nbme 23 block 1 Flashcards
Anterior spinal artery occlusion–> Loss of motor function, pain, and temperature sensation below the lesion
Anterior cord syndrome–
Syringomyelia, trauma –> Motor deficits more pronounced in UPPER EXTREMETIES
Central cord syndrome-
Brown-Séquard syndrome is also known as _________??—> IPSILATERAL motor loss, CONTRALATERAL pain/temperature loss.
Hemicord syndrome-
Various localized conditions —–Does not fit broad neurological symptoms and blood findings.
Segmentary syndrome
Affects dorsal columns
Vitamin B12 deficiency: Causes subacute combined degeneration
Hyper segmented neutrophils: Key peripheral blood smear finding
Posterior cord syndrome
___________ and ________hormones (2) Addison’s disease Hyperpigmentation, hypotension, hyperkalemia.
Adrenocorticotropic hormone and cortisol
_____________ hormone Hypothyroidism Fatigue, weight gain, cold intolerance.
Thyroid-stimulating hormone/ TSH
________________–Leukemia, signs of bone marrow failure, abnormal cells on blood smear.
Acute myeloblastic leukemia
_______________–Vasculitis Palpable purpura, abdominal pain, arthralgia.
Henoch-Schönlein purpura
_________________________- Autoimmune thrombocytopenia Isolated thrombocytopenia WITHOUT THROMBOSIS
Immune thrombocytopenic purpura
__________________________Pentad: thrombocytopenia, hemolytic anemia, renal failure, neurologic symptoms, fever.
Thrombotic thrombocytopenic purpura TTP
__________________Decreased platelets, thrombosis
Timing: 5-10 days post-heparin initiation
Treatment: Discontinue heparin, alternative anticoagulation
Heparin-induced thrombocytopenia (HIT):
_____________ Proprioception for lower body Ataxia without spasticity or specific sensory loss.
Dorsal spinocerebellar
___________Proprioception and vibration for upper body Symptoms affecting upper extremities.
Fasciculus cuneatus
_____________ Pain and temperature sensation Loss of pain and temperature sensation
Spinothalamic
_________________Proprioception for lower body Ataxia without spasticity or specific sensory loss.
Ventral spinocerebellar
If you see a patient with MS presenting with loss of proprioception and vibration sense in the lower extremities, then think_________________ damage.
fasciculus gracilis
If you see quadriplegia, impaired horizontal eye movements, and dysarthria with vascular risk factors, then think _________syndrome and localize the lesion to the pons.
locked-in syndrome
________________stroke (area) or lesion Impaired respiration, heart rate, CN IX-XII dysfunction.
Medulla/Medullary stroke
_____________stroke or lesion Vertical gaze palsy, impaired consciousness
Midbrain stroke
_____________ lesion Movement disorders, not quadriplegia or gaze palsy.
Putamen/ Basal ganglia lesion
If you see uniformly decreased immunoglobulins and recurrent bacterial infections with a normal oxidative burst, then think _______________disease and look for absence of germinal centers in lymph nodes.
Common Variable Immunodeficiency (CVID)
______________ Would indicate a defect in neutrophil function such as Leukocyte Adhesion Deficiency (LAD), characterized by delayed umbilical cord separation and poor wound healing, not uniformly decreased immunoglobulins
Absent neutrophil chemotaxis
___________________: Suggestive of HIV/AIDS, which would present with opportunistic infections and failure to thrive, and would not typically have normal immunoglobulin levels.
Decreased CD4+ T-lymphocyte count
_______________: Associated with recurrent infections, particularly Neisseria infections, and specific complement tests would be abnormal.
Decreased complement concentrations
_______________ Characteristic of Chronic Granulomatous Disease (CGD), which would show an abnormal oxidative burst test.
Impaired intracellular bactericidal activities in neutrophils
______________________________
CVID is characterized by impaired B cell differentiation leading to hypogammaglobulinemia and recurrent infections. The absence of germinal centers reflects the lack of functional B cells producing antibodies, consistent with the uniformly decreased immunoglobulins observed.
Absence of Germinal Centers in Lymph Nodes
Absent neutrophil chemotaxis, Recurrent infections, delayed umbilical cord separation, poor wound healing.
