (monosodium urate crystals) in the joint, triggering a neutrophil-driven inflammatory response.
- Sudden, excruciating pain (often waking the patient at night).
- First metatarsophalangeal (MTP) joint is most common, but ankle, knee, or other joints can be affected.
- Risk factors: Male sex, older age, dietary purines (red meat, alcohol), obesity, diuretic use.
- Autoimmune inflammation (e.g., rheumatoid arthritis): Typically causes symmetrical polyarthritis, not sudden monoarthritis.
- Cartilage degeneration (osteoarthritis): Gradual onset, no redness/heat, and less severe pain.
- Calcium pyrophosphate (CPP) crystals (pseudogout): Usually affects the knee or wrist, not the ankle; associated with older age and metabolic disorders.
- Joint aspiration showing negatively birefringent needle-shaped crystals (urate) under polarized microscopy.
- Increased bone formation due to excessive activity of osteoblasts
- Autoimmune attack on bone marrow cells
- Abnormal deposition of collagen fibers in bone
- Reduced bone mass due to increased osteoclast activity and decreased bone formation
- Increased osteoclast activity: Excessive bone resorption.
- Decreased osteoblast activity: Reduced bone formation (often due to aging, estrogen deficiency, or calcium/vitamin D insufficiency).
- Imbalance in bone remodeling: Resorption outpaces formation.
- Increased bone formation (osteoblast activity): Occurs in Paget’s disease, not osteoporosis.
- Autoimmune attack on bone marrow: Seen in multiple myeloma or rheumatoid arthritis, not osteoporosis.
- Abnormal collagen deposition: Occurs in osteogenesis imperfecta (brittle bone disease), not typical osteoporosis.
- Postmenopausal women (estrogen loss → ↑ osteoclasts).
- Aging (↓ osteoblast function).
- Glucocorticoid use (↓ bone formation).
- The presence of a headache predominantly on the left side indicates the tumor is also on the left side of the brain.
- The initial evaluation is with imaging.
- Elevated intracranial pressure induced by a tumor does not result in headaches.
- There is a specific, classic headache pattern associated with brain tumors.
- "The initial evaluation is with imaging."
- This is accurate. When a brain tumor is suspected, neuroimaging (such as MRI or CT scan) is the first step in evaluation. MRI with contrast is the gold standard for detecting brain tumors.
- "The presence of a headache predominantly on the left side indicates the tumor is also on the left side of the brain."
- False. Headache location does not reliably localize the tumor. Brain tumor headaches are often diffuse and caused by increased intracranial pressure (ICP) rather than direct tumor location.
- "Elevated intracranial pressure induced by a tumor does not result in headaches."
- False. Increased ICP from a tumor commonly causes headaches, often worse in the morning or with Valsalva maneuvers.
- "There is a specific, classic headache pattern associated with brain tumors."
- False. While some features (e.g., morning headaches, worsening with straining) may suggest a tumor, there is no single classic pattern. Headaches from brain tumors vary widely.
- Thyroid-stimulating hormone
- Electroencephalogram
- Magnetic resonance imaging of the brain
- Erythrocyte sedimentation rate
- Thyroid-stimulating hormone (TSH) – To assess for hyperthyroidism, which can present with anxiety, tachycardia, and tremors.
- Electroencephalogram (EEG): Only indicated if seizure activity (e.g., temporal lobe epilepsy) is suspected.
- MRI of the brain: Reserved for cases with focal neurologic deficits or concern for structural abnormalities (e.g., tumor).
- Erythrocyte sedimentation rate (ESR): A nonspecific marker of inflammation; not useful for anxiety workup unless autoimmune/infectious causes are suspected.
- It occurs suddenly and is the worst headache of the patient's life.
- It is associated with fever, stiff neck, and a decreased level of consciousness.
- It is typically throbbing, initially unilateral in the temporal area, and may become bilateral.
- It is often associated with neurological deficits and an altered level of consciousness.
- Throbbing headache localized to the temporal region
- Unilateral onset, often becoming bilateral
- Scalp tenderness (especially when combing hair)
- Jaw claudication (pain while chewing)
- Visual disturbances (e.g., transient or permanent vision loss)
- Elevated ESR/CRP
- Autosomal dominant with complete penetrance
- X-linked recessive
- Polygenic with variable expressivity
- Mitochondrial inheritance
- Polygenic: Multiple genes contribute to the risk of developing OCD.
- Variable expressivity: Even among individuals with genetic susceptibility, symptoms can vary widely in severity and presentation.
- Influenced by environmental factors: Stress, trauma, and infections may interact with genetic predisposition.
- Autosomal dominant with complete penetrance would mean a single gene mutation always causes OCD, which is not the case.
- X-linked recessive would show a specific gender-linked pattern, which is not observed in OCD.
- Mitochondrial inheritance would involve maternal transmission only, which is not a recognized pattern for OCD.
- Disseminated intravascular coagulation (DIC)
- Deficiency of ADAMTS13 enzyme
- von Willebrand Disease
- Hemophilia B
- Severe deficiency of ADAMTS13 enzyme (due to autoantibodies or genetic mutation).
- This leads to uncleaved ultra-large von Willebrand factor (vWF) multimers, causing microthrombi in small vessels.
- Microangiopathic hemolytic anemia (MAHA) occurs due to RBC shearing by fibrin strands.
- Disseminated intravascular coagulation (DIC):
- Also causes thrombocytopenia + schistocytes, but typically occurs in sepsis, trauma, or malignancy (not spontaneous).
- Lab findings include prolonged PT/aPTT, low fibrinogen, and elevated D-dimer (unlike TTP).
- von Willebrand Disease (vWD):
- Causes mucocutaneous bleeding but not thrombocytopenia or schistocytes.
- Hemophilia B:
- Presents with joint/muscle bleeding (not bruising/petechiae) and prolonged aPTT, but normal platelets and RBC morphology.
- ADAMTS13 activity <10% confirms TTP.
- Treatment: Plasma exchange (PLEX) is urgent to remove autoantibodies and replenish ADAMTS13.
- Mycoplasma genitalium
- Ureaplasma urealyticum
- Neisseria gonorrhoeae
- Chlamydia trachomatis
- Chlamydia trachomatis (obligate intracellular bacterium, not visible on Gram stain).
- Mycoplasma genitalium is another cause but is less common than Chlamydia.
- Neisseria gonorrhoeae:
- Causes purulent discharge with Gram-negative intracellular diplococci on Gram stain.
- Ureaplasma urealyticum:
- A rare cause of NGU but not as common as Chlamydia.
- Mycoplasma genitalium:
- Increasingly recognized but still less prevalent than Chlamydia in NGU.
- NAAT (PCR) testing is the gold standard to confirm Chlamydia or Mycoplasma.
- Empirical treatment for NGU:
- Azithromycin 1g single dose (covers Chlamydia) or
- Doxycycline 100mg BID x 7 days (also covers Mycoplasma).
- Men in their late 30s
- Adolescents of both sexes
- Elderly women
- Women in their early 20s
- Late childhood to early adolescence (peaking around 10–12 years old).
- A smaller second peak occurs in early adulthood (20s–30s).
- Neurodevelopmental factors: OCD is linked to prefrontal-striatal-thalamic circuit dysfunction, which often manifests during brain maturation in adolescence.
- Puberty-related hormonal changes may trigger symptoms.
- Early-onset OCD is more common in males, but by adulthood, the sex ratio equalizes.
- Men in late 30s / Women in early 20s: Less typical for new-onset OCD (though adult-onset occurs).
- Elderly women: OCD rarely develops de novo in this group (more likely exacerbation of preexisting symptoms).
- 22 years
- 25 years
- 15 years
- 18 years
- Frontal lobe myelination: Continues into the early-to-mid 20s.
- Synaptic pruning: Refinement of neural connections lasts until around age 25.
- Risk-taking vs. impulse control: Adolescents and young adults (teens to early 20s) exhibit higher risk-taking behaviors due to immature PFC.
- 15 years: The brain is still undergoing significant changes (e.g., puberty-related hormonal effects).
- 18 years: While legal adulthood begins, cognitive and emotional regulation networks are not fully matured.
- 22 years: Close, but some studies suggest full maturation extends slightly beyond this age.
- Higher vulnerability to addiction, mental health disorders, and poor judgment before full maturation.
- Educational and policy decisions (e.g., age limits for alcohol, military enlistment) often consider this timeline.
- Thrombopoietin
- von Willebrand factor
- Factor VIII
- Tissue factor
- Tissue factor (exposed on subendothelial cells) binds Factor VII, forming the TF-VIIa complex.
- This activates Factor X → Xa, leading to thrombin (IIa) generation and fibrin formation.
- von Willebrand factor (vWF): Mediates platelet adhesion (primary hemostasis), not coagulation cascade initiation.
- Factor VIII: A cofactor for Factor IX in the intrinsic pathway, but not the initiator.