Leukocyte adhesion deficiency
Decreased CD4+ T-lymphocyte count Opportunistic infections, failure to thrive, specific serological markers.
HIV/AIDS
Decreased complement concentrations Recurrent Neisseria infections, specific complement tests.
Complement deficiency (c5-c9)
Impaired intracellular bactericidal activities in neutrophils /Recurrent infections with catalase-positive organisms, abnormal oxidative burst test.
Chronic granulomatous disease
defect in BTK gene (bad tyrosine kinase)/ x-linked inheritance pattern –> no mature B cells so no germinal centers and cant give LIVE VACCINES
Brutons x linked agammaglobulinemia
Paraneoplastic syndrome often associated with small cell lung cancer
Lambert-Eaton Myasthenic Syndrome (LEMS):
Acetylcholinesterase —- Progressive muscle weakness that WORSENS with activity, NOT improves.
Myasthenia Gravis
Binding of acetylcholine on the POSTsynaptic membrane –> Progressive muscle weakness that WORSENS with activity, presence of anti-AChR antibodies.
Myasthenia Gravis
Direct depolarization of muscle fibers by Ca²⁺ —-> Myopathy with CONSTANT weakness, not improvement with repetitive testing.
Direct muscle damage or channelopathy
Postsynaptic membrane potential —->Progressive muscle weakness that worsens with activity, not improves.
Myasthenia Gravis
if you see muscle weakness that improves with repetitive testing, a history of smoking, and a hilar lung mass, then think _________ associated with small cell lung cancer and impaired presynaptic release of acetylcholine.
Lambert-Eaton Myasthenic Syndrome (LEMS)
_________Contraindicated in pregnancy due to its effects on fetal bone and teeth.
Bone and teeth: Primary targets of toxicity in the fetus.
Tetracycline
Ear— Ototoxicity Typically associated with _______________, not tetracycline.
aminoglycosides
Kidney Nephrotoxicity _______ and __________are more commonly associated with this.
Aminoglycosides and NSAIDs
Common in chronic renal failure
Secondary hyperparathyroidism:
____________retention: Due to decreased renal excretion
Phosphate
___________: Due to decreased renal activation of vitamin D and phosphate retention
Hypocalcemia
___________ Compensatory response to hypocalcemia and hyperphosphatemia
Elevated PTH
_______________: Leads to phosphate retention (↑ phosphate)
Chronic Renal Failure
_______________: Results from decreased renal production of 1,25-dihydroxyvitamin D (active vitamin D), which reduces calcium absorption from the gut.
Hypocalcemia
__________________ The parathyroid glands secrete more PTH in response to low calcium and high phosphate levels to maintain calcium levels.
Secondary Hyperparathyroidism:
Stellate Ganglion: Part of the ________________ nervous system
sympathetic nervous system
__________ Nervous System: Increases heart rate, dilates bronchi, inhibits glandular secretion, decreases peristalsis, and causes vasoconstriction.
Sympathetic nervous system
Heart Rate: Increases via stimulation of the ___________ nervous system
sympathetic nervous system
Bronchodilation: _______ stimulation relaxes the bronchi
sympathetic
Bronchoconstriction: ______ stimulation constrics the bronchi
Parasympathetic
Glandular Secretion: Decreases; ___________stimulation reduces secretions
sympathetic
Glandular Secretion: Increases; ___________stimulation reduces secretions
parasympathetic
Peristalsis: Decreases; ___________stimulation inhibits gastrointestinal motility.
sympathetic
Peristalsis: Increases; ___________stimulation increases gastrointestinal motility.
parasympathetic
Vasoconstriction: _________ stimulation typically causes vasoconstriction
sympathetic
___________ stimulation typically causes vasodilation
parasympathetic
Integral membrane proteins are anchored within the membrane primarily due to the _______ interactions between their nonpolar amino acid side chains and the hydrophobic tails of the phospholipids in the lipid bilayer.
hydrophobic
________________proteins are anchored within the membrane primarily due to the hydrophobic interactions between their nonpolar amino acid side chains and the hydrophobic tails of the phospholipids in the lipid bilayer.
integral membrane proteins
Hydrophobic Interactions: Integral membrane proteins have regions rich in _________ amino acids that interact favorably with the _____ lipid tails, anchoring the protein within the membrane.
hydrophobic; hydrophobic
Membrane Structure: The phospholipid bilayer of cell membranes has ________ heads facing the aqueous environment and __________tails facing inward, creating a _________ core.
hydrophilic; hydrophobic ; hydrophobic
____________: These proteins span the membrane, and their hydrophobic regions interact with the lipid bilayer, ensuring their stable insertion.
Integral Proteins
_____bonds stabilize protein structure but are not the primary anchoring mechanism for integral membrane proteins.
Disulfide bonds
Hydrogen bonds are not the primary interaction within the ________core of the membrane.
hydrophobic
Ionic bonds are not favored in the ____________ environment of the membrane core.
hydrophobic
β-pleated sheets are structural elements but do not primarily interact with the ______membrane core.
hydrophobic
____________These proteins can have transmembrane domains consisting of α-helices or β-barrels rich in hydrophobic amino acids.
Integral Membrane Proteins:
_____________: Typically composed of 20-25 hydrophobic amino acids forming an α-helix that interacts with the lipid bilayer.
Membrane-Spanning Regions
Function: ____________ serve various functions including transport, signal transduction, and enzymatic activity, necessitating stable anchoring within the membrane.
Integral proteins
Prostate cancer metastasis to the spine most commonly occurs via the _______________. This network of valveless veins allows for direct hematogenous spread of cancer cells from the prostate to the vertebral column.
vertebral venous plexus (Batson’s plexus).
_________ Provides a direct route for prostate cancer cells to metastasize to the vertebrae due to its valveless nature and direct communication with the pelvic venous plexus.
Vertebral Venous Plexus (Batson’s Plexus):
____________The primary mechanism for metastasis in prostate cancer, particularly to the spine.
Hematogenous Spread:
If you see prostate cancer with metastasis to the spine, think of the ________as the route of spread.
vertebral venous plexus
GABA A receptors are _________and do not mediate calcium entry for synaptic plasticity.
inhibitory
Glycine is an_______ neurotransmitter, not primarily involved in synaptic plasticity via calcium entry.
inhibitory
Metabotropic glutamate receptors do not directly mediate calcium entry; they act through _______________systems.
second messenger systems
_________mediate calcium entry and are crucial for synaptic plasticity in the visual cortex.
NMDA receptors
: Serotonin receptors are not primarily involved in synaptic plasticity via ________entry.
calcium entry
Inspiratory pause on right upper quadrant palpation –>_________, indicative of acute cholecystitis.
Murphy’s sign
Palpable gallbladder – Commonly seen in ___________, associated with pancreatic cancer.
Courvoisier’s sign
Periumbilical ecchymoses –>Associated with acute pancreatitis (__________)
Cullen’s sign
Rebound tenderness and guarding in the right lower quadrant —Indicative of ____________.
acute appendicitis
Tenderness of the epigastrium on palpation Can be seen in_____________ not specific for cholecystitis.
peptic ulcer disease or pancreatitis,
NSAID-Induced Gastric Ulceration: NSAIDs inhibit cyclooxygenase (COX), reducing ______ synthesis, which decreases gastric mucosal protection and leads to gastric ulcers.
prostaglandin
Misoprostol: A synthetic prostaglandin E1 analog used to prevent NSAID-induced gastric ulcers. Misoprostol acts on__________receptors to increase mucus and bicarbonate secretion and enhance mucosal blood flow.
prostaglandin E receptors
Clopidogrel Mechanism: Clopidogrel is an antiplatelet agent that inhibits the ____________on platelets. This prevents ADP-mediated activation of the GPIIb/IIIa receptor complex, which is essential for platelet aggregation.
ADP receptor (P2Y₁₂)
what drug changes the tertiary structure of fibrinogen?
NO drug- trap in answers
Enhancing cAMP-mediated inhibition of platelet thromboxane A₂ synthesis is which drug with what MOA?
Phosphodiesterase inhibition— Dipyridamole, Cilostazol
Increasing prostacyclin (PGI₂) biosynthesis in vascular endothelium-what drug with what MOA?
PGI₂ analog Epoprostenol
Preventing ADP-stimulated platelet activation ADP receptor (P2Y₁₂) inhibition -what drugs?