- Thrombopoietin: Stimulates platelet production in bone marrow; unrelated to acute clotting.
- The extrinsic pathway (TF-driven) is the physiologically relevant trigger in vivo.
- The intrinsic pathway (activated by contact with collagen/negatively charged surfaces) is less critical for normal clotting.
- Thrombotic Thrombocytopenic Purpura
- Disseminated intravascular coagulation
- Hemophilia A
- von Willebrand Disease
- Hemophilia A (Factor VIII deficiency), an X-linked recessive disorder (thus predominantly affects males).
- Prolonged aPTT (normal PT and platelet count).
- Severity correlates with Factor VIII levels:
- Severe (<1% activity): Spontaneous bleeding.
- Moderate (1-5%): Bleeding after minor trauma.
- Mild (5-40%): Bleeding only after surgery/major injury.
- Thrombotic Thrombocytopenic Purpura (TTP): Causes thrombocytopenia + microangiopathic hemolysis, not joint/muscle bleeding.
- Disseminated Intravascular Coagulation (DIC): Acquired condition with diffuse thrombosis/bleeding, not hereditary.
- von Willebrand Disease (vWD): Causes mucocutaneous bleeding (e.g., epistaxis, menorrhagia) but rarely hemarthrosis (unless severe Type 3).
- Low Factor VIII activity with normal vWF levels.
- Post-traumatic stress disorder
- Generalized anxiety disorder
- Panic disorder
- Medication-induced anxiety disorder
- Medication-induced anxiety disorder (substance/medication-induced anxiety in DSM-5).
- Stimulants (e.g., methylphenidate, pseudoephedrine).
- Bronchodilators (e.g., albuterol).
- Corticosteroids (e.g., prednisone).
- Opioids (e.g., tramadol—also has SNRI effects).
- SSRIs/SNRIs (initial activation syndrome).
- Generalized anxiety disorder (GAD): Requires chronic, excessive worry (not acute onset).
- Panic disorder: Recurrent unexpected panic attacks, not linked to medication.
- PTSD: Requires a traumatic stressor, not medication use.
- Stabilization in height and weight
- Rapid increase in height and weight and appearance of secondary sexual characteristics
- Weight gain primarily in the form of adipose tissue followed by linear growth
- Earlier growth spurt for boys compared to girls
- Growth spurt: Rapid increase in height (linear growth) and weight (due to muscle and bone growth).
- Secondary sexual characteristics:
- Girls: Breast development (thelarche), pubic hair (adrenarche).
- Boys: Testicular enlargement, pubic hair.
- Stabilization in height/weight: Occurs in late adolescence after growth plates fuse.
- Weight gain as adipose tissue first: Seen in girls during pre-puberty, but not the defining feature of early adolescence.
- Earlier growth spurt in boys: False—girls typically start their growth spurt 1–2 years earlier than boys.
- HSV primarily causes lesions in the frontotemporal region of the brain.
- HSV can become latent and reside within nerve ganglia, leading to potential recurrences.
- HSV infection heals within two to three weeks and never recurs.
- HSV infection in pregnant women always results in vertical transmission to the newborn.
- HSV-1: Typically establishes latency in the trigeminal ganglion (oral herpes).
- HSV-2: Typically establishes latency in the sacral ganglia (genital herpes).
- "HSV primarily causes lesions in the frontotemporal region of the brain":
- While HSV can cause herpes encephalitis (most common in the temporal lobe), this is rare and not a defining feature of typical HSV infections.
- "HSV infection heals within two to three weeks and never recurs":
- False—HSV lesions heal, but the virus remains dormant and can reactivate.
- "HSV infection in pregnant women always results in vertical transmission":
- False—Transmission risk is highest during primary HSV infection near delivery, but not guaranteed.
- Antivirals (e.g., acyclovir) can suppress recurrences but do not eliminate latency.
- Neonatal HSV is a severe complication but preventable with C-section if active lesions are present at delivery.
- Platelets are almost immediately destroyed by the autoimmune process.
- Platelet transfusions can worsen the thrombocytopenia.
- IVIG and steroids directly increase platelet production.
- Platelets can induce an allergic reaction.
- IVIG:
- Blocks Fc receptors in the spleen/liver, preventing platelet destruction.
- Provides a rapid but temporary rise in platelet count (within 24–48 hours).
- Steroids (e.g., prednisone):
- Suppress antibody production and reduce splenic clearance of platelets.
- Slower onset but more sustained effect than IVIG.
- Platelet transfusions:
- Not first-line because transfused platelets are quickly destroyed by the same autoimmune process.
- Reserved for severe bleeding (e.g., intracranial hemorrhage).
- "Platelet transfusions worsen thrombocytopenia": Incorrect—they don’t exacerbate the disease but are ineffective due to rapid destruction.
- "IVIG/steroids directly increase production": No—they reduce destruction (bone marrow production is usually normal in ITP).
- "Platelets induce allergic reactions": Rare and unrelated to ITP pathophysiology.
- TIAs involve permanent brain injury.
- TIAs usually last more than one hour.
- TIAs are caused by bleeding in the brain.
- TIAs usually resolve within a short period without infarction.
- TIA:
- Neurologic deficits resolve completely (typically within <1 hour, though by definition <24 hours).
- No acute infarction on imaging (diffusion-weighted MRI is the gold standard to rule out small infarcts).
- Stroke:
- Permanent infarction occurs (visible on imaging).
- Symptoms persist beyond 24 hours (though most strokes are evident much sooner).
- "TIAs involve permanent brain injury": False—this defines a stroke, not a TIA.
- "TIAs usually last >1 hour": False—most resolve within 60 minutes (though the formal cutoff is 24h).
- "TIAs are caused by bleeding": False—TIAs are ischemic (due to temporary clot/hypoperfusion); bleeding causes hemorrhagic stroke.
- TIA is a medical emergency—10-15% risk of stroke within 90 days (highest in first 48h).
- ABCD2 score helps stratify risk and guide urgent evaluation (e.g., carotid imaging, anticoagulation for AF).
- Neuromyelitis optica (Devic disease)
- Multiple sclerosis
- Acute demyelinating encephalomyelitis (ADEM)
- Neurosarcoidosis
- CD4+ and CD8+ T-cell infiltration targeting myelin in the brain/spinal cord.
- Episodic relapses (in relapsing-remitting MS) with plaques visible on MRI.
- Th1/Th17-driven autoimmunity against myelin proteins (e.g., MBP, PLP).
- Neuromyelitis optica (NMO/Devic disease):
- Antibody-mediated (anti-AQP4 IgG) pathology (B-cell/plasma cell predominant).
- Targets astrocytes, not just myelin.
- Acute disseminated encephalomyelitis (ADEM):
- Monophasic (typically post-infectious), not recurrent.
- Neurosarcoidosis:
- Non-caseating granulomas (macrophage/T-cell mix), not purely T-cell-driven demyelination.
- Frequent episodes of intense fear occurring only in social situations
- Avoidance of situations that cause panic or where panic might be expected to occur
- Excessive anxiety and worry occurring more days than not for at least 6 months
- Recurrent panic attacks that are exclusively triggered by exposure to specific phobic objects or situations
- Avoidance Behavior:
- Patients avoid places/situations where panic attacks occurred (e.g., crowds, public transport) due to fear of being trapped or helpless.
- This leads to social isolation, job loss, or inability to leave home.
- Panic Attacks:
- Recurrent, unexpected episodes of intense fear (peaking within minutes) with physical symptoms (e.g., palpitations, sweating, derealization).
- Attacks are not exclusively triggered by phobic objects (that would indicate a specific phobia).
- "Frequent fear only in social situations": Suggests social anxiety disorder, not panic disorder.
- "Excessive anxiety for ≥6 months": Fits generalized anxiety disorder (GAD), not panic disorder.
- "Panic attacks triggered by phobic objects": Describes specific phobia, not panic disorder (which involves unexpected attacks).
- Amitriptyline
- Sumatriptan
- Acetaminophen
- Ibuprofen
- Amitriptyline (a tricyclic antidepressant, TCA).
- Mechanism:
- Modulates central pain pathways (serotonin/norepinephrine reuptake inhibition).
- Reduces headache frequency and severity (not just acute relief).
- Dosing:
- Low doses (e.g., 10–75 mg nightly) are typically effective.
- Evidence:
- Supported by guidelines (e.g., AAN, ICHD-3) as first-line prophylaxis.
- Sumatriptan: A 5-HT1B/1D agonist for acute migraine attacks (not TTH prophylaxis).
- Acetaminophen/Ibuprofen: Used for acute pain relief in TTH but not preventive therapy (risk of medication-overuse headache).
- Behavioral therapy (e.g., relaxation training, biofeedback) is equally effective but may not be preferred by all patients.
- Migraine disorders
- Alzheimer disease
- Multiple sclerosis
- Parkinson disease
- Demyelination of trigeminal nerve fibers in the pons (a common MS plaque location).