Clopidogrel, Prasugrel, Ticagrelor
Stimulating biosynthesis of cell adhesion molecules is MOA of what drug?
no drug-trick q
A serious fungal infection caused by a group of molds. It primarily affects immunocompromised individuals, especially those with diabetes mellitus, particularly when in diabetic ketoacidosis (DKA).
Mucormycosis:
Aspergillosis Incorrect: Common in immunocompromised patients but typically involves the ___________, not associated with black eschar in nasal mucosa.
lungs
Incorrect: Does not present with black eschar or proptosis; usually causes mucocutaneous or disseminated infections in severely immunocompromised patients. white not black lesions
Candidiasis
_______________incorrect: Common in certain geographic areas (e.g., Southwestern U.S.), typically presents with pulmonary symptoms, not black eschar.
coccidioidomycosis
Incorrect: Typically presents with meningitis or pulmonary symptoms in immunocompromised patients, not associated with black eschar or proptosis.
Cryptococcosis
Incorrect: Typically presents with pulmonary symptoms and is associated with bird or bat droppings; does not cause black eschar or proptosis.
Histoplasmosis
Correct: Black eschar, proptosis, and ophthalmoplegia in a patient with diabetic ketoacidosis are classic signs of mucormycosis.
Mucormycosis
This is a parasitic disease caused by the Leishmania species, typically transmitted by the bite of infected sand flies (Phlebotomus spp. or Lutzomyia spp.). The disease is endemic in parts of India.
Visceral Leishmaniasis (Kala-azar):
: The vector for Leishmania donovani, the causative agent of visceral leishmaniasis
Sand Fly
: Vector for Onchocerca volvulus (river blindness).
black fly
Vector for Loa loa (Loiasis).
deer fly
Incorrect: Not a common vector for systemic infections like kala-azar.
gnat
Correct: Vector for Leishmania donovani, causing visceral leishmaniasis
Sand fly
Incorrect: Vector for Trypanosoma brucei (African sleeping sickness)
Tsetse fly
If you see a patient with a sudden onset of cool, discolored limb with difficulty walking, think of an _____________causing acute limb ischemia.
embolic event
Ascorbic acid Incorrect: Vitamin C deficiency causes _____, not yellowing of the skin
scurvy
Folic acid deficiency causes____________
anemia, megaloblastic without peripheral neuropathy
Incorrect: Used to treat viral hepatitis,
Interferon alfa plus ribavirin
B1-Thiamine deficiency causes
beriberi,
deficiency causes various neurological symptoms, not yellowing of the skin.
Pyridoxine B6
If you see a patient, especially a child, with yellow-tinged skin and nonicteric sclerae, think of ________ and DIETARY causes.
carotenemia
Acute Gout Attack: The patient presents with a classic case of acute gouty arthritis, characterized by severe pain in the great toe (podagra) and the presence of negatively birefringent crystals on joint fluid analysis. treatment of choice?
indomethacin
Incorrect: Provides pain relief but does not address inflammation in gout.
Acetaminophen
Incorrect: Used for long-term uric acid reduction, not for acute attacks.-chronic not acute gout
Allopurinol
Correct: Effective for treating acute gout, especially in patients who cannot take NSAIDs
Colchicine
Incorrect: First-line for acute gout, but contraindicated due to the patient’s NSAID allergy.
Indomethacin
Incorrect: Used for chronic gout management by increasing uric acid excretion.
Sulfinpyrazone
if you see a patient with acute severe pain in the great toe, swelling, and negatively birefringent crystals in joint fluid, think of an acute gout attack.
Consider _____________for treatment if the patient has contraindications to NSAIDs.
colchicine
_______ These stones are associated with recurrent urinary tract infections (UTIs), particularly with urease-producing bacteria (e.g., Proteus, Klebsiella). The urease enzyme hydrolyzes urea to ammonia, increasing urine pH and leading to the formation of stones.
Struvite Stones (Magnesium Ammonium Phosphate Stones):
Suggests a chronic infection, often associated with struvite stones.