- Neurovascular compression (classic TN) is more common, but MS-related TN tends to be:
- Bilateral (vs. unilateral in classic TN).
- Younger onset (classic TN typically occurs after age 50).
- Migraine disorders: TN is not a migraine symptom (though migraine and TN can coexist).
- Alzheimer’s/Parkinson’s diseases: These are neurodegenerative and do not typically cause TN.
- Sharp, unilateral pain often mistaken for cluster headache
- Throbbing headache, commonly associated with nausea and vomiting
- A dull, bilateral ache with no focal deficit, possibly with a diminished level of consciousness
- Severe headache with photophobia and stiff neck
- Dull, bilateral headache (due to vascular stretching and autoregulatory dysfunction).
- No focal neurologic deficits (distinguishing it from hypertensive encephalopathy or stroke).
- Possible altered mental status (if BP is extremely high, e.g., >180/120 mmHg).
- Sharp, unilateral pain (cluster headache-like): Suggests trigeminal autonomic cephalalgias or migraine, not hypertension.
- Throbbing headache with nausea/vomiting: Classic for migraine or malignant hypertension (if + papilledema/renal injury).
- Severe headache + photophobia/stiff neck: Indicates meningitis or subarachnoid hemorrhage, not hypertensive urgency.
- Writing full sentences
- Pouring liquids without spilling
- Catching a bounced ball reliably
- Hopping on one foot
- Gross motor skills:
- Hops on one foot (2–4 times).
- Catches a bounced ball most of the time.
- Fine motor skills:
- Pours liquid with minimal spilling.
- Copies simple shapes (e.g., circle, cross).
- Writes some letters or numbers (but not full sentences).
- Pouring liquids without spilling: Achieved by age 4–5 (with practice).
- Catching a bounced ball: Expected by age 4.
- Hopping on one foot: Typically mastered by age 4.
- 10-20%
- 90-100%
- 60-70%
- 30-40%
Correct Answer: 30–40%
Why This Range?
- Studies Show ~30–40% Transmission:
- A systematic review (Sexually Transmitted Infections, 2014) found the per-partner transmission risk for anogenital warts is ~30–40% over 6–12 months.
- Higher rates (60–70%) are often cited for any HPV infection (including subclinical), but visible warts transmit less frequently.
- Factors Reducing Transmission:
- Condom use lowers risk by ~50%.
- Intact skin barriers (no microtears) decrease inoculation.
- Host immunity clears many infections before warts develop.
- Why Not 60–70%?
- That range applies to HPV DNA detection (e.g., PCR-positive swabs), but visible warts represent a smaller subset of infections.
Key Point:
While HPV is highly contagious, the 30–40% range better reflects the risk of clinical genital warts (not just asymptomatic infection). Question 44 Which of the following describes a primary function of the prefrontal cortex (PFC) in relation to depressive symptoms, and what is the common alteration seen in depression? Group of answer choices- The PFC controls motor functions, and increased PFC activity is linked to anhedonia
- The PFC manages sleep cycles, and reduced PFC function leads to insomnia
- The PFC regulates appetite, and decreased PFC activity is associated with hyperphagia
- The PFC is involved in emotional regulation, and reduced PFC activity is associated with depressive symptoms
- Primary Function of PFC:
- Top-down control of limbic regions (e.g., amygdala) to modulate emotional responses.
- Dorsolateral PFC (dlPFC): Cognitive control (e.g., rumination).
- Ventromedial PFC (vmPFC): Emotional valuation and inhibition.
- Depression-Related Alterations:
- Reduced PFC activity (hypometabolism on fMRI/PET scans).
- Dysfunctional connectivity with limbic areas, leading to:
- Impaired emotion regulation.
- Rumination (linked to dlPFC deficits).
- Anhedonia (vmPFC-amygdala disconnect).
- Motor functions: Controlled by the motor cortex; PFC’s role is cognitive, not motor.
- Sleep cycles: Regulated by the hypothalamus, brainstem; PFC indirectly affects sleep via stress pathways.
- Appetite: Primarily modulated by the hypothalamus; PFC’s role is in decision-making (e.g., food choices).
- Antidepressants (e.g., SSRIs) and therapy (e.g., CBT) can normalize PFC activity.
- Transcranial magnetic stimulation (TMS) targets the dlPFC to improve depressive symptoms.
- Chlamydia trachomatis
- Staphylococcus aureus
- Mycoplasma genitalium
- Gardnerella vaginalis
- Chlamydia trachomatis (NAAT-positive in this case).
- Neisseria gonorrhoeae (ruled out by the negative NAAT).
- Chlamydia trachomatis is the #1 cause of PID in the U.S., often presenting with mild or subclinical symptoms.
- NAAT (PCR) is the gold standard for detecting Chlamydia.
- Untreated PID can lead to infertility, ectopic pregnancy, or chronic pelvic pain.
- Mycoplasma genitalium: An emerging cause of PID but less common than Chlamydia.
- Staphylococcus aureus: Associated with toxic shock syndrome or abscesses, not typical PID.
- Gardnerella vaginalis: Causes bacterial vaginosis (BV), not PID (though BV may increase PID risk).
- Empiric coverage for Chlamydia (e.g., doxycycline) + gonorrhea (e.g., ceftriaxone) is recommended, even if NAAT is negative for one pathogen.
- Primarily limited to joint inflammation and the skeletal system
- Encompass a group of disorders affecting the cardiovascular system due to autoimmune inflammation
- A heterogeneous group of disorders that can affect nearly every organ in the body, often characterized by inflammation and altered immune responses
- A diverse group of chronic disorders primarily characterized by inflammation, pain, and damage to joint structures only
- North America
- Sub-Saharan Africa
- Asia
- Europe
- Prolactin inhibits the release of gonadotropin-releasing hormone (GnRH)
- Prolactin decreases the production of progesterone
- Prolactin increases the release of FSH, leading to anovulation
- Prolactin stimulates excessive estrogen production
- No withdrawal bleeding
- Normal withdrawal bleeding
- Heavy menstrual bleeding
- Irregular bleeding unrelated to progesterone administration
- They typically affect both sides of the head.
- Onset of symptoms is typically gradual.
- Neurologic deficits, such as weakness or numbness, can occur.
- They are the most common type of headache.
- Pregnancy and the immediate post-partum period
- Use of anticoagulant medications
- Ear, Nose, and Throat (ENT) infections
- Hypercoagulable states
- Chronic liver disease and hereditary hemorrhagic telangiectasia
- Hemophilia A and Vitamin K deficiency
- Disseminated Intravascular Coagulation (DIC) and Immune Thrombocytopenic Purpura (ITP)
- von Willebrand Disease and scurvy
- Osteoarthritis
- Scleroderma
- Rheumatoid arthritis
- Systemic lupus erythematosus
- They are definitive indicators of the progression of Alzheimer disease.
- They are protective factors that prevent the progression of the disease.
- They are only found in the late stages of Alzheimer disease.
- They are associated with Alzheimer disease, but it's unclear whether they are a cause or a result of the disease.
- The use of classification and seriation while engaging with the environment
- The ability to solve problems using trial and error
- The application of logic to physical objects and abstract ideas
- The ability to understand that a word or object can stand for something else
- Accumulation of cholesterol crystals within the synovial fluid
- Deposition of calcium pyrophosphate dihydrate crystals in the synovium
- Immune complex deposition in the synovial lining of the joint
- Formation of monosodium urate crystals leading to neutrophil activation
- Resistance to easy bruising
- Skin thinning (atrophy)
- Striae (stretch marks)
- Telangiectasia (small, dilated blood vessels near the surface of the skin)
- Preoperational stage
- Formal operational stage
- Sensorimotor stage
- Concrete operational stage
- Recurrent and persistent thoughts experienced as intrusive and unwanted, and causing significant anxiety or distress
- Conscious worries about real-life problems that one can control but chooses not to
- Pleasurable fantasies that distract from everyday tasks and responsibilities
- Voluntary thought patterns that help to relieve anxiety caused by stress
- GPIIbIIIa crosslinks with fibrinogen.
- Fibrinogen is converted into fibrin by thrombin.
- Cross-linking of GPib on the platelet surface to exposed collagen via von Willebrand factor
- The platelets are activated and release their granules into the microenvironment.
- Using insect repellents, such as permethrin or DEET
- Checking for ticks after leaving a tick-infested area
- Wearing socks over pants
- Taking an antibiotic prophylactically before outdoor activities
- Increased consumption of platelets due to drug-induced vascular damage
- Direct bone marrow suppression leading to decreased platelet production
- Formation of drug-dependent antibodies that bind to and destroy platelets
- Impaired platelet function without affecting platelet count
- Early disseminated Lyme disease
- Early localized Lyme disease
- Early localized ehrlichiosis
- Early disseminated ehrlichiosis
- Progressive dementia, consistent with Alzheimer disease or similar disorder
- Acute onset, fluctuating course of cognitive impairment, consistent with delirium
- Chronic cognitive impairment, consistent with Parkinson dementia
- Chronic neurological disorder, consistent with vascular dementia
- Conjunctivitis and pneumonia
- Gastrointestinal infection
- Congenital heart defects
- Neonatal jaundice
- Ureaplasma urealyticum
- Neisseria meningitidis
- Mycoplasma genitalium
- Chlamydia trachomatis
- Reassure the parents that the weight is appropriate for the infant's age.