Recurrent Pyelonephritis:
Cloudy Urine and High pH: Alkaline urine is typical with ________stones due to the presence of ammonia. ph>7
struvite
Large Calculus: Struvite stones can grow large and form _____________ often requiring surgical removal or lithotripsy.
staghorn calculi,
______________ disrupts microtubule polymerization, not DNA crosslinking.
colchicine
_____________Incorrect: Both drugs affect microtubules, not DNA crosslinking.
Colchicine and vinblastine
____________ is a nucleoside analog that inhibits DNA polymerase, not crosslinking. Cyclophosphamide is correct.
Cytosine arabinoside
_______________Incorrect: Both drugs inhibit DNA synthesis by other mechanisms (thymidylate synthase inhibition and dihydrofolate reductase inhibition, respectively), not crosslinking.
Fluorouracil and methotrexate
________________________ Correct: Both are alkylating agents that interfere with DNA synthesis by crosslinking.
Lomustine and cyclophosphamide
If you see a question asking about drugs that interfere with DNA synthesis by crosslinking, think of alkylating agents such as _______________________
lomustine and cyclophosphamide
Asbestosis: This is a form of pneumoconiosis caused by inhalation of asbestos fibers, commonly seen in construction workers. It is characterized by interstitial fibrosis, which results in a __________lung disease pattern.
restrictive
Characterized by reduced lung volumes (decreased FVC) and normal or increased FEV1/FVC ratio.
Restrictive Lung Disease:
Decreased ________: Due to interstitial fibrosis, which impairs gas exchange.
DLCO
History and Physical Findings: The patient’s occupational history, bilateral diaphragmatic pleural plaques, and end-inspiratory crackles are indicative of __________.
asbestosis
FEV1/FVC: Decreased, FVC: Decreased, DLCO: Decreased Incorrect: This pattern is seen in _______________lung diseases.
obstructive lung disease
FEV1/FVC: Decreased, FVC: Decreased, DLCO: Normal Incorrect: _____________pattern with normal DLCO is atypical for asbestosis.
Obstructive
FEV1/FVC: Normal, FVC: Decreased, DLCO: Decreased Correct: Classic pattern of __________ lung disease due to interstitial fibrosis in asbestosis.
restrictive
FEV1/FVC: Normal, FVC: Decreased, DLCO: Normal Incorrect: __________ pattern without diffusion impairment, not typical for asbestosis.
Restrictive
FEV1/FVC: Normal, FVC: Normal, DLCO: Normal Incorrect: This indicates ______lung function, not consistent with the patient’s symptoms and findings.
normal lung function
If you see a patient with a history of construction work, progressive shortness of breath, end-inspiratory crackles, bilateral pleural plaques, and interstitial lung changes, think of asbestosis. Expect pulmonary function tests to show a _____pattern with decreased DLCO.
restrictive
This is the most common cause of hypothyroidism in iodine-sufficient areas. It is characterized by the autoimmune destruction of the thyroid gland, leading to the replacement of thyroid tissue with lymphoid tissue.
Hashimoto’s Thyroiditis:
Diffuse fibrosis of the thyroid parenchyma Incorrect: This is more characteristic of ______________
Riedel’s thyroiditis
________ is a rare chronic inflammatory disease of the thyroid gland. It is characterized by the replacement of normal thyroid tissue with dense fibrous tissue, which can extend into surrounding neck structures. This fibrosis can lead to a hard, fixed thyroid mass and symptoms of compression such as dysphagia, dyspnea, or hoarseness.
Key Features :
Dense fibrosis: Extensive fibrotic process replaces normal thyroid parenchyma.
Hyalinization: The fibrotic tissue often undergoes hyalinization, contributing to the hardness of the gland.
Compression symptoms: Due to the infiltration of fibrosis into surrounding tissues.
Rock-hard goiter: The thyroid gland feels very hard on palpation, often compared to a “woody” texture.
Riedel’s thyroiditis
Hyalinization and scarring of the thyroid parenchyma
reidels thyroiditis
Multiple giant cell granulomata throughout the thyroid parenchyma Incorrect: Seen in ______________
subacute granulomatous (De Quervain’s) thyroiditis.
Patchy areas of liquefaction necrosis in the thyroid parenchyma are characteristic features seen in ___________________
is a self-limited inflammatory thyroid disorder that often follows a viral upper respiratory infection. It is characterized by a painful, enlarged thyroid gland and typically presents with systemic symptoms such as fever and malaise.