- Inform the parents that while the infant’s weight is below the expected milestone, it is not concerning.
- Suggest that the weight gain is ahead of the expected curve and counsel on potential overfeeding.
- Advise the parents that the infant is not gaining enough weight and further evaluation is needed.
- Nausea and vomiting are typical accompanying symptoms.
- Short duration of attacks, with peaks of five to ten minutes
- Pain described as deep, intense, and boring, typically around the orbital area
- More common in young adult men, often starting in their 30s
- Skeletal abnormalities and unusual skin pigmentation
- Rapid onset of fatigue and weakness
- High platelet count and increased hemoglobin
- Overproduction of red blood cells
- Its rapid movement and evasion mechanisms
- Its extremely thin diameter of 0.2 microns
- Its ability to be stained
- Its lack of a cell wall
- Impulsions
- Delusions
- Compulsions
- Obsessions
- First metatarsophalangeal joint, known as podagra
- Talocrural joint, known as talagra
- Acromioclavicular joint, termed acragra
- Tibiofemoral joint, referred to as gonagra
- Anemia
- Renal impairment
- Hypertension
- Thrombosis
- Platelets
- Erythrocytes
- Coagulation system
- Blood vessels
- Traumatic brain injury
- Ischemic stroke leading to hemorrhagic transformation
- Berry aneurysm in the Circle of Willis
- Acute hypertensive crisis
- 5%
- 50%
- 1%
- 20%
- Alexia: Inability to properly perceive written words
- Dysarthria: Slurred or stuttering speech due to motor weakness or incoordination
- Dysphagia: Inability to carry out learned motor tasks
- Apraxia: Inability to carry out learned motor tasks
- Recommend a developmental evaluation as this may indicate a delay in language milestones.
- Reassure that this is all within normal developmental limits.
- Encourage additional interactive play techniques since this demonstrates advanced development.
- Advise on interventions for delayed motor development, as block stacking should be mastered by now.
- Low purine diet
- Overhydration
- Increased excretion of uric acid
- Increased production of uric acid
- By stimulating the immune system to produce more uric acid
- By causing lysis of cells and subsequent release of purines
- By increasing the excretion of uric acid through renal tubular acidosis
- By disrupting the balance of pro-inflammatory and anti-inflammatory cytokines
- Morning stiffness lasting for hours
- Presence of Heberden's nodes
- Soft and tender joint swelling
- Symmetrical involvement of the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints
- Acrosin
- 5-alpha reductase
- Aromatase
- 21-hydroxylase
- Chancroid
- Human Papillomavirus (HPV)
- Syphilis
- Herpes Simplex Virus (HSV)
- Gradual onset of headache with photophobia and stiff neck
- Headache with abrupt onset that is diffuse and sometimes localized near the vertex
- Unilateral, sharp, and stabbing pain in the temporal region
- Throbbing headache accompanied by nausea and vomiting
- Gamma-aminobutyric acid (GABA)
- Serotonin
- Acetylcholine
- Glutamate
- A nodular and fixed prostate
- An enlarged, firm, and smooth prostate
- A tender, warm, and swollen prostate
- A nontender, soft, boggy prostate
- Hydrocele
- Inguinal hernia
- Hypospadias
- Epispadias
- Difficulty in initiating movements, along with tremors and stiffness
- Sudden loss of muscle control leading to falls, and memory loss
- Rapid deterioration of cognitive functions and loss of balance
- Rapid, involuntary movements primarily in the hands and feet
- Bradykinesia (difficulty initiating and performing movements)
- Resting tremor (typically seen in the hands or fingers)
- Muscle rigidity (stiffness in the limbs and trunk)
- Postural instability (difficulty maintaining balance, leading to falls).
- Associated symptoms of fatigue and myalgia
- Diffuse headache which develops over several days
- Fever and meningismus
- Altered level of consciousness and neurological exam abnormalities
- Fever and meningismus (neck stiffness, photophobia, and headache).
- Diffuse headache, often developing over several days.
- Associated symptoms like fatigue and myalgia (muscle aches).
- B-cells
- CD4 T-cells
- Macrophages
- Neutrophil precursor cells
- Huntington disease
- Chronic ethanol intoxication
- Parkinson disease
- Wilson disease
- Spontaneous bruising and bleeding, including oozing from venipuncture sites
- Isolated deep vein thrombosis with no bleeding
- Excessive clotting without any bleeding manifestations
- Prolonged bleeding following surgical procedures only
- Decreased pain with elevation of the testicle (Prehn's sign)
- Nausea and vomiting
- Absent cremasteric reflex
- High-riding testicle
- Carpometacarpal joints
- Proximal interphalangeal joints
- Metacarpophalangeal joints
- Distal interphalangeal joints
- Advise the parent that the toddler is likely experiencing failure to thrive and recommend nutritional intervention.
- Inform the parent that while the weight is below the expected percentile, it is not concerning if the toddler is following their growth curve.
- Suggest that the toddler's weight gain is excessive and provide counseling on diet modification.
- Reassure the parent that this is an expected weight gain for a toddler between 1 and 2 years of age.
- Decreased serum cortisol levels in the morning
- Decreased serum adrenocorticotropic hormone (ACTH) levels in the afternoon
- Elevated serum insulin-like growth factor 1 (IGF-1)
- Decreased serum thyroxine (T4) and elevated thyroid-stimulating hormone (TSH) levels
- History of chronic physical illness
- Family history of anxiety disorders
- Personal history of abuse or trauma
- Male sex
- Family history of anxiety disorders: Genetic predisposition plays a major role.
- Personal history of abuse/trauma: Childhood or adult trauma (e.g., physical, emotional, or sexual abuse) increases risk.
- Chronic physical illness: Conditions like COPD, diabetes, or chronic pain are linked to higher anxiety rates.
- Women are ~2x more likely than men to develop anxiety disorders (e.g., GAD, panic disorder).
- Possible reasons include hormonal fluctuations, societal pressures, and differences in coping mechanisms.
- 12 months of unprotected intercourse without conception
- 6 months of unprotected intercourse without conception
- 24 months of unprotected intercourse without conception
- 18 months of unprotected intercourse without conception
- <35 years old: 12 months of regular, unprotected intercourse without conception.
- ≥35 years old: 6 months (due to declining fertility with age).
- Evidence-Based Threshold:
- ~85% of couples conceive within 1 year of trying (if no fertility issues).
- After 12 months, evaluation for underlying causes (e.g., ovulatory dysfunction, tubal blockage, male factor) is recommended.
- Age Considerations:
- For women ≥35, evaluation begins at 6 months due to accelerated ovarian reserve decline.
- 6 months: Appropriate only for women ≥35.
- 18/24 months: Delays diagnosis and intervention unnecessarily in a 30-year-old.
- Stepwise cognitive decline
- Impaired visual-spatial coordination
- Motor symptoms of parkinsonism
- Impaired speech and language skills
- Language Deficits (Primary Progressive Aphasia, PPA):
- Nonfluent/agrammatic variant: Halting speech, grammar errors.
- Semantic variant: Loss of word/object meaning.
- Logopenic variant (less common in FTD, more Alzheimer’s-related): Word-finding pauses.
- Behavioral Variant FTD (bvFTD):
- Personality changes (apathy, disinhibition, compulsions).
- Preserved memory early on (vs. Alzheimer’s).
- Stepwise cognitive decline: Suggests vascular dementia.
- Impaired visual-spatial coordination: Seen in Alzheimer’s disease (parietal lobe involvement).
- Parkinsonism: Occurs in FTD with motor neuron disease (FTD-MND) or corticobasal degeneration, but not a hallmark of typical FTD.
- Evidence of overfeeding
- Normal physiological weight loss
- Possible dehydration requiring immediate intervention
- Indicative of failure to thrive
- Physiological weight loss:
- 5–7% loss of birth weight by day 3–4 of life (due to fluid shifts, meconium passage, and limited initial intake).
- Return to birth weight by day 10–14.
- This baby’s 5% loss by day 10 is normal (likely already stabilizing/gaining).
- Overfeeding: Newborns rarely overfeed; weight loss would be <3% if excess intake.
- Dehydration: Suspect if >10% loss, poor feeding, or dry mucous membranes.
- Failure to thrive: Requires persistent weight loss/growth faltering (not a single data point).
- Breastfed babies often lose slightly more (7–10%) but still normalize by 2 weeks.
- Intervene only if:
- Loss exceeds 10%.
- No regain by 2 weeks.
- Signs of dehydration (e.g., fewer wet diapers, lethargy).