Key Features
Granulomatous inflammation: Presence of granulomas with multinucleated giant cells.
Liquefaction necrosis: Areas of necrosis within the thyroid parenchyma, leading to patchy destruction of thyroid tissue.
Painful thyroid gland: One of the hallmark symptoms, often radiating to the jaw or ears.
Transient thyrotoxicosis: Followed by hypothyroidism and eventual recovery of thyroid function.
subacute granulomatous thyroiditis (De Quervain’s thyroiditis).
Replacement of thyroid parenchyma by lymphoid cells Correct: Characteristic finding in
hashimotos thyroiditis
If you see a patient with a goiter, signs of hypothyroidism (low T3 and T4, high TSH), and positive antithyroid antibodies, think of ___________ with replacement of thyroid parenchyma by lymphoid cells.
Hashimoto’s thyroiditis
This is a non-atherosclerotic, non-inflammatory vascular disease that causes abnormal growth within the wall of an artery. It most commonly affects the renal and carotid arteries and can lead to hypertension, especially in young women.
Key Features
Hypertension: Often severe and resistant to treatment, typically in young patients.
Renal Artery Aneurysm: can lead to aneurysms, stenosis, and dissection of the affected arteries.
“String of Beads” Appearance: On angiography, the renal arteries often show a characteristic “string of beads” appearance due to alternating areas of stenosis and aneurysmal dilation.
Fibromuscular dysplasia
Key Features: Typically occurs in older patients with a history of atherosclerosis. Causes renal artery stenosis but not usually aneurysms in young patients.
Atherosclerotic Renal Artery Disease:
Key Features: Involves calcification within the renal artery, usually secondary to chronic renal disease or hypertension, but not typically causing aneurysms in a young patient.
Calcific Nephrostenosis:
Key Features: A systemic necrotizing vasculitis affecting medium-sized arteries, often associated with Hepatitis B. Can cause aneurysms but presents with systemic symptoms like fever, weight loss, and muscle pain.
Polyarteritis Nodosa:
Key Features: Characterized by multiple renal cysts, hypertension, and renal insufficiency. Does not cause renal artery aneurysms.
Polycystic Kidney Disease:
Key Features: Characterized by multiple renal cysts, hypertension, and renal insufficiency. Does not cause renal artery aneurysms.
Clinical Approach
Diagnosis:
Angiography: To visualize the characteristic “string of beads” appearance.
Blood Pressure Monitoring: Severe hypertension is a common presentation.
Imaging: CT or MRI to detect aneurysms or stenosis.
Treatment:
Antihypertensive Therapy: To control blood pressure.
Percutaneous Angioplasty: For treating significant renal artery stenosis.
Surgery: In cases of severe aneurysms or complicated stenosis.
Polycystic Kidney Disease:
Pathophysiology
_____________Involves the abnormal growth of the smooth muscle and fibrous tissue in the arterial walls, leading to areas of stenosis and aneurysm formation.
Fibromuscular Dysplasia:
cyclophosphamide and some other chemo agents kill mitotic cells. which of the following cell compartments is most rapidly depleted during cyclophosphamide therapy?
granulocytes
_________ are essential components of the immune system, each with specialized functions in responding to infections and mediating inflammatory and allergic reactions. Understanding their roles and characteristics is crucial in diagnosing and managing various medical conditions, particularly infections, allergies, and hematologic disorders.
Granulocytes
what are the 3 granulocytes?
Basophils, Eosinophils, Neutrophils
what is the target of cyclophosphamide?
rapidly dividing cells
is an alkylating agent used in chemotherapy that targets rapidly dividing cells. Granulocytes, which include neutrophils, eosinophils, and basophils, are rapidly dividing cells and are highly susceptible to the effects of chemotherapeutic agents like cyclophosphamide.
Cyclophosphamide
Mechanism of Action:_____________cross-links DNA, preventing cell division, and is most effective against cells that are rapidly proliferating.
Cyclophosphamide
These cells have a high turnover rate and are produced in large quantities by the bone marrow. They are among the first cell types to be depleted during chemotherapy.
Granulocytes:
: One of the common side effects of cyclophosphamide and other chemotherapeutic agents is____________, leading to decreased production of all blood cell lines, particularly affecting granulocytes.
bone marrow suppression
